CASE CONFERENCE

body stuffers cocaine

Two Crack Cocaine Body Stuffers From the Divisions of Emergency Medicine,* Gastroenterology,t and Trauma and Critical Care Surgery,¢ and the Department of Radiology,~ University of Mississippi Medical Center, Jackson. Receivedfor publication December 2, 1991. Revision received March 24, 1992. Acceptedfor publication March 30, 1992.

Charles V Pollack, Jr, MA, MD* David W Biggers, MD* Frederick B Carlton,Jr, MD, FACEP* James LAchord,MD, FACEPt Philip E Cranston,MD, FACEP§ J Todd Eggen,DO* John A Griswold,MD*

[Pollack CV Jr, Biggers DW, Carlton FB Jr, Achord JL, Cranston PE, Eggen JT, Griswold JA: Two crack cocaine body stuffers. Ann Emerg Med November I992;21:1370-1380.] INTRODUCTION Today's cases involve two young men who presented to our university hospital emergency department after ingesting packets containing rocks of crack cocaine. Because these packets were not specifically prepared for gut transit before ingestion, the patients are classified as "body stuffers" rather than "body packers." The management of this problem is not well delineated in the literature. The discussants are Charles V Pollack, Jr, MA, MD, and David W Biggers, MD, co-chief residents in emergency medicine; Frederick B Carlton, Jr, MD, Director of Emergency Medicine; James L Achord, MD, Director of Gastroenterology; Philip E Cranston, MD, Director of Computed Tomography Body Imaging; J Todd Eggen, DO, Assistant Clinical Professor of Medicine (Emergency Medicine); and John A Griswold, MD, Associate Director of Trauma and Critical Care Surgery, all of the University of Mississippi Medical Center. Dr Pollack will serve as moderator. CASE

PRESENTATIONS

Case 1

Charles V Pollack, Jr, MA, MD: A 29-year-old man presented to the ED stating he had swallowed five or six "dime rocks" of crack cocaine wrapped in plastic approximately 24 hours before arrival. He complained of a generalized headache of several hours' duration but was otherwise asymptomatic. He had presented because of nervousness and fear that "the bag would hang up." He denied recent use of alcohol or any other drugs. There was no history of any seizure activity, palpitations, respiratory difficulty, or chest or abdominal pain. The ingestion had been prompted by a knock on his door that he feared might be law enforcement personnel. His medical history was remarkable for polysubstance abuse for 15 years and for a gunshot wound to the leg in 1986. He was taking no prescription medications. On physical examination, he was an anxious-appearing man who was slightly diaphoretic. His vital signs were blood

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pressure of 182/86 mm Hg; t e m p e r a t u r e , 37.5 C orally; pulse, 108; and respirations, 20. Cardiac monitor revealed a sinus tachycardia without ectopy. A p e r i p h e r a l IV line was established. Examination of the head, eyes, ears, nose, and throat was unremarkable. The neck was supple, and chest and cardiac auscultation was normal. The abdominal, rectal, and genitourinary examinations were u n r e m a r k a b l e . Inspection of the extremities revealed no cyanosis, edema, or needle track marks. The patient was mildly tremulous, but his nenrologic examination was otherwise normal. Radiographs of the chest and abdomen were obtained. L a b o r a t o r y studies revealed a p e r i p h e r a l WBC count of 12,600/mm 3 with a n o r m a l differential; hematocrit was 42.3%, and platelet count was normal. Serum electrolytes, glucose, blood urea nitrogen, and creatinine also were normal. The urinalysis was within normal limits, and urine myoglobin screen was negative. Serum creatiuine phosphokinase (CPK) was 1,213 U/L (normal range, 33 to 281 U/L) and was sent for isoenzyme fractionation. A 12-lead ECG revealed sinus tachycardia. Urine toxicology screen by thinlayer chromatography revealed only the presence of cocaine metabolites. Philip E Cranston, MD: Plai n radiographs of the chest and abdomen of this patient were i n t e r p r e t e d as n o r m a l in the ED. On subsequent review, even with all of the historical information, I agreed that there were no abnormalities and no radiographically identifiable foreign bodies. D r Pollack: The patient was admitted to the ED observation unit and was kept on the cardiac monitor. Because of the elevated C P K measurement and pending repeat urine myoglobin screening, an IV infusion of 5% dextrose in halfnormal saline with 2 ampules of sodium bicarbonate was initiated at 150 mL/hr. He agreed to d r i n k 75 g of activated charcoal followed by 1.5 L/hr of polyethylene glycol 3350 and electrolytes. The patient began having liquid stools approximately three hours later; the first charcoal-stained stool a p p e a r e d at about 5.5 hours after initiation of GoLytely®. Each stool was examined for evidence of a plastic bag; none was found. Repeat CPK measurement eight hours after the first assay revealed a total C P K of 784 U/L. Fractionation of the original CPK measurement revealed 100% MM b a n d ; urine myoglobin screening remained negative. Electrolytes remained normal. The IV fluid was changed to 5% dextrose in half-normal saline without bicarbonate. The patient's pulse gradually decreased to approximately 80. He never complained of chest pain or exhibited any seizure activity. After 11 hours, the patient began to refuse his Go-Lytely®; he was passing clear liquid stools without charcoal staining at that time. Approximately two hours later, he r e p o r t e d that he had passed the plastic bag and immediately flushed it "so there wouldn't be any evidence." He had freely allowed inspection of all previous stools. He agreed to remain on the monitor thereafter, but one hour later, after passing another clear liquid stool, he demanded discharge. He had competent

