Anesthesia in cocaine users

Abstracts

JUSTIFICATIVA E OBJETIVOS: A cocaína é a droga ilícita mais freqüentemente associada a óbitos, e suas implicações perioperatórias nos pacientes agudamente intoxicados ou com história de uso crônico precisam ser bem conhecidas pelos anestesiologistas. O conhecimento da neurofisiologia, da farmacologia e das conseqüências fisiopatológicas decorrentes do uso da cocaína poderá facilitar o cuidado desses pacientes. O objetivo deste trabalho foi revisar as informações sobre a cocaína e suas interações com a anestesia. CONTEÚDO: O artigo discute a farmacologia da cocaína, as conseqüências fisiopatológicas decorrentes do seu uso e as interações com a anestesia. CONCLUSÕES: A compreensão e o reconhecimento precoce das complicações associadas ao uso de cocaína são essenciais para o manuseio adequado de pacientes usuários desta droga. O anestesiologista deve estar preparado, pois tanto as anestesias regionais quanto a geral apresentam riscos significativos nesses pacientes.

COMPLICAÇÕES; DROGAS

REVIEW ARTICLE

Anesthesia in cocaine users^*

Anestesia en el paciente usuario de cocaína

Ana Luft^I; Florentino Fernandes Mendes, TSA^II

^IAnestesiologista; Pós-Graduanda em Ciências Médicas da Fundação Faculdade Federal de Ciências Médicas de Porto Alegre (FFFCMPA), nível de Mestrado

^IIDoutor em Medicina — Faculdade de Ciências Médicas da Santa Casa de São Paulo; Professor de Anestesiologia da FFFCMPA

^{Correspondence to}

SUMMARY

BACKGROUND AND OBJECTIVES: Cocaine is the illicit drug most frequently associated with death, and the anesthesiologist should be aware of the perioperative complications of this drug in patients with acute intoxication or with a history of chronic use. The knowledge of the neurophysiology, pharmacology, and physiopathological consequences of cocaine abuse may facilitate the care of these patients. The objective of this work was to review the information on cocaine and its interactions with anesthesia.

CONTENTS: This paper discusses the pharmacology, physiopathological consequences of cocaine use, and its interactions with anesthesia.

CONCLUSIONS: The knowledge and early recognition of the complications associated with the use of cocaine are essential for the adequate management of cocaine users. The anesthesiologist should be prepared because both regional and general anesthesia carry significant risks in those patients.

Key Words: COMPLICATIONS: illicit drugs; DRUGS: cocaine.

RESUMEN

JUSTIFICATIVA Y OBJETIVOS: La cocaína es la droga ilícita más frecuentemente asociada a decesos, y sus implicaciones perioperatorias en los pacientes agudamente intoxicados o con historial de uso crónico necesitan ser muy bien conocidas por los anestesiólogos. El conocimiento de la neurofisiología, de la farmacología y de las consecuencias fisiopatológicas provenientes del uso de la cocaína podrá facilitar el cuidado de esos pacientes. El objetivo de este trabajo fue revisar las informaciones sobre la cocaína y sus interacciones con la anestesia.

CONTENIDO: El artículo discute la farmacología de la cocaína, las consecuencias fisiopatológicas provenientes de su uso y las interacciones con la anestesia.

CONCLUSIONES: La comprensión y el reconocimiento precoz de las complicaciones asociadas al uso de la cocaína son esenciales para el manejo adecuado de pacientes usuarios de esa droga. El anestesiólogo debe estar preparado, pues tanto las anestesias regionales como la general presentan riesgos significativos en esos pacientes.

INTRODUCTION

Several factors are responsible for the increase in cocaine use, including the ease of administration, availability, purity of the drug, reduction in costs, and the false perception that its use is safe. Cocaine is the illicit drug most frequently associated with death ¹. Perioperative implications in patients with acute intoxication or chronic users are well known to the anesthesiologist. During the perioperative evaluation, a detailed history on drug abuse should be obtained. This evaluation will help planning the perioperative management and is an opportunity to reduce the anxiety about the surgery. The knowledge of the neurophysiological, pharmacological, and physiopathological consequences of cocaine use may facilitate the control of these patients during procedures requiring anesthesia.

