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Anesthetic implications of acute methylenedioxymethamphetamine intoxication in a patient with traumatic intracerebral hemorrhage

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Anesthetic implications of acute methylenedioxymethamphetamine intoxication in a patient with traumatic intracerebral hemorrhage
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  281 M.E.J. ANESTH 20 (2), 2009 CASE REPoRTS ANESTHETIC IMPLICATIONS OF ACUTEMETHYLENEDIOXYMETHAMPHETAMINEINTOXICATION IN A PATIENT WITH TRAUMATICINTRACEREBRAL HEMORRHAGE - Case Report- s aMuel D e M arIa j r  * , e than o b ryson ** , a  nD e lIzabeth a.M. f rost *** Abstract The use of the street drug methylenedioxymethamphetamine (MDMA), commonly referredto as ecstasy, has become increasingly prevalent amongst teenagers and young adults in the UnitedStates and many other parts of the world. While most anesthesiologists are facile with the intricaciesof managing patients intoxicated by alcohol, cocaine and narcotics the new “club” drugs presenta challenge, especially under emergency conditions. MDMA, in particular, is the most commonlyabused club drug and potentially one of the most dangerous in the perioperative period. We presenta case report of traumatic subarachnoid hemorrhage in a patient with acute MDMA intoxicationand a review of the anesthetic implications. Case A 19-year-old man with an unknown medical and surgical history presented to the EmergencyDepartment after a motor vehicle collision in which he was the unrestrained driver. The patient presented initially with a Glasgow Coma Score (GCS) of 9 and was emergently intubated in thefield. A passenger in the vehicle stated the patient was at a “rave” before the accident. He did notknow whether the patient took any illicit substances but stated that there was “X” at the party.The patient was of average height and weight. Initial vital signs upon arrival to the EmergencyDepartment included heart rate 115 beats per minute, blood pressure 157/88 mmHg, respiratoryrate 12 breaths per minute, and O 2 saturation 99% on FiO 2 0.4 via mechanical ventilator. Rectaltemperature was 38.2°C. He had numerous facial abrasions but no open lacerations or obviousfractures. Neurologic examination did not reveal any focal deficits and the patient was movingall four limbs spontaneously. His lungs were clear and his cardiovascular exam was remarkableonly for tachycardia. Laboratory evaluation indicated sodium of 124 meq/L. Cerebral computedtomography revealed a left-sided intracerebral hematoma and blood in the fourth ventricle withslight midline shift. From Department of Anesthesiology, Mount Sinai Medical Center, N.Y., N.Y., USA.* MD, Resident.** MD, Assistant Professor.*** MD, Professor.Corresponding author: Dr. Elizabeth A.M. Frost, Department of Anesthesiology, Mount Sinai Medical Center, N.Y., N.Y.,USA, One Gustave L Levy Place, New York, NY 10029. Tel: (212) 241-9240, Fax: (212) 876-3906.E-mail: elzfrost@aol.com  282 SAMUEL DEMARIA JR ET. AL Ecstasy is a hallucinogenic amphetamine analogknown amongst recreational drug users as XTC, X,E and Adam. The drug is classified as a club drugalong with GHB (gamma hydroxybutyrate), ketamineand flunitrazepam because of its use predominantlyat dance parties (“raves”) and dance clubs. MDMAwas patented in 1914 by Merck Pharmaceuticals as anappetite suppressant. Given its purported entactogeniceffects (i.e., feelings of enhanced communicationwith and closeness to others), it was promoted as a psychotherapy adjunct in the 1970’s. Despite this potential clinical use, abuse of MDMA prompted theDrug Enforcement Administration (DEA) to issue aschedule 1 drug classification in 1985. Since that time,MDMA abuse in the US has steadily climbed.MDMA is most often abused orally as a small pill or capsule. As it is produced illegally, the purityof street MDMA is highly variable, with numerouscompounds commonly mixed into the final product.Indeed, the concentration of MDMA itself may varyand accidental overdoses are likely. Any acute MDMAintoxication should be approached as polysubstanceintoxication.MDMA