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family members in attendance. His vital signs were normal, and he was no longer tremulous. The risks of retained cocaine, including myocardial infarction, stroke, sudden death, seizures, and renal failure, were explained to him, and he was allowed to sign out against medical advice. It is interesting to note that his next ED visit occurred five weeks later due to a gunshot wound to the groin, reportedly sustained in an argument over the price of crack cocaine. Case 2 David W Biggers, MD: An 18-year-old man was brought by friends to the ED after two generalized seizures, each lasting one to two minutes. Previously, he had been agitated and diaphoretic. He stated that 24 hours earlier he had ingested several unknown "pills." He r e p o r t e d no history of emesis, headache, or seizures. He denied illicit drug use. He would not offer any reason for the ingestion, and he denied any suicidal thoughts, depression, or regular medication use. On initial examination, vital signs were pulse, 150; blood pressure of 142/82 mm Hg; temperature, 36.5 C; and respirations, 16. Monitoring revealed a n a r r o w complex tachycardia and a pulse oximetry reading of 98% on room air. An IV line was initiated; bedside glucose assay was normal. In general, the patient was alert, fully oriented, and mildly anxious. H e a d and eyes, ears, nose, and throat examination revealed warm, moist skin over the forehead. Pupils were 5 mm and reactive bilaterally. Oral mucous membranes were moist, and the neck exanunation was normal. The chest was clear to auscultation, and cardiac examination revealed a regular tachycardic r h y t h m with no r u b , murmur, or gallop. The abdomen was soft and nontender with hyperactive bowel sounds. The extremities were normal, and there was no muscular tenderness. A mild resting tremor was noted in the u p p e r extremities; neurologic examination was otherwise unremarkable. At the completion of the examination, the patient suffered a witnessed tonic-clonic seizure that resolved spontaneously after one minute. He remained postictal with the same cardiac r h y t h m and blood pressure of 156/80 mm Hg. Due to the impression of new-onset seizures and a poorly detailed history of drug ingestion, the patient was electively nasotra1, Abdominal radiograph of patient 2, revealing unusual density in right lower quadrant (arrow)

Figure

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cheally intubated and p r e p a r e d for gastric lavage. Lorazepam I mg IV and phenytoin 1 g IV (50 mg/min) were administered for seizure prophylaxis. Gastric lavage with a 40F orogastric tube r e t u r n e d no pill fragments or foreign bodies. On being informed of the serious nature of the patient's condition, the patient's friends volunteered the history that the patient h a d actually swallowed a cellophane w r a p p e r containing approximately 20 "small rocks" of crack cocaine the previous day in fear of a drug arrest. Having h a d previous similar experience as a body stuffer, the patient promptly treated himself with laxatives and 2 gallons of milk. Nevertheless, he experienced the first seizure ten hours after ingestion, a second seizure 13 hours later, and a t h i r d seizure (in the ED) one hour after the second. Portable chest and abdominal radiographs were taken. ECG revealed a sinus t a c h y c a r d i a with a QRS d u r a t i o n of 0.07 second; there was no ventricular ectopy. Initial laboratory studies revealed a WBC count of ll,200/mm3; the hematocrit was 45.7%, and the platelet count was 473,000/mm 3 . Serum electrolytes, glucose, blood urea nitrogen, and creatinine were all within normal limits; serum CPK was 800 U/L. There was no myoglobin i n t h e urine, and the urine toxicologic screen by thin-layer chromatography revealed only cocaine metabolites. Dr Cranston: The chest r a d i o g r a p h was u n r e m a r k a b l e ; the portable k i d n e y - u r e t e r - b l a d d e r film suggested a faint radiopaque density in the right lower q u a d r a n t that was suspicious for a foreign body (Figure 1). We suggested that computed tomography of the abdomen might provide a more certain diagnosis of foreign body due to its inherently greater contrast resolution. We consulted with the physicians in the ED; the patient at that time remained postictal with no further seizure activity and stable vital signs. He was intubated

and on a T-piece with no a p p a r e n t respiratory difficulty. He was thought to be sufficiently stable to go to computed tomography. Abdominal scanning without oral or IV contrast material revealed two interesting findings: two focal high-density areas in the distal ileum that a p p e a r e d to correspond to the abnormality on plain film (Figure 2) and an amorphous density in the gastric fundus (Figure 3). The patient remained stable and was quickly r e t u r n e d to the ED. D r Biggers: Based on the clinical picture and the radiographic findings, it was suspected that either the cocaine had not been securely w r a p p e d and had been absorbed or that cocaine was leaching out of a secure container that might still be in the stomach. The surgery and gastroenterology services were notified, and administration of activated charcoal was withheld pending a decision regarding u p p e r endoscopy to investigate the possible gastric foreign body. J a m e s L A c h o r d , MD: Our service was consulted regarding the a p p a r e n t foreign body in the stomach. Although we knew that any attempt at endoscopic removal of a bag containing cocaine would be potentially hazardous because of the risk of r u p t u r e or dispersal with release of additional toxin, we thought it i m p o r t a n t to know if u n a b s o r b e d drug remained in the patient's stomach. U p p e r endoscopy was performed without difficulty, and an empty plastic sandwich bag was found against the posterior wall of the gastric fudus. The bag was removed easily with a snare, uncovering a relatively superficial 1-cm ischemic mucosal ulcer with surrounding edema. There were no other abnormalities. D r Biggers: Immediately after endoscopy, the patient received 100 g of activated charcoal by nasogastric tube, and whole-bowel irrigation was begun with Go-Lytely® solution at a rate of 2 L/hr. The patient was admitted to the medical ICU, where he was monitored for two days. His medications

Figure 2.

Figure 3.

Lower abdominal computed tomography (patient 2), revealing small focal densities in right lower quadrant (arrow)

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Upper abdominal computed tomography (patient 2), revealing amorphous density in gastric fundus (arrow); subsequently, this was thought most likely to represent the empty bag removed at endoscopy

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included lorazepam, phenytoin, and famotidine, and he received three additional doses of activated charcoal. Blood pressure and pulse rate remained controlled without p h a r macologic intervention; no dysrhythmias developed. Serial ECGs and CPK-MB measurements demonstrated no evidence of myocardial ischemia. The hematocrit remained stable. No foreign bodies were passed in the rectal effluent, and whole-bowel irrigation was discontinued after 24 hours. After extubation, the patient did well with no a p p a r e n t neurologic sequelae. Plain radiographs on hospital day 3 revealed the abdominal right lower q u a d r a n t densities to be no longer present; the patient refused repeat computed tomography scanning. He was discharged on the fifth hospital day with psychiatric evaluation scheduled on an outpatient basis. Question: Was any p a r t i c u l a r consideration given to the possibility of a coingestant, such as amphetamines? D r Biggers: Not in this case, although the gut decontamination p r o c e d u r e that we followed, with muhidose activated charcoal and whole-bowel irrigation, would have adequately managed most common coingestants. If the patient h a d not responded to symptomatic support, we would have been forced to investigate that issue further. BISCUSSl0N D r Pollack: We will begin our discussion of the management of cocaine body stuffers by defining the problem. Dr Eggen will differentiate these patients from body packers, who deliberately smuggle illicit drugs in their gastrointestinal tracts.