The objective of this paper was to review the information on cocaine and its interactions with anesthesia.

HISTORY

The word crack has been used for a little over 15 years, but the use of cocaine products is very old. There are reports on the use of the leaves of the bush Erythoxylon coca (native to South America, in the Amazon region) on Peruvian tribes 2,000 years before the discovery of this continent. When chewed, the leaf releases low doses of cocaine, the active substance of the plant. In 1862, Schroff and Demarle observed that cocaine produced analgesia in the tongue and began to use it for the relief of laryngeal pain, contributing to popularize its use in England and the United States ². During the 1880's, Freud undertook experiments with cocaine, using it in the treatment of opioid addiction. At the same time, Carls Koller, a Viennese ophthalmologist, introduced cocaine as a local anesthetic for ophthalmologic procedures. In 1898, several physicians used cocaine as a local anesthetic in spinal anesthesia ².

In Europe, at the end of the 19^th Century, since the aspiration of the white powder produced a greater effect, its consumption reached the proportion of an epidemic. In 1914, cocaine was prohibited in the Americas and Europe as a consequence of the complications associated with its use. The prohibition had important consequences, and its use only reappeared in the beginning of the 1970s, reaching a peak in 1985 in the United States, and five years later in Brazil ³. Studies to evaluate the abuse of drugs in Brazil showed that, since 1987, hospital admissions related to cocaine have been increasing. In the last five years it represents the second cause of hospital admission among the illicit drugs, supplanted only by alcohol ^4-7.

PRESENTATION

Cocaine comes in two forms, hydrochloride (white power) and freebase (crack), made by the combination of the hydrochloride and alkali (sodium bicarbonate or ammonium). The hydrochloride can be dissolved in water and injected intravenously or, more commonly, used by inhalation.

PHARMACOKINETICS

Cocaine is a benzoylmethylecgonine; ecgonine is a tropine derivative, a component similar to atropine and scopolamine. It is the only naturally occurring local anesthetic ⁸. After intravenous administration, its plasma half-life varies from 60 to 90 minutes, but it can be longer after nasal or oral administration ⁹. When inhaled, it reaches the brain circulation in 6 to 8 seconds, and intravenously in 12 to 16 seconds. Its nasal use causes severe vasoconstriction, what limits absorption. The peak plasma concentration is achieved in 60 minutes and persists for up to 6 hours.

Approximately 80 to 90% of cocaine is metabolized. Metabolisms start in the plasma by hydrolysis of the ester radical; ecgonine methyl ester is the first metabolite, being degraded to bezoylecgonine, the main urine metabolite. Norcaide, another metabolite, is produced by demethylation in the liver through the cytochrome P450 system. From 1 to 5% of the active substance remain unchanged, and the metabolites are eliminated in the urine 6 to 14 hours after administration ². Tests to detect the use of cocaine can be performed in the blood, urine, and hair. The urine toxicological test is the test of reference. It identifies the metabolite bezoylecgonine, which can be detected 4 to 48 hours after exposure to the drug ¹⁰.

