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which leads to vasoconstrictive effects, as well as endorphin release. The drug also
blocks sodium channels, resulting inlocal anesthesia and up-regulation of stimulating amino acids [31, 32]. This can cause a sympathomimetic symptom storm in
acute intoxication, with symptoms including hypertension, psychomotor agitation,
tachycardia, mydriasis, and pupillary dilation.
J. P. Gallagher et al.
Procedural Considerations
Acute intoxication can result in extreme blood pressure lability, which is compounded by anesthetic interactions. With severe variations in intraoperative blood
pressure, acutely intoxicated patients have higher rates of complications such as
cardiac arrhythmias, myocardial infarction, and intracranial hemorrhage [33, 34].
Hyperthermia and seizures can occur from CNS activation. There are multiple
pulmonary effects from chronic use, including bronchospasms, venous thromboembolisms, pneumothorax, diffuse alveolar hemorrhage, and eosinophilic pneumonia [35–38].
Upon cessation of use, withdrawal symptoms include hyper-somnolence,
depression, and profound fatigue. Some patients may also experience signicant
agitation in the withdrawal phase, which presents a challenge for those who remain
admitted postoperatively in emergency settings. Withdrawal can last between 2
and 4weeks, and more severe or prolonged symptoms are suggestive of increased
use [39].
Anesthetic Interactions
Ketamine and halothane should be avoided, given the increased risk of cardiac
arrhythmias and increased systemic vascular resistance [9, 27]. Etomidate administration is also associated with an increased risk of myoclonus, seizures, and hyperreexia and should be avoided, with propofol and thiopental generally considered
preferred agents for induction [27].
Extreme hypertension has been reported intraoperatively in patients with cocaine
use, which is thought to be related to anesthetic interactions as well as systemic
activation during surgery.
On the contrary, chronic use can result in the depletion of catecholamines,
and patients will rarely develop profound hypotension during procedures, requiring vasopressor support to maintain perfusion [23, 40, 41]. Patients with chronic
use are also at higher risk of developing agitation and psychomotor instability
that can require escalating doses of anesthetic to achieve adequate sedation
[35, 40].
Cocaine
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Perioperative Recommendations
Current guidance on preoperative screening for cocaine use is based on expert opinion.
Recommendations include avoiding general anesthesia in patients with signs of acute
intoxication due to CNS stimulation and risk for interactions with common anesthetics, especially for elective procedures. However, the half-life of cocaine is relatively
short at 60–90min, and the drug should be eliminated by 8h in most cases [3, 42, 43].
However, UDS testing can remain positive for up to 7days and cannot reliably guide
procedural timing in non-toxic patients. Studies have shown that non- toxic patients
with positive UDS have similar outcomes to their non-using counterparts [3, 43, 44].
In the absence of clear guidelines for procedural management, cases must be
managed individually with close monitoring in the postoperative setting to prevent
and manage possible hemodynamic instability, especially in cases of acute withdrawal [42]. It is reasonable to proceed with anesthesia in non-toxic patients who
present after 8h of ingestion with hemodynamic stability and without acute abnormalities on ECG or with CNS examination [9, 42].
In cases of trauma and emergent procedures in acutely intoxicated patients, caution should be exercised when prescribing beta-blockers, as this can precipitate
unopposed alpha-receptor stimulation. In cases with chronic use, patients may
experience hypotension due to catecholamine depletion, which can require vasopressor support if refractory to intravenous uids (Fig.8.2).
Preoperative Considerations
EKG
CNS exam
Perioperative Risks
Hypertension
Coronary spasm, arrhythmias
Hyperthermia
Seizures
Venous thromboembolism
Diffuse alveolar hemorrhage, bronchospasm
Increased anesthetic needs
Fig. 8.2 Procedural guidance with recent Cocaine use
Postoperative Considerations
Increased pain tolerance
Withdrawal symptoms -Hyper-somnolence, depression,
Procedural Timing
Proceed if non-toxic regardless of
UDS findings
Consider delay by 8 hours if toxic
Drugs to avoid:
Ketamine, halothane,
etomidate, B-blockers
fatigue
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J. P. Gallagher et al.