Body Stuffers Versus Body Packers J Todd Eggen, DO: Two p r i m a r y differences are usually a p p a r e n t between drug body stuffers and body packers: p r e p a r a t i o n and quantity. Body packers are hired specifically to smuggle drugs, especially cocaine or heroin, which are typically carefully packed and w r a p p e d in containers that are designed to survive gastrointestinal tract transit. 1,2 The sophistication of the w r a p p i n g - - i n latex (sometimes condoms) with or without a covering of aluminum foill,3---has increased markedly over the past decade. It is suspected that most body packers, or "mules," escape detection and any significant toxic effects of the drug. The one notable exception is "packers" from Nigeria, who typically use a single latex wrap with electrical tape, comprising a r a t h e r high-risk procedure. The n a t u r e of the smuggling business dictates that it is most efficient for large quantities of drug to be carried by each body packer. Because the lethal exposure for cocaine may be quite small, the magnitude of the potentially higher exposure becomes clinically meaningless; the risk of leaching or package perforation, however, with its attendant complications appears to increase in p r o p o r t i o n to the n u m b e r of packages ingested. Body stuffers, on the other hand, are not as well p r e p a r e d for their mission, which usually is to avoid apprehension while in the possession of illicit substances.4 The typical body

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stuffer presentation, as in both of our cases, is that of a user or seller of cocaine who, on the verge of arrest, "swallows the evidence." The cocaine may not be wrapped, or it may be contained in aluminum foil or in an open and relatively porous container such as a sandwich bag. Glass or plastic "crack vials" are sometimes swallowed. Most often, large quantities of cocaine are not involved in these cases. Due to the poor wrapping, however, a lethal exposure may occur. Radiographic detection of the containers may be more difficult in the stuffer than in the packer, in whom the carefully wrapped packages are more likely to provide air-liquid or air-solid interfaces. X,z Both types of patients are equally unlikely, under routine circumstances, to give an accurate history. Another significant difference between stuffers and packers is that stuffers are much more likely to be exposed to coingestants. Body packers usually are not drug abusers and are engaged in transporting one drug, whereas users and street sellers--who are most likely to be body s t u f f e r s - - t r y to hide any adverse evidence in their possession. This may include additional illicit or prescription drugs that complicate ED presentation and management. These definitions and differences were first described by Roberts et al in 1986. 4 These authors further related the commonly encountered scenario of the clandestine body stuffer who is asymptomatic on arrest but later found seizing, comatose, or dead in his jail cell. These cases reinforce the importance of vigilant monitoring in patients suspected of body stuffing. Aside from support and monitoring, however, there is no widely accepted management regimen for body stuffers in the literature. Radiographic studies are not consistently helpful, as Dr Cranston will point out, because the n u m b e r of ingested containers is generally small and, hence, air-fluid and air-foreign object interfaces arc not likely to be evident. Symptoms and entire toxidromes may v a r y widely or overlap because of the presence of coingestants. Surgery is rarely helpful because the container is not sealed and usually has been lealdng since ingestion; surgical intervention is indicated only for intestinal obstruction or significant clinical deterioration. Endoscopy has not been studied in this setting. Gut decontamination, such as with whole-bowel irrigation, is important, b u t end points are unclear. On the other hand, when I conducted an informal poll of poison control centers two years ago, I found that the management of body packers (particularly in areas that are m a j o r drug-smuggling entry points such as Miami, New York City, and Los Angeles) is relatively standardized, if only on the basis of accumulated anecdotal experience. In asymptomatic or mildly toxic patients, serial radiographic studies are performed, and patients are supported and observed. Surgery is performed only for signs of intestinal obstruction or for sudden catastrophic deterioration (for which container rupture is presumed). Whole-bowel irrigation or catharsis is p u r s u e d aggressively until all containers are passed or accounted for and then confirmed by u p p e r gastrointestinal contrast study.S

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D r P o l l a c k : Dr Carlton will review the manifestations and ED management of cocaine intoxication.

Toxicology of Ingested Cocaine F r e d e r i c k B Carlton, Jr, MD: At one time, it was held that orally ingested cocaine would cause little systemic toxicity because the drug, as a hydrochloride salt with a pic a of 6.8, was thought to be nearly entirely hydrolyzed by gastric acid. It is now known that the entire spectrum of cocaine intoxication and threats to life can occur after exposure by the nasal, oral, rectal, IV, or inhalation routes. The p r i m a r y toxic effects of cocaine are exhibited in the cardiovascular and central nervous systems, from which the initial manifestations are t a c h y c a r d i a , hypertension, and agitation. Ventricular ectopy and arrhythmias are relatively common. In severe intoxications, hypotension and f r a n k shock may ensue. Myocardial injury is a significant risk in cocaine intoxication; even in young, otherwise healthy adults, a complaint of chest pain in this setting must always be evaluated thoroughly. Central nervous system effects are most often manifest as a hyperadrenergic state with restlessness and delirium; seizures, as seen in case 2, are quite common. Cocaineinduced hypertension is occasionally associated with intracerebral or subarachnoid hemorrhage; vasospastic ischemic cerebral infarcts also may occur. The r e s p i r a t o r y center is stimulated initially; h y p e r p n e a may be followed, however, by medullary r e s p i r a t o r y depression and arrest. Nausea and vomiting are common even after exposure by a nonoral route. Prolonged or repetitive seizure activity may result in rhabdomyolysis and renal t u b u l a r injury. The most common systemic manifestations of acute cocaine toxicity are hyperthermia, which may be life threatening, and metabolic acidosis, which may be profound. In the ED management of cocaine ingestion, an accurate history of the amount of drug involved is valuable but, as in case 2, frequently cannot be obtained. As a rule of thumb, in most areas, crack cocaine rocks sell on the street for about $1 p e r milligram, so a "dime rock" (a $10 aliquot) p r o b a b l y consists of approximately 10 mg of crack. Crack is alkaloidal cocaine that when smoked makes a popping s o u n d - - h e n c e the name " c r a c k . " Although as little as 25 mg of cocaine can be lethal, 6 a human LD50 has not been definitively established (500 mg is a generally accepted amount3). There is m a r k e d interindividual variability in cocaine absorption kinetics after oral exposure. The emergency physician's priority in the management of a patient after a cocaine ingestion is stabilization. Patients who are asymptomatic on arrival may deteriorate r a p i d l y and should be managed expectantly. Ensurance of airway patency and adequate oxygenation is, as always, the first priority. An IV line should be immediately established to have r a p i d venous access should the patient begin seizing; a cardiac monitor and, if available, a pulse oximeter should be applied immediately. Patients with seizures or deteriorating mental status should be iutubated as soon as possible to pro-