PHARMACODYNAMICS

The effects of cocaine can be explained by its action on several receptors. Cocaine blocks the reuptake of catecholamines in the sympathetic pre-synaptic receptors, resulting in accumulation of catecholamines in the synaptic cleft, and increased stimulation of receptor cells. The psychostimulating effect can be explained by its capacity to increase the levels of dopamine, norepinephrine, and serotonin in the brain ¹¹. Cocaine exerts a local anesthetic effect by blocking the sodium channels in neurons, which blocks the transmission of nervous impulses. The systemic effects result from its ability to simultaneously increase the levels of catecholamines and to block its reuptake, leading to a continual antagonism of both alpha and beta receptors ¹². The exposure to cocaine produces a myriad of signs and symptoms. Acute exposure can be associated with hyperthermia, hypertension, tachycardia, mydriasis, stupor, and respiratory and cardiac depression, and it can also inhibit the classical response to trauma and hemorrhagic shock. In the myocardial cell, it decreases the speed of depolarization, the amplitude and speed of conduction of the action potential, causing cardiac arrhythmias and sudden death ^2-13. The use of cocaine brings a feeling of power and infatigability; in high doses, it causes agitation, insomnia, hallucination, and seizures ¹⁴. The chronic use is associated with the development of psychosis and paranoia ¹⁵. Both presentations of cocaine, the hydrochloride and free-base (crack), have a highly addictive potential.

ANESTHESIA

The knowledge and early recognition of the cardiovascular complications related to cocaine are essential for their proper management. Studies in anesthetized animals suggest that the parenteral administration of cocaine induces the peripheral accumulation of norepinephrine and hypertension ¹⁶. However, recent studies in non-anesthetized humans showed that the hypertensive effect of inhaled cocaine is caused by a large increase in cardiac output coinciding with the peripheral constriction and direct sympathetic cardiac stimulation ¹⁶. Thus, the reason why beta-adrenergic antagonists may precipitate hypertensive crisis, which may lead to death, when used to treat cocaine toxicity is now known ¹². The isolated use of beta-adrenergic antagonists may increase alpha agonist action, worsening the hypertension.

After acute administration, the rapid increase in blood pressure is associated with sudden death caused by subarachnoid hemorrhage and rupture of aortic aneurism ¹². Ventricular tachycardia and sudden death with ventricular fibrillation have also been documented. The most common etiology is ischemia secondary to cardiac overload. In general anesthesia, the most frequent problem is severe hypertension, which occurs during induction, laryngoscopy, and tracheal intubation. Drugs, such as ketamine, that increase the levels of circulating catecholamines, and those that sensitize the myocardium to the actions of epinephrine, such as halothane, should be avoided or used with extreme caution.

Individuals admitted to emergency rooms with non-traumatic chest pain should be questioned about cocaine use. Aortic dissection and rupture, arrhythmias, myocarditis, and dilated cardiomyopathy should also be considered in patients complaining of thoracic pain ^17,18. The association of cocaine, myocardial infarction (MI), and myocardial ischemia was noticed initially in 1982. The ECG in those patients may be abnormal even without patent ischemia (absence of MI). Forty-three percent of cocaine users with chest pain without myocardial infarction present electrocardiographic changes as criteria to start reperfusion treatment. Creatinophosphokinase is elevated in 50% of cocaine users without ischemia. This increase is probably secondary to rhabdomyolysis, and is not a good indicator of ischemia. The concentrations of serum troponin are more sensitive and specific to detect myocardial infarction. The pathogenesis of ischemia includes fixed or decreased oxygen myocardial delivery, vasoconstriction of the coronary vessels, both in normal and atherosclerotic segments, which is more pronounced in the latter. As a result, cocaine users with coronary heart disease are more prone to myocardial infarction, platelet aggregation, and thrombi formation. However, angiography in approximately half of cocaine users with myocardial infarction does not show evidence of atherosclerotic disease. The lethality of cocaine is related to the increase the maximal uptake of oxygen associated with coronary vasoconstriction. The myocardial demand of oxygen is increased, which may lead to ischemia or infarction. The vasoconstriction of coronary vessels occurs first by stimulation of alpha-adrenergic receptors and can be reversed by adrenergic antagonists, such as phentolamine, and exacerbated by beta-adrenergic antagonists, such as propranolol. Continual vasodilation, especially in the coronary vessels, and reduction in sympathetic cardiac activity may decrease the cardiac morbidity related to cocaine ¹⁶. Coronary artery vasoconstriction can be caused both by cocaine and its metabolites, explaining why ischemia or infarction may occur several hours after cocaine use. First line agents recommended for the treatment include oxygen, aspirin, nitroglycerine, and benzodiazepines. And, as second line agents, verapamil, phentolamine, thrombolityc agents, or primary angioplasty ¹⁷. In animal models, calcium channel blockers increase cocaine toxicity and its use is questionable ¹⁹. Labetolol, which has alpha and beta-blocking properties, reverts the hypertension caused by cocaine, but has no demonstrable effect on coronary vasoconstriction. The antagonism of beta-adrenergic receptors is greater than its effects on alpha-adrenergic receptors ²⁰. For this reason, one should avoid using propranolol. The association between cocaine and tobacco can exacerbate the effects of cocaine on myocardial oxygen supply and demand by increasing cardiac frequency and systemic blood pressure and decreasing the caliber of diseased coronary arteries ²¹. Alcohol and cocaine, which produce the metabolite cocaethylene that also blocks the reuptake of dopamine in the synaptic cleft, potentiating the systemic effects of cocaine, is another combination that frequently causes death.