Methamphetamines
Physiologic Effects andPharmacodynamics
Methamphetamines are stimulants that can be used via inhalation, intravenous,
intranasal, or ingestion. They primarily promote norepinephrine release as an
indirect agonist but can also target dopamine and serotonin receptors [45]. Onset
and duration vary depending on the route of use. Timing to peak effect is less than
15min with intravenous and intranasal use and up to 3h when ingested [46–48].
Duration of intoxication can be up to 9–12h for all formulations, although typically longest when ingested orally. However, it can be detected much longer with
UDS, with up to 7–9days depending on the dose, route, and chronicity of use
[48, 49].
Intoxication is associated with a variety of CNS and peripheral effects. At lower
doses, intoxication causes increased attention, hyperfocus, and improved motor
coordination related to the effects of dopaminergic signaling [50, 51]. At increased
doses, patients can experience anxiety and paranoia, with up to 10% progressing to
acute psychosis when an overdose occurs [48, 52, 53]. With norepinephrine release
at higher doses, hemodynamic changes include tachycardia, tachypnea, and signicant hypertension [48]. Potential adverse events related to this include malignant
hypertension, risk of cardiac arrhythmias, and a signicant increase in non-ischemic
cardiomyopathy with chronic use. Patients are also at elevated risk of hemorrhagic
stroke due to hypertension [54–56]. Withdrawal symptoms can include fatigue,
impaired concentration, depression, and irritability. While the most signicant
symptoms occur in the rst 48–72 h, up to 25% of patients can have persistent
symptoms of depression for months after use [48].
Procedural Considerations
Results have been mixed in the operative setting regarding outcomes for patients
with a history of methamphetamine use who receive general anesthesia. Trauma
patients appear to have higher rates of perioperative cardiovascular complications,
higher incidence of ICU admissions requiring laparotomy, and higher rates of rhabdomyolysis [57]. They are also more likely to have intraoperative hypotension and
vasopressor requirements in a time-dependent manner where risk remains at 7days
from last use [58, 59]. However, these effects do not persist, and there appear to be
similar rates of mortality and hospitalization length in patients with prior use [60].
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In addition, for UDS-positive patients requiring emergent surgeries, it appears that
drug use plays a much smaller role in hemodynamic instability than factors such as
age and intravascular depletion [61].
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Anesthetic Interactions
Similar to cocaine, methamphetamines are stimulating agents, and acute intoxication can be associated with labile blood pressure and refractory intraoperative hyper
or hypotension. It is recommended to avoid anesthetics that can worsen tachycardia
and adrenergic stimulation.
Perioperative Recommendations
Current data suggests that patients who are acutely intoxicated with methamphetamines are at higher risk of signicant hypotension, as well as increased anesthetic requirements [61, 62]. They are also at increased risk for cardiac
complications in the perioperative and postoperative setting. Due to these risks, it
is reasonable to postpone surgeries for up to 48h in elective cases where patients
present acutely intoxicated. However, these assessments must be made clinically,
as UDS does not appear to be a reliable screening tool for acute intoxication. In
patients who are non- toxic with a positive UDS and>48h from most recent use,
they may tolerate proceeding with general anesthesia on a case-by-case basis.
Patients demonstrating signs of acute withdrawal postoperatively should be managed in an inpatient setting.
If a patient presents with acute intoxication and surgery cannot be delayed, there
are several intraoperative considerations. Providers should avoid physical restraints
due to the risk of agitation, muscle contractions, and risk of rhabdomyolysis or cardiovascular complications [57]. Chemical restraints with benzodiazepines can be
used, as well as rst-generation antipsychotics if agitation persists. Patients are initially at elevated risk for refractory hypertension, which may then progress to signicant hypotension as catecholamine depletion develops. These patients may
require treatment with vasopressor support [61]. There is also an increased risk of
coronary spasm with beta-blocker use, and they are not recommended in cases with
acute intoxication [63].
Finally, induction with succinylcholine can induce rhabdomyolysis and should
be avoided (Fig.8.3) [64, 65].