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tect the airway and allow ventilatory support. An ECG should be obtained p r o m p t l y to provide a baseline tracing. Next, patients who are asymptomatic should undergo gut decontamination while they are closely observed for signs of toxicity. Gastric emptying in the body stuffer may be hazardous because of the possibility of r u p t u r i n g a previously intact bag, compromising the patient's airway, encountering foreign objects that are too large for the lavage tube, or propelling with lavage fluid the bags and their contents into the small bowel where they are more likely, respectively, to cause a mechanical obstruction and induce mesenteric ischemia. On the other hand, body stuffers are often brought to the ED by law enforcement personnel shortly after ingestion, so the offending packet frequently is still in the stomach. If the patient is awake and seizure free and there is a reliable history of ingestion within 60 minutes of arrival, induced emesis with syrup of ipecac may provide gastric decontamination while avoiding some of these risks. Although some note that this a p p r o a c h is controversial, three series used ipecac in this setting and r e p o r t e d no complications.a,7, 8 Ipecac should not be given to the patient who has had a seizure, whose mental status is deteriorating, or whose gag reflex is decreased or absent because of the greatly increased risk of aspiration; instead, the patient may be electively endotracheally intubated, and lavage can be performed if indicated by history and clinical situation. Regardless of whether gastric emptying is attempted, activated charcoal (1 g/kg) should be administered to patients with a history of cocaine ingestion. Charcoal adsorbs cocaine, serves as a m a r k e r for gastrointestinal transit, and may be effective in reducing the absorption of coingestants or adulterants. Activated charcoal may be given concomitantly with syrup of ipecac, if the latter is used. 9 Although activated charcoal is thought to be useful in treatment of body stuffers, it may be even more efficacious in treatment of body packers, in whom it may adsorb small amounts of cocaine leaching out of bags that remain grossly intact. ~0,11 Catharsis is also helpful. Whole-bowel irrigation with a n o n a b s o r b e d polyethylene glycol electrolyte solution is probably the safest and most effective means of purging the bowel of intact ingested drug packets.S,7 In drug stuffers, however, the relatively u n p r e p a r e d bags of drug rarely survive complete gastrointestinal transit intact. Activated charcoal therefore should be given along with whole-bowel irrigation, as cocaine adsorption by charcoal increases with increasing p H as the material moves through the gastrointestinal t r a c t . 12,13

Mildly symptomatic patients (ie, those manifesting hyperadrenergic symptoms and perhaps discrete, brief seizures) should be managed primarily with benzodiazepines. Patients should be monitored carefully for signs of coronary ischemia (eg, chest pain, ST-segment changes, arrhythmias) and hemodynamic or neurologic deterioration as well as for the a p p e a r a n c e of myoglobin in the urine. Cocaine-induced seizures usually respond rapidly to IV diazepam; the use of

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phenytoin and p h e n o b a r b i t a l has not been studied in detail. The hypertension and tachycardia associated with cocaine intoxication are usually self-limited and require no specific therapy; diazepam also is of benefit for these problems. Many other drugs, such as B- and combined a/B-adrenergic blockers, calcium channel blockers, and neuroleptics, have been studied as potential therapeutic agents in the management of acute cocaine toxicity. A great deal of controversy still surrounds this issue; Dr Pollack will address this next. Patients with significant signs of cocaine toxicity on initial presentation (eg, severe hypertension, a r r h y t h m i a s , ventilatory compromise, r e c u r r e n t seizures, severe hyperthermia) require more specific management that must be initiated in the ED while an ICU bed is p r e p a r e d . Riggs and Weibley r e p o r t e d the cases of four cocaine body stuffers in 1990.14 These patients had tachycardia, hypertension, and agitation at ED presentation. Two developed seizures in the ED; one develope d abdominal pain consistent with intestinal angina. All were hospitalized in an ICU for at least 48 hours, and all recovered without a p p a r e n t sequelae. Severely symptomatic body stuffers and packers also are potential surgery candidates. Although surgical mortality is high, surgical consultants should be kept aware of the patient's condition, as removing a leaching or open bag from the gut may decrease the drug load sufficiently to enhance the success of intensive medical management. Most surgeons, as I suspect Dr Griswold will tell us, would consider surgical intervention in these patients only as a last resort. As was discussed with case 2, consideration should be given in each body stuffer to the possibility of not only coingestants but also adulterants and diluents. Some of these substances may require specific toxicologic management. Of the samples examined over a decade in one drug analysis laboratory, 39% of anonymously submitted cocaine samples contained adulterants, and an additional 24% were cut with sugars and other diluents. 15 Typical adulterants included lidocaine and other "caine" anesthetics, caffeine, ephedrine, amphetamine, phenacetin, heroin and other opioids, quinine, and theophylline. Sugars used to dilute cocaine included mannitol, inositol, lactose, glucose, and sucrose. In addition, some substances may be substituted totally for cocaine, including all the adulterants listed plus phencyclidine and LSD. 15 As a general rule, adulterants pose fewer clinical problems when ingested r a t h e r than taken by the IV route.

Management of Acute Cocaine Toxicity D r P o l l a c k : More significant manifestations of cocaine intoxication that can occur after body stuffing require aggressive management to be initiated in the ED b u t are better handled with invasive monitoring in the medical ICU setting. As Dr Carlton has told us, there has been much controversy surrounding the best pharmacologic means of managing these patients. There arc two i m p o r t a n t points to keep in mind. First, cocaine-assoclated hypertension and ventricular ectopy are usually transitory and rarely require specific treatment other than support and benzodiazepines. Second,