closely resembles the hallucinogenmescaline and the stimulant amphetamine. Thesestructural relationships are predictive of its effects.MDMA increases the release and decreases the reuptakeof serotonin and dopamine and may also have directagonist properties at serotonergic and dopaminergicreceptors as well as monoamine oxidase (MAO)inhibitor effects. In vitro studies suggest an indirectagonist effect on norepinephrine release 5 . Effects may be felt within 20 minutes of ingestion and can last upto 8 hours.Effects include heightened alertness, “closeness”to others, increased emotional lability, decreasedaggression and increased sexual arousal. Hypertension,tachycardia and hyperpyrexia are common. Mydriasis, bruxism, sweating and agitation with later lethargy,fatigue, anorexia and depressed mood follow.The drug is metabolized principally throughthe cytochrome P450 (CYP450) 2D6 enzyme. PhaseII metabolism of MDMA is poorly understood. Onemetabolite has been shown to be a 2D6 inhibitor in vitro. 2D6 inhibitors (e.g., cocaine, methadone,haloperidol, fluoxetine, paroxetine) block the mainThe patient was transported to the operating roomfor emergent evacuation of the hematoma. A 20 gaugeintra-arterial catheter was placed in his left radial artery prior to induction. Tachycardia persisted. Anesthesiawas induced with propofol 140 mg, fentanyl 100 mcgand rocuronium 50 mg. The hemodynamic statusremained stable during the induction period. A bladder temperature probe was placed and a temperature of 38.4°C was recorded. A forced air blanket set to ambientair (24°C) was applied and cold normal saline hydrationwith 1.5 liters and sodium chloride 3% (500 ml) wasadministered during the four hour case. The patientreceived an infusion of remifentanil (0.05-0.1 mcg/kg/hr) and propofol (75-125 mcg/kg/min) throughoutthe case as well as a low concentration of isoflurane(0.5%) in oxygen and air. Electrolyte sampling prior toclosure showed a sodium of 133 meq/L. Temperature prior to transport to the ICU was 36.4°C, heart rate 87 beats per minute and blood pressure 138/89 mmHg.Sedation was continued for 24 hours and his tracheawas extubated 2 days later.Following surgery, he had right-sided weaknessthat improved over the next week. Three weeks after the event, neurological examination was normal. Hewas discharged home without neurologic sequelae. Discussion While alcohol, cocaine/amphetamine and opiateuse occasionally complicate the perioperative period,the rise of designer and club drugs demands a new paradigm in anesthetic management. The club drug,ecstasy (methylenedioxymethamphetamine, MDMA)has effects that may confuse the diagnosis, especiallyin the head injured patient.In the US, there were an estimated 19.7 million people (or about 8.1 percent) over the age 12 usingillicit drugs in 2005. About 500,000 of these had takenMDMA at least once during the year prior to beingsurveyed 1 . According to the Texas Commission onAlcohol and Drug Abuse people attending “raves”,where ecstasy is prevalent, range in age 13 to 40years 2 . MDMA is available at 70% of these gatheringsaccording to one study 3 . A 2001-2002 survey in Chicagoshowed that roughly 40% of 18-40 year olds had goneto a “rave” and roughly half of these participants hadtaken a club drug 4 .  M.E.J. ANESTH 20 (2), 2009 283 ANESTHETIC IMPLICATIONS OF ACUTE METHYLENEDIOXYMETHAMPHETAMINE INTOXICATION IN APATIENT WITH TRAUMATIC INTRACEREBRAL HEMORRHAGE severe hyponatremia. All three of these patients werefound to have recently ingested MDMA 9 .Other effects attributed to acute MDMAintoxication include hepatotoxicity with hepatonecrosisand fulminant liver failure, pneumothorax and pneumomediastinum, acute renal failure fromrhabdomyolysis and creatine phosphokinaseelevations lasting up to 4 days after hospitalization.Cerebrovascular events like subarachnoid hemorrhage,cerebral infarct and venous sinus thrombosis arerelatively uncommon.Most toxicology screens will not detect MDMAand its metabolites and a history is vital although oftennot available. A directed physical exam is also critical,with particular attention directed to vital signs (withsuspicion