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J. P. Gallagher et al.
Preoperative Considerations
UDS not reliable
Perioperative Risks
Hypertension
Arrhythmias
Hyperthermia
Seizures
Rhabdomyolysis
Increased anesthetic needs
Increased pain tolerance
Postoperative Considerations
Avoid physical restraints – use antipsychotics and benzodiazepines for agitation
Withdrawal symptoms - depression, fatigue, irritability
Fig. 8.3 Procedural guidance with recent Amphetamine use
Acute intoxication: Delay 48 hr if elective.
Non-toxic with +UDS or chronic use: Proceed
Drugs to avoid:
succinylcholine
Procedural Timing
on a case-by-case basis.
B-blockers,
Opioids
Physiologic Effects andPharmacodynamics
Opioid analgesics act on multiple different opioid receptors in the central and
peripheral nervous system and range from medications with misuse potential,
including natural (morphine) and synthetic (fentanyl) compounds, to illicit drugs
(heroin). Potency varies signicantly by the compound, with heroin being 3–5 times
more potent than morphine and fentanyl up to 50–100 times more potent [66].
Opioids can be taken via intravenous, subcutaneous, ingestion, and inhalational
routes. The onset of action and duration of acute intoxication is dependent on the
formulation and route of ingestion and is difcult to generalize. Effects are derived
from targeting three opioid receptors (mu, kappa, delta), primarily in the central and
peripheral nervous system and the gastrointestinal tract [67].
Opiates primarily act as depressants, and symptoms of acute intoxication include
analgesia, euphoria, and delayed mentation. Withdrawal symptoms last up to 1week
and typically peak at 36–48h [68]. Symptoms can include severe nausea/vomiting,
anxiety, diaphoresis, rhinorrhea, malaise, and insomnia [69].
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Procedural Considerations
Patients may demonstrate miosis, slowed gastrointestinal motility, and respiratory
depression, which is the primary adverse outcome of overdose and can be fatal [70].
Patients are also commonly treated with a concomitant medication for opioid use
disorder, such as methadone, naloxone, or buprenorphine, and these must be managed during admission. Due to opioid tolerance with chronic use, patients may also
require increased doses of analgesia postoperatively, which can worsen outcomes
and increase the risk of worsening opioid use disorder [71–73]. Patients are also
more likely to be chronically ill, which also increases morbidity and mortality from
emergent or elective procedures [71].
Anesthetic Considerations
Patients with chronic opioid use have an increased association with spinal and
epidural infections, likely related to bacterial seeding with intravenous use
[74]. Chronic use can also result in cross-tolerance with other depressants and
anesthetics due to receptor down-regulation. Patients may also experience an
exaggerated pain response postoperatively, requiring increased analgesia
[9, 27].
Perioperative Recommendations
Patients using opioids must rst be assessed for chronicity of use and opioid prescriptions. Those with acute intoxication should be evaluated for respiratory
depression and hemodynamic instability. Patients with lethargy or hypoventilation require emergent intervention and procedural delay. Chronic use requires
considerations for likely increased sedation needs intraoperatively, as well as
increased postprocedural analgesia compared to opioid naïve patients. These
cases are best managed with the assistance of pain specialists to incorporate multimodal approaches with opioid and non-opioid pain management strategies.
These can include local anesthetic blocks, ketamine infusions, and non-pharmacologic support [75]. They may also benet from opioid agonist therapy or weaning opioid doses to prevent withdrawal while admitted [73]. In patients with acute
intoxication requiring emergent intervention, patients are at elevated risk for pulmonary edema, hypoxia, and aspiration due to delayed gastric emptying
(Fig.8.4) [9].
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J. P. Gallagher et al.