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the cardiovascular and neurologic manifestations of cocaine toxicity are linked inextricably and often may be managed with the same drug. 16 Occasionally, coexisting signs and symptoms such as chest pain or neurologic abnormalities p r o m p t the emergency physician to attempt pharmacologic management of the hypertension associated with cocaine intoxication. In the past, B-adrenergic blockers were thought to be the best drugs for this indication.6,17-19 F u r t h e r work, however, has documented mounting evidence that B-blockers may both potentiate cocaine-induced myocardial damage and have deleterious effects on mortality in general. In 1990, Lange et al r e p o r t e d that p r o p r a n o l o l potentiated cocaine-induced coronary vasoconstriction in stable volunteers undergoing cardiac catheterization. 20 Smith and colleagues in 1991 r e p o r t e d that B-blockers adversely affected survival in a rat model of cocaine toxicity. 21 It is postulated that B-blockade allows unopposed cocaine stimulation of a-adrenergic receptors, which in turn promotes p e r i p h e r a l and coronary vasospasms with exacerbation of hypertension. F o r this reason, labetalol, which also has some a-blocking activity, has been touted as a possible antidote to cocaine toxicity.22,23 The efficacy of labetalol has not been supported, however, in the laboratory. 24 The short-acting B-blocker esmolol has not demonstrated as effective in several case reports.25 Likewise, the use of calcium channel blockers does not offer clear benefits in managing the hemodynamic effects of cocaine intoxication. Empirically, calcium channel blockers may be expected to help reverse some of the vasospastic effects of cocaine peripherally, as well as in the central nervous system, myocardium, and mesenteric tree. There have been no clinical trials, however, that have demonstrated consistent efficacy from this class of drugs. In a human volunteer study in 1987, p r e t r e a t m e n t with diltiazem before administration of IV cocaine blunted only the hyperthermic manifestation of intoxication; cardiovascular and other autonomic effects were not altered. 26 Derlet and Albertson r e p o r t e d that rats p r e t r e a t e d with dihiazem, nifedipine, or verapamil before exposure to cocaine both had higher mortality rates and developed seizures significantly faster than did control animals. 27 In another r a t model, Smith et al r e p o r t e d that verapamil had no effect on cocaine-induced seizure activity or mortality. 21 While the evidence against safe use of calcium channel blockers is not as strong as that against B-blockers, it remains a p p a r e n t that the former likewise cannot be considered an "antidote" for cocaine intoxication. Pure a-adrenergic blockers such as phentolamine may be more reliably beneficial, but p r o b a b l y the safest drugs to use in cocaine-induced hypertension are p u r e vasodilators such as nitroprusside, which has the a d d e d advantages of r a p i d onset of action and easy titration to effect. 16,28 Arrhythmias associated with cocaine intoxication are usually limited to supraventricular tachycardias that, again, do

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not require specific management other than control of the central sympathetic stimulus with benzodiazepines. Judicious use of mixed a/B-blockers or calcium channel blockers is indicated if atrial t a c h y a r r h y t h m i a s persist. On the contrary, ventricular tachycardia and fibrillation are p r o b a b l y the underlying causes of many cases of cocaineassociated sudden death. 2903° While s t a n d a r d indications for cardioversion and defibrillation in the management of ventricular tachycardia/ventricular fibrillation should be followed in the cocaine-toxic patient, pharmacologic management of these ventricular dysrhythmias remains another area of uncertainty. Lidocaine p r o b a b l y should be avoided because its Type I r h y t h m effect is very similar to that of cocaine. 16 F u r t h e r m o r e , the combination of cocaine and lidocaine has been r e p o r t e d to increase mortality and the frequency of seizures in a r a t model. 31 Phenytoin may be useful in that its antiarrhythmic activity occurs by a different mechanism from lidocaine. It also may be of benefit in managing concomitant cocaine-induced seizure activity and should be considered early. One study has suggested a role for sodium bicarbonate in the management of cocaine-associated ventricular tachycardia/ventricular fibrillation. 32 Myocardial infarction is a well-known complication of acute cocaine overdose and may occur in young patients with no known coronary a r t e r y disease and no other cardiac risk factors. Loss of critical myocardial mass is another significant contributor to the incidence of cocaine-associated sudden death. 3z The incidence of cocaine-induced myocardial infarction is not known, but there are many case reports in the literature. Typical risk factors for coronary artery disease (especially cigarette smoking) a p p e a r to apply to cocaine-induced myocardial ischemia as well, and patients who have sustained cocaine-related myocardial infarctions in the past are at substantial risk for reinfarction if they abuse the drug again. 34,35 Diagnosis in the ED may be difficult because ECG changes typical of ischemia often are not evident early, and laboratory evaluation with CPK isoenzymes often is inconclusive. Angiography in patients with known cocaine-induced myocardial infarctions may be normal, leading to speculation that coronary vasospasm is an important factor in these infarctions; pre-existing fixed lesions are, however, seen more often.20, 36 If acute coronary ischemia is suspected in the ED, management should proceed in a manner similar to that if cocaine were not involved (ie, monitoring, supplemental oxygen, nitrates, and thrombolytic therapy as indicated). Cardiovascular collapse may follow the intense sympathetic storm of cocaine intoxication. Both synaptic depletion of norepinephrine and myocardial dysfunction secondary to dysrhythmias or infarction contribute to the development of hypotension. Fluid resuscitation alone often is not sufficient to restore a perfusing blood pressure; routine ED adjunctive measures, such as placing the patient in Trendelenburg position or the use of a pneumatic antishock garment, should be used. Pharmacologic support should include the early use of