heightened if patient is hyperthermic) andcardiopulmonary findings. Initial studies that may helpthe anesthesiologist’s approach are mostly nonspecifictests such as the electrocardiogram and electrolytes.Succinylcholine should be used cautiously giventhe risk of compounding the malignant hyperthermia-like effects of the drug, raising intracranial pressure or  potentially worsening hyperkalemia, if present. Also,the bruxism often associated with ecstasy may makeintubation more challenging in spite of patient habitus.If the patient is conscious and capable of protecting hisor her airway, anxiolysis with midazolam or diazepammay be useful and also raises seizure threshold.Management of hyperthermia, cardiovascular instability, electrolyte derangements and renal andhepatic dysfunction are imperative. Wide swings inhemodynamic parameters are to be avoided given these patients’ higher risk of cardiomyopathy and coronaryor cerebral vasospastic events. An intra-arterial blood pressure monitor, placed prior to induction, isadvised.Propofol and thiopental are appropriate inductionagents as ketamine may induce catecholamine releasefrom potentially exhausted stores. Etomidate tends tohave stable hemodynamic effects but may increaseseizure activity, which may be attenuated by pre-induction benzodiazepines. Paralysis with a non-depolarizing agent immediately slows heat productionand help lower body temperature. Also, unlikesuccinylcholine, non-depolarizers are not associatedwith malignant hyperthermia. For this reason,metabolic pathway of MDMA and may substantiallyincrease the effects. Benzodiazepines are metabolized principally by the 3A4 enzyme and likely have limitedmetabolic interaction with MDMA. Pro-serotonergicdrugs (e.g., fluoxetine, amphetamines, St. John’swort, tramadol, lithium,) may increase the severity of MDMA’s pro-serotonin effects.Hyperthermia is the most common adverse effectand a leading cause of MDMA-related mortality. Themechanism relates most likely to serotonergic effects inthe hypothalamic thermoregulatory center compounded by sustained muscle hyperactivity from long periods of dancing in a warm environment (e.g., club), increasedmetabolic rate and rigidity. In genetically susceptible pigs, MDMA has been identified as a trigger of malignant hyperthermia (MH). Hyperpyrexia leadingto rhabdomyolysis, disseminated intravascular coagulation (DIC) and multi-organ failure is themost dreaded consequence 6 .   Increased temperatureincreases cerebral blood flow and intracranial pressureand could worsen head trauma. Also, hyperthermiais not uncommon after head injury which will thuscompound the differential diagnosis.Sympathetic stimulation from MDMAintoxication increases myocardial oxygen demand andcauses tachycardia, vasoconstriction, hypertensionand occasionally acute myocardial infarction anddilated cardiomyopathy if prolonged. Cerebralautoregulation may fail, allowing dangerous increasesin cerebral blood flow. Significant hypotension andlow cardiac output may be encountered after the initialhyperdynamic state due to catecholamine depletion or autonomic dysregulation.Electrolyte disturbances in MDMA abusers are particularly dangerous. Hyponatremia which oftenresults from excessive water intake from increased physical activity (i.e., dancing at parties where MDMAis present) has been associated with MDMA-relatedseizures, stupor and incontinence 7 . Increases in plasmaADH levels can be induced by MDMA use which maycompound the increased intake of water by users 8 .The occurrence of severe hyponatremia is an unusualcomplication in young patients with mild head injuries.One retrospective review of patients in a Thai hospitaldemonstrated that of over one thousand mild headinjuries reviewed, only three patients demonstrated  284 SAMUEL DEMARIA JR ET. AL Hyperthermia must be treated promptly toavoid rhabdomyolysis and DIC. Basic measuresinclude cold fluids, active cooling with ice packs andavoidance of warming blankets. Given the presumedcentral mechanism of MDMA-induced hyperthermia,dantrolene use is controversial as the drug inhibitsthe release of calcium from sarcoplasmic reticulum.Dantrolene may help exertional heat stroke whichmay be similar to MDMA-induced hyperthermia.Hall and Henry noted that during hyperthermia, thecalcium levels required for excitation-contractioncoupling are reduced such that hyperthermia alonecan cause contraction and subsequent heat productionand increased metabolic demand 10 . They suggestedthat dantrolene, which raises the calcium requirementsfor excitation-contraction coupling, may be of some benefit even if it does not directly counteract centralcauses of hyperthermia.In summary, patients acutely intoxicated byecstasy may be hyperthermic, hyperdynamic and havemany other dangerous complications. Neurologicalsequelae, in particular, present a challenge in termsof evaluation and treatment of the patient. We presenta case of traumatic intracranial hemorrhage possiblyworsened by concurrent ecstasy abuse. A conservativeapproach to such patients using thorough preoperativeassessment, a gentle anesthetic induction andappropriate monitoring is crucial to a good outcome.rocuronium may be ideally situated to both initiatea rapid sequence induction and maintain paralysis.Severe hypertension and raised intracranial pressuremay occur during direct laryngoscopy and commonlyused methods to blunt this response (e.g., intravenouslidocaine, opioids) are correct.Maintenance of anesthesia for head trauma isgenerally with volatile anesthetics. However, volatilegases are known triggers of malignant hyperthermiaand are best used conservatively if a patient has ingestedMDMA. A narcotic infusion with remifentanil, whichis metabolized by blood and tissue esterases, servesthe dual role of blunting sympathetic output andlowering the amount of gaseous anesthetic necessaryfor surgery. Other narcotics, such as fentanyl, are alsosuitable. Serial sodium measurements and appropriatecorrection are important.Potential intraoperative pitfalls are many.Intraoperative hypertension and tachycardia should betreated with labetalol, with its alpha and beta blockingeffects. Pure beta blockade worsens hypertension bytipping the balance of catecholamine action to alpha-1receptors. Intraoperative hypotension requires rapidinfusion of crystalloid or the use of direct alpha-1agonists. Avoiding indirect agonists such as ephedrine prevents the theoretical catastrophe generated whenan already exhausted sympathetic nervous system is prompted to release catecholamines. References 1. US Department of Heath and Human Services. National Survey onDrug Use and Health. Washington DC: US Department of Healthand Human Services, 2005.2. K  otarba   JA: Research Briefs. The Rave Scene in Houston Texas. AnEthnographic Analysis. Austin, Tex. Texas Commission on Alcoholand Drug Abuse, October 1993.3. National Institute on Drug Abuse. The Monitoring the Futurenational results on adolescent drug use: overview of key findings,2001. Ann Arbor, Mich: University of Michigan Institute for SocialResearch, 2002.4. F enDrICh   M, W Islar    JS, J ohnson   TP, H ubbell   A: A contextual profile of club drug use among adults in Chicago.  Addiction; 2003,98:1693-1703.5. S MIth   KM, L arIve   LL, R  oManellI   F: Club drugs:methylenedioxymethamphetamine, flunitrazepam, ketaminehydrochloride, and gamma-hydroxybutyrate.  Am J Health Syst  Pharm ; 2002 Jun 1, 59(11):1067-76.6. G Ill   JR, H ayes   JA, D e S ouza IS, et   al : Ecstasy (MDMA) deaths in New York City: a case series and review of the literature.  J ForensicSci ; 2002, 47:121-126.7. M allICk    A, B oDenhaM   AR: MDMA-induced hyperthermia: asurvivor with an initial body temperature of 42.9°C.  J Accid Emerg  Med; 1997, 14:336-338.8. H enry   JA, F allon   JK, K  ICMan   AT: Low-dose MDMA (“Ecstasy”)induces vasopressin secretion [letter].  Lancet; 1998, 351:1784.9. R  ukskul   P: Ecstasy (MDMA) ingestion related with severehyponatremia in patients with mild head injury.  J Med Assoc Thai ;2005 Jan, 88(1):41-4.10.   H all AP, H enry   JA: Acute toxic effects of ‘Ecstasy’ (MDMA)and related compounds: overview of pathophysiology and clinicalmanagement.  British Journal of Anaesthesia; 2006, 96(6):678-685.
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