The chronic use of cocaine can cause left ventricular hypertrophy, systolic dysfunction, dilated cardiomyopathy, and myocardial depression. Several arrhythmias and conduction defects related to cocaine use have been reported, but the arrhythmogenic potential of the drug has not been defined. Being a sympathicomimetic agent, it increases ventricular irritability and decreases the fibrillation threshold ¹⁷. Bacterial endocarditis is another risk associated with the use of this drug (venous access, contaminants, increased heart rate, and hypertension, which cause valvular and vascular dysfunction, predisposing to bacterial invasion) ²². Despite the severe hypertension that might follow anesthetic induction and tracheal intubation, several anesthesiologists prefer to use general anesthesia due to the possibility of increased toxicity of local anesthetics and relative hipovolemia related to the chronic use of cocaine, as well as thrombocytopenia ²³. Due to the severe vasoconstriction associated with the use of this drug, patients with severe trauma associated with hipovolemia may have normal mean arterial pressure. Hypotension seems to be more pronounced with spinal anesthesia, and the response to ephedrine is reduced secondary to the depletion of norepinephrine stores ¹¹. This effect is analogous to the tachyphylaxis that occurs after repeated doses of ephedrine. Low doses of phenilephrine usually restore blood pressure to normal levels ²⁴. The reduction in platelet count with chronic cocaine use has been described; if the individual uses other drugs, such as alcohol and opioids, which are also associated with thrombocytopenia, one should request a platelet count ^23,25. Several theories have tried to explain the thrombocytopenia induced by cocaine. Elevated catecholamine levels, such as norepinephrine, cause direct arterial vasoconstriction; alpha-adrenergic agonists bind to receptors on the platelets, activating them and, in theory, the combination of arterial vasospasm and platelet activation increases the risk of thrombocytopenia in cocaine users. Other possible etiologies include bone marrow depression, autoimmune response with antiplatelet antibodies, hypersplenism, chronic hepatitis, sepsis, and AIDS ²⁶.

Cocaine could also precipitate seizures. They might be secondary to acute hyperthermia, to an increase in muscular activity, and to the severe vasoconstriction that hinders dissipation of body heat ²⁷. Animal studies demonstrated that cocaine a dose-dependent effect on the thermoregulator center in the hypothalamus, causing significant changes in body temperature ^28,29. There might be ischemic or hemorrhagic strokes secondary to vasospasm, thrombosis of the cerebral artery, and vasculitis, or by rupture of an aneurysm or vascular malformations ^30-33.