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norepinephrine to counteract presumed physiologic depletion of this catecholamine. Indirect sympathetic support with other pressors such as dopamine or dobutamine also may be useful. Central nervous system manifestations of cocaine intoxication frequently p r o m p t the ED presentation of body stuffers, as in both case 1 (anxiety) and case 2 (seizures). Seizures that do not respond to benzodiazepines are problematic in that p r e f e r r e d second-line t h e r a p y is not well defined. Both phenytoin and p h e n o b a r b i t a l have been r e p o r t e d variously as being effective and relatively ineffective. Phenytoin has the a d d e d advantage of antiarrhythmic activity; p h e n o b a r b i t a l in anticonvulsant doses has a mild sedative effect, the benefit of which must be weighed against potential r e s p i r a t o r y depression. As in refractory seizures not related to cocaine, intubation, paralysis, and general anesthesia should be considered in the a p p r o p r i a t e clinical setting. Stroke may occur in association with acute cocaine toxicity; subarachnoid hemorrhage, p a r e n c h y m a l or intraventricular hemorrhage, and ischemic cerebrovascular accidents have all been reported. 37,38 Subarachnoid bleeds usually occur in the presence of a pre-existing vascular lesion with acute hypertension, although the patient may be normotensive by presentation to the ED. Hypertension and cocaine-associated vasospasm also may be mechanisms for i n t r a c e r e b r a l bleeds and ischemic events. 38 Management of these complications in the body stuffer is no different than in other cases, with the exception of emphasis on gut decontamination and the caveats regarding the use of B-blockers for acute blood pressure control. As always, consideration should be given to an occult traumatic etiology for sudden onset of lateralizing neurologic signs; body stuffers are notoriously poor historians. Significant h y p e r t h e r m i a often complicates cocaine intoxication; this may in t u r n be complicated by cerebral edema, acute renal failure, and disseminated intravascular coagulation. Control of h y p e r t h e r m i a is vitally important in the successful management of severely toxic patients. 16,29,39 Ice and water packing or submersion followed by exposure to fanning provides the most r a p i d means for effective cooling. 16 Seizure activity, tremor, and anxious or psychotic hyperactivity contribute to the development of hyperthermia. Management of these manifestations with benzodiazepines contributes to t h e r a p y of h y p e r t h e r m i a as well. There is no role for dantrolene in the management of cocaine-induced h y p e r t h e r m i a A 6 Haloperidol and other neuroleptics should be avoided in the management of cocaine-toxic patients because of the risk of developing heat-generating dystonic reactions or neuroleptic malignant syndrome4°; hypertension also may be exacerbated by haloperidol, ai Myoglobinuria and resulting renal t u b u l a r injury are significant manifestations of cocaine toxicity.3,42 Repetitive seizure activity is common and may result in rhabdomyolysis. Screening for urine myoglobin is important in managing

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these patients because renal insult may occur with only minimally elevated CPK measurements and occasionally even in the absence of documented seizure activity.43,4a E a r l y treatment with hydration and alkalinization is essential to avoid significant renal compromise. Respiratory depression, metabolic acidosis, and mesenteric ischemia are other significant manifestations of cocaine intoxication. Medullary r e s p i r a t o r y drive is affected directly by cocaine; acidosis usually results from tissue ischemia and lactic acidosis associated with repetitive seizure activity and vasospasm. Ischemic gut p r o b a b l y occurs due to prolonged vasoconstriction in the mesenteric bed. a5 These complications are best managed without p a r t i c u l a r r e g a r d to the toxic etiology. In summary, "conjoint t h e r a p y " (ie, using the same drug to treat disparate manifestations) is i m p o r t a n t in the management of cocaine intoxication. As already noted, the toxic effects of cocaine on the cardiovascular and nervous systems are linked. Most studies have shown that benzodiazepines provide the most efficacious means of reducing the occurrence of seizures, cardiovascular compromise, and systemic manifestations of cocaine intoxication.2a, 46-a8 This therapy, coupled with general support and specific management of disease processes that also occur in nontoxic settings (eg, acute myocardial infarction, cardiovascular collapse, respiratory depression, myoglobinuria, and so on), affords the intoxicated body stuffer the best chance of survival. Dr Cranston will now review the potential contributions of imaging studies to the management of body stuffers.

Role of Radiology in Managing Body Stuffers D r Cranston: Plain abdominal radiographs of body packers have been shown to reveal the presence of drug containers in 75% to 90% of cases. 1,2,a9 This means that plain r a d i o g r a p h y misses up to one fourth of body packers. One can easily imagine, based on these data, that plain radiographic recognition of body stuffers, who generally ingest only a small amount of drugs, is even less reliable. The key to detecting these foreign bodies is the t r a p p i n g of air in the package that provides an air-fluid or air-foreign object interface.5,50 The stomach and ascending colon are therefore the most common locations in which we detect foreign bodies in the gut because of the contrast afforded by gastric and colonic air that surrounds the objects. 49 Likewise, we are least successful on plain r a d i o g r a p h y with foreign bodies of the rectosigmoid colon, where the presence of stool usually masks the object. In general, plastic or glass vials of crack cocaine are even more difficult to detect on plain films than are packets, si The hinited contrast resolution of routine radiographs can be overcome to some extent by the use of radiographic contrast media and more advanced studies such as computed tomography. 52-z4 Magnetic resonance imaging is less useful for visualizing packets of cocaine "because of the relative paucity of protons.55 Barium or gastrograffin swallows can outline nicely the foreign objects in the gut with little risk

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and provide an easy and quick method of confirming a suspicious history in the asymptomatic patient.Za, 56 (Contrast and therapeutic enemas have been associated with rectal packet rupture among packersla; fortunately, stuffers usually use the antegrade route of concealing evidence.) With computed tomography, we can obtain much better contrast resolution that is more likely to delineate foreign b o d i e s - - e s p e c i a l l y solitary or small o b j e c t s - - i n the gut. This was demonstrated in case 2, in which the foreign body suggested on plain radiographs was much more clearly visualized with computed tomography. Toxic patients may not be sufficiently stable, however, to undergo computed tomography scanning. In addition, motion artifact adversely affects the interpretation of computed tomography scans. Due to the expense of these scans, their use therefore should be limited to relatively cooperative patients in whom radiographic confirmation of the presence of a foreign body is clinically necessary for further management decisions. D r PoUaek: Dr Achord will now review the role of endoscopy in the management of the body stuffer.

Role of Endoscopy in Managing Body Stuffers D r A c h o r d : The literature on endoscopic management of body packers and body stuffers is sparse, but in any event I believe that endoscopy plays only a small role. Our methods of retrieving foreign bodies through a scope involve the use of snares that clamp down on and pull the o b j e c t - - e x a c t l y what we wish to avoid in the case of a fragile foreign body that contains a highly toxic substance. Body packers, with their carefully p r e p a r e d cargo, are much better managed by encouraging gastrointestinal transit of the bags. In body stuffers, empty bags will pass through a normal gastrointestinal tract. Where we might be able to offer some benefit in the ED is when a bag is evident in the stomach either radiographically or by history, and we need to know if the bag is empty or full, as in case 2. One should not lose sight of the fact, however, that the vessel itself is harmless. I suspect that the ulcerated area associated with the bag in that patient's stomach would have healed just fine even without H2-blockers. The physiologic stress of hyperadrenergic stimulation and the emotional stress of the situation that p r o m p t e d the ingestion, however, are likely to result in mucosal injury, so I think coverage with this class of drugs, as in any medical ICU stay, is indicated. Endoscopic investigation of the cocaine toxic or potentially toxic patient is further complicated by the adrenergic stimulation's adverse effects on the patient's ability to cooperate. These patients are difficult to sedate short of rapid-sequence induction and endotracheal intubation, and they are likely to bite and disable the endoscope. It also should be remembered that endoscopy itself is not an entirely benign procedure and must be a p p r o a c h e d with caution in a patient in danger of developing seizure activity, gag reflex loss, and r e s p i r a t o r y depression. There is one case r e p o r t e d in the literature of successful endoscopic retrieval of a packet of