Preoperative Considerations
Consider pain specialist care for multimodal
approach to perioperative nerve blockade and post-
operative analgesia
Hypoxia, pulmonary edema, aspirate
Postoperative Considerations
Withdrawal symptoms – Nausea/vomiting, anxiety, diaphoresis, rhinorrhea, malaise,
Perioperative Risks
Increased anesthetic needs
Drugs to avoid: depressants
Increased pain tolerance
insomnia
Procedural Timing
Proceed if non-toxic
Acute intoxication: Airway support
Fig. 8.4 Procedural guidance with recent Opioid use
Alcohol
Physiologic Effects andPharmacodynamics
Alcohol misuse is a leading cause of preventable death worldwide [72]. Alcohol is
a depressant and acts on multiple receptors, primarily by disrupting the inhibitory
neurotransmitter GABA and its counter-enzyme, glutamate. It is ingested orally,
and the onset of action is within 15–30 min in a dose-dependent manner [76].
Symptoms of acute intoxication include decreased awareness, disinhibited behaviors, slurred speech, and somnolence. Chronic use can lead to increased tolerance
and decreased effects of acute intoxication despite elevated blood alcohol levels on
serum testing. These patients are also at elevated risk of alcohol withdrawal syndrome, which can be fatal [76].
Procedural Considerations
Acute intoxication is associated with multiple periprocedural risks, including aspiration, agitation, and increased anesthetic requirements for sedation. Chronic alcohol use also has signicant complications on multiple organ systems, which can
affect perioperative management. Patients are at risk of developing cardiomyopathy,
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chronic liver disease, and profound electrolyte and nutritional abnormalities. In
addition, patients must be monitored for alcohol withdrawal postoperatively, as this
can progress to seizures and delirium tremens in patients with chronic use.
Symptoms begin at approximately 24h from the last consumption with anxiety,
tremors, and psychomotor agitation, and they peak at 48–72h. If possible, patients
should be monitored in a setting with a standardized protocol for the treatment of
withdrawal [77].
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Anesthetic Considerations
Alcohol has multiple sedating effects and acts via a similar mechanism as many
anesthetics, including opioids, propofol, and thiopentone [78]. Patients may require
lower doses of anesthetics to achieve adequate sedation in patients with recent or
chronic alcohol use.
Perioperative Recommendations
Patients with acute intoxication are at elevated risk for poor outcomes and intraoperative complications, specically related to anesthetic interactions, risk of aspiration and airway compromise, and risk of signicant hemodynamic instability during
procedures. They may also present with symptoms of confusion, decreased mental
functioning, and aggression. In these cases, it is reasonable to delay procedures until
acute effects have resolved [79, 80]. Serum alcohol testing is generally considered
a reliable marker for acute intoxication, although it is difcult to standardize, as
patient symptoms partially depend on chronicity of use rather than the quantitative
value of the test.
Patients with a history of chronic use but who do not appear acutely intoxicated
should be screened for recency of use and history of withdrawal symptoms. In those
who are at high risk of withdrawal, cases should be delayed at least 72 h, and
patients should be monitored in a controlled setting with a standardized program for
managing withdrawal symptoms. Chronic misuse and dependence are associated
with pathologies that can complicate procedural care, such as cirrhosis and cardiomyopathy. Cases in which the patient has a history of signicant chronic use should
involve screening for sequelae of liver disease, such as esophageal varices, renal
injury, and coagulopathy [77]. This evaluation is critical, even in urgent or emergent
cases, to prevent complications from surgery. Patients may also be treated prophylactically for withdrawal with benzodiazepines in emergent cases associated with
acute intoxication to prevent seizures and delirium tremens (Fig.8.5).
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Preoperative Considerations
Electrolyte abnormalities
Serum alcohol testing
Coagulopathy
Screen for evidence of chronic liver disease
(imaging, lab work)
Perioperative Risks
Aspiration
Agitation
Reduced anesthetic needs
Increased pain tolerance
Drugs to avoid:
Propofol, opioids
Postoperative Considerations
Increased pain tolerance
Withdrawal symptoms – diaphoresis,
tachycardia, anxiety, hallucinations, seizures
Fig. 8.5 Procedural guidance with recent Alcohol use
J. P. Gallagher et al.
Procedural Timing
Delay elective procedures at least 72 hr if recent
consumption and high risk of withdrawal
Disclosures The authors have no grants or nancial support to acknowledge or disclose in the
development of this chapter.
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