Cocaine increases the effects of local anesthetics, which might lead to intoxication. Regional anesthesia with high doses of local anesthetics should be avoided, since it is impossible to predict a safe dose ¹¹. Seizures related to cocaine use are resistant to gabaergic and antiseizure drugs that exert their effects through sodium or calcium channels. Traditional antiseizure drugs, such as benzodiazepines, barbiturates, phenytoin, and inhalational anesthetics, have proved ineffective in the treatment of cocaine-induced seizures. The physiological changes related to cocaine can be treated with a₂-adrenergic agonists, such as dexmedetomidine and clonidine, with peripheral a₁-antagonists, such as phentolamine, with hydration, and with benzodiazepines ¹⁸.

Pulmonary complications secondary to cocaine use affect approximately 25% of the individuals, varying from asthma exacerbations to fatal pulmonary hemorrhage ³⁴. Epistaxis, perforation of the nasal septum, oropharyngeal ulcers secondary to vasoconstriction and ischemic necrosis, are frequent in the respiratory tract ³⁴.

As a direct irritant of the airways, cocaine damages bronchial epithelial cells, stimulating and exposing vagal receptors, causing severe bronchospasm, and exacerbating asthma ^35-37. In the lungs, cocaine impairs the function of alveolar macrophages and the production of cytokines, which might result in immunosuppression and infectious complications ³⁸. The activation of polymorphonuclear cells, resulting in sudden inflammation, might also occur ³⁹. Sustained inhalation might cause pneumothorax and pneumomediastinum, and could be associated with a reduction in pulmonary diffusion, possibly due to the vasoconstriction of pulmonary capillaries ¹². Non-cardiogenic pulmonary edema due to endothelial toxicity, with increased cellular permeability, might occur ^34,35,39 and the increase in vascular resistance might cause acute left ventricular failure, resulting in cardiogenic pulmonary edema ².

Among the gastrointestinal complications in cocaine users are acute ischemia secondary to severe arterial vasoconstriction and reduction in blood flow secondary to the stimulation of a-adrenergic receptors, which could lead to duodenal ulcer and perforation, usually three days after the exposure to the drug. Its anticholinergic action causes hypomotility, an increase in gastric emptying, and prolonged exposure to gastric acid, which contributes to ulcer formation ⁴⁰.

Cocaine abuse is particularly problematic in obstetrics. Its use during pregnancy is associated with obstetric and anesthetic emergencies. Pregnancy increases the cardiovascular toxicity of cocaine. In pregnant women, uterine blood flow is decreased during the exposure to cocaine. Hydralazine is used for the treatment of maternal hypertension, but it has not been demonstrated that it restores uterine blood flow ⁴¹. It can be very difficult to differentiate convulsions caused by cocaine in pregnant women with eclampsia and preeclampsia. The combination of hypertension, proteinuria, and seizures secondary to the acute use of cocaine can be mistaken by eclampsia, and laboratory exams are necessary to make the differential diagnosis ⁴². The management of these patients includes treatment with magnesium sulfate. Parturients undergoing cesarean sections frequently complain of pain during the surgery, even under adequate regional anesthesia, and need complementary analgesia with opioids ¹¹.

Prolonged response to succinylcholine can also be observed in chronic cocaine users, with low levels of pseudocholinesterase. In the acute intoxication, cocaine competes with succinylcholine for metabolism by pseudocholinesterase, decreasing the metabolism of both ⁴³. The choice of anesthetic technique should be individualized, taking into consideration the several clinical manifestations of acute and chronic cocaine abuse.

Cocaine exerts its effects in several receptors and by several mechanisms, and it is difficult to predict how it will interact with drugs that act on the central nervous system and cardiovascular system. The understanding and early recognition of complications are essential for the adequate management. Both general and regional anesthesia have significant risks, and the anesthesiologist should be prepared to adequately manage these patients.

REFERENCES

Submitted em 11 de maio de 2006

Accepted para publicação em 24 de janeiro de 2007

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*

Received from Serviço de Anestesia Santa Casa, CET/SBA Faculdade de Ciências Médicas de Porto Alegre

Publication Dates

• Publication in this collection
  10 May 2007
• Date of issue
  June 2007

History

• Received
  11 May 2006
• Accepted
  24 Jan 2007