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cocaine from the stomach, s7 but this occurred in a body packer who h a d ingested especially well w r a p p e d containers. I do not believe that endoscopy is of significant clinical use in body stuffers. Other modalities that involve the gut, however, are useful. In carefully selected patients, induced emesis may be helpful.a,7, 8 Whole-bowel irrigation is, I think, tremendously valuable in these patients both for decreasing gut transit time and acting as a m a r k e r of transit progress. Polyethylene glycol-electrolyte solutions simply are not absorbed, and their use is very safe, even in patients with renal failure and other pre-existing fluid and electrolyte abnormalities. Activated charcoal, which p r o b a b l y is best given in a multiple dose regimen in this setting, also is very i m p o r t a n t because even intact bags can leach cocaine or heroin in a process analogous to dialysis. The drug p r o b a b l y is present in the patient's bloodstream long before we begin to see symptoms manifest.ll D r P o l l a c k : Dr Griswold will now address the role of surgical management in these patients.

Role of Surgery in Managing Body Staffers J o h n A Griswold, MD: When the practice of cocaine packet i n g e s t i o n - - b y either body packing or body stuffing-first became known, prophylactic surgical intervention was thought to be a p p r o p r i a t e . Removal of these potentially lethal packets was viewed as preventive therapy. 5a It soon became obvious, however, that medical management was superior in the absence of traditional indications for surgical exploration, 59 which in this setting most often are represented by mechanical obstruction, as might occur from bags plugging the ileocecal valve or acting as a lead point for intussusception. The risk of obstruction is lower for body stuffers because the ingested packets usually are generally smaller in number and size. Patients who become toxic due to leaching o f cocaine from the packets also a p p e a r to benefit more from medical than from surgical therapy, unless there is an associated bowel obstruction or perforation. Most indications for surgical t h e r a p y arise in chronic cocaine abusers. The vasoconstrictive activity of cocaine appears to have a propensity to involve the blood supply to the mucosa of the gastrointestinal tract. This can result in ulceration that qnicldy progresses to bleeding or perforation. 40 Perforation of the proximal gastrointestinal tract is now reported quite frequently and eventually may become a more common cause of duodenal perforation than peptic ulcer disease. Mucosal ischemia appears to be dose dependent and therefore is encountered more often in the chronic user, but it also may be seen in the patient who has ingested packets that are slowly leaking in a limited area.a2, 45 In the body stuffer or packer, it remains important to obtain surgical consultation early, before the development of any surgical complications. While we may not need to be involved in the early management of the patient, this allows us to be p r e p a r e d for timely intervention, should it become necessary, before problems are compounded.

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CONSENSUS

DEVELOPMENT

D r P o l l a c k : Our cases today are somewhat atypical of body stuffers in that presentation was delayed after ingestion. Nevertheless, their management provides us with the opportunity to develop a consensus on how we will handle these patients in our ED in the future. Asymptomatic or mildly symptomatic patients can be managed, at least initially, in the ED and observation unit, although inquiries should be made concerning the availability of a medical ICU bed. The patient should have an IV line established on arrival and be kept on a cardiac monitor and pulse oximeter. Basehne ECG and l a b o r a t o r y studies should be performed, and the urine should be screened periodically for myoglobin. (The latter may be made more economical by checking for hemoglobin in the urine with a simple dipstick and then forwarding only positive results to the l a b o r a t o r y for confirmation with the more expensive myoglobin screen.) A plain radiograph of the abdomen should be checked for evidence of foreign body. If the history is consistent with a truly acute ingestion and the patient is awake and has not had a seizure, ipecac may be given. Gastric lavage in the asymptomatic patient probably is not indicated. Activated charcoal (1 g/kg body wt) should be given, and consideration should be given to multiple-dose charcoal administration. Whole-bowel irrigation should be initiated at 1.5 to 2 L/hr, and the rectal effluent should be examined for foreign bodies and the appearance of charcoal from above. Surgical consultants should be notified of the patient's current status and be kept informed about any deterioration, p a r t i c u l a r l y any signs or symptoms consistent with mesenteric ischemia or bowel obstruction. Other signs of toxicity for which patients should be constantly monitored include severe agitation, hyperthermia, tachycardia, hypertension, chest pain with or without ECG signs of ischemia, and seizure activity. Agitation should be treated with benzodiazepines to the point of sedation. Diazepam or lorazepam also would be the first-line therapy for seizure activity. Should severe hypertension or myocardial ischemia develop, nitroprusside , nitroglycerin, or perhaps calcium channel blockers should be used preferentially over B-blockers. Hyperthermia should be managed aggressively. If after the passage of clear and then charcoal-stained rectal effluent there is no evidence of the cocaine packet, plain radiographic studies should be supplemented by contrast studies or computed tonmgraphy scanning in an attempt to locate the container. F u r t h e r management is dependent on the condition of the patient. Patients who manifest more severe signs of toxicity in the ED (eg, repeated or prolonged seizures, significant hyperthermia, myocardial infarction, or hypotension) should be t r a n s f e r r e d to an intensive care setting where more aggressive monitoring and treatment can accompany gastrointestinal decontamination. Surgery and perhaps gastroenterology should be consulted, and medical management should follow the guidelines outlined for severe toxicity.

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REFERENCES 1. McCarron MM, Wood JD: The cocaine "body packer" syndrome: Diagnosis and treatment. JAMA 1983;250:1417-1420. 2. Caruana DS, Weinbach B, Goerg D, Gardner LB: Cocaine-packet ingestion: Diagnosis, management, and natural history. Ann Intern Med 1984;100:73-74.

27. Derlet RW, Albertson TE: Potentiation of cocaine toxicity with calcium channel blockers. Am J Emerg Med 1989;7:464-468. 28. Ramoska E, Sacchetti AD: Propranolol-induced hypertension in treatment of cocaine intoxication. Ann Emerg Med 1985;14:1112-1113. 29. Lathers CM, Tyau LSY, Spine MM, eta]: Cocaine-induced seizures, arrhythmias and sudden death. J Clin Pharmaco11988;28:584-593.

3. Lewin NA, Goldfrank LR, Weisman RS: Cocaine, in 6oldfrank LR, Flomenbaum NE, Lewin NA, et al (ads): Goldfrank's Toxicologic Emergencies, ed 4. NenNalk, Connecticut, Appleton & Lange, 1990, p 499-508.

30. Billman GE: Mechanisms responsible for the cardiotoxic effects of cocaine. FASEBJ 1999;4:2469-2479.

4. Roberts JR, Price D, 6oldfrank L, et al: The bodystuffer syndrome: A clandestine form of drug overdose. Am J Emerg Med 1986;4:24-27,

31. Derlet RW, Albertson T: Potentiation of cocaine toxicity with lidocaine (abstract). Ann Emerg Med 1990;19:464-465.

5. Hoffman RS, Smilkstein M J, 6oldfrank LR: Whole bowel irrigation and the cocaine body-packer: A new approach to a common problem. Am J Emerg Med 1990;8:523-527.

32. Parker RP, Beckman KJ, Bauman JL, et al: Sodium bicarbonate reverses cocaineinduced conduction defects (abstract). Circulation 1989;80(suppl II):ll-l&

6. Gay GR: Clinical management of acute and chronic cocaine poisoning. Ann Emerg Med 1982;11:562-572.

33. Karch SB, Tazellar H, Billingham M, et al: Cocaine-associated sudden death syndrome (abstract). Ann Emerg Mad 1986;15:650.

7. Marc B, 6herardi RK, Baud FJ, et al: Managing drug dealers who swallow the evidence. Br Med J1989;299:1082.

34. Mathias DW: Cocaine-associated myocardial ischemia: Review of clinical and angiographic findings. Am J Mad 1986;81:675-678.

8. Linden CH, Rumack BH: Ipecac for ingested drug packets (abstract). VetHum Toxicol 1984;26:404.

35. Smith HWB, Liberman HA, Brody SL, et al: Acute myocardial infarction temporally related to cocaine use: Clinical, angiographic, and pathophysiologic observations. Ann Intern Med 1987;107:13-18.

9. Freedman GE, Pasternak S, Krenzelok EP: A clinical trial using syrup of ipecac and activated charcoal concurrently. Ann Emerg Med 1987;16:164-166. 10. Gherardi RK,Baud FJ, LePorc P, et al: Detection of drugs in the urine of bodypackers. Lancet1988;1:1076-1078. 11. Wetli CV, Mittleman RE: The "body packer syndrome"--Toxicity following ingestion of illicit drugs packaged for transportation. J Forens Sci 1981;26:492-500. 12. Makosiej F, Hoffman RS, Howland MA, et el: Cocaine adsorption to activated charcoal: The effects of pH (abstract). VetHum Toxico11990;32:350. 13. Kirshenbaum LA, Sitar DS, Tenenbein M: Interaction between whole-bowel irrigation solution and activated charcoal: Implications for the treatment of toxic ingestions. Ann Emerg Med 1990;19:1129-1132. 14. Riggs D, Weibley RE: Acute toxicity from oral ingestion of crack cocaine: A report of four cases. Pediatr Emerg Care 1990;6:24-26. 15. Messinger TA: A decade of drug analysis results: 1973-1983. PharmChem News 1984;13:1-7. 16. Goldfrank LR, Hoffman RS: The cardiovascular effects of cocaine. Ann Emerg Med 1991;20:165-175. 17. Rappolt RT, Gay GR, Inaba DS: Propranolol: A specific antagonist to cocaine. Clin Toxicol 1977;10:265-271. 18. Jonsson S, 0"Meara M, Young JB: Acute cocaine poisoning: Importance of treating seizures and acidosis. Am J Med 1983;75:1061-1064. 19. Robin ED, Wong RJ, Ptashne KA: Increased lung water and ascites after massive cocaine overdosage in mice and improved survival related to beta-adrenergic blockade. Ann Intern Mad 1989;110:202-207. 20. Lange RA, Cigarroa RG, Floras ED, et al: Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Mad 1990;112:897-903. 21. Smith M, Garner D, Niemann JT: Pharmacologic interventions after an LD50 cocaine insult in a chronically instrumented rat model: Are beta-blockers contraindicated? Ann Emerg Med 1991;20:768-771.

36. Ascher EK, Stauffer JCE, 6aasch WH: Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaineassociated acute myocardial infarction. Am J Cardio11988;16:939-941. 37. Lowenstein DH, Massa SM, Rowbotham MC, at al: Acute neurologic and psychiatric complications associated with cocaine abuse. Am J Mad 1987;83:841-846. 38. Spivey WH, Euerle B: Neurologic complications of cocaine abuse. Ann Emerg Mad 1990;19:1422-1428. 39. Catravas JD, Waters IW, Walz MA, at al: Acute cocaine intoxication in the conscious dog: Pathophysiologic profile of acute lethality. Arch Int Pharmacodyn 1978;235:328-340. 40. Derlet RW, Albertson TE, Rice P: The effect of haloperidol in cocaine and amphetamine intoxication. J Emerg Med 1989;7:633-637. 41. Lee HS, LaMaute HR, Pizzi WF, et al: Acute gastroduodenal perforations associated with use of crack. Ann Surg 1990;211:15-17. 42. Cregler LL, Mark H: Medical complications of cocaine abuse. NEnglJMed 1986;315:1495-1500. 43. Singhal PC, Rubin RB, Peters A, et al: Rhabdomyolysis and acute renal failure associated with cocaine abuse. J Toxicol Clin Toxico11990;28:321-330. 44. Merigian KS, Roberts JR: Cocaine intoxication: I-lyperpyrexia, rhabdomyolysis and acute renal failure. J Toxicol Clin Toxica11987;25:135-148. 45. Nalbandian H, Sheth N, Dietrich R, et al: Intestinal ischemia caused by cocaine ingestion: Report of two cases. Surgery1985;97:374-376. 46. Guinn MM, Bedford JA, Wilson MC: Antagonism of intravenous cocaine lethality in nonhuman primates. Clin Toxico11980;16:499-508. 47. Catravas JO, Waters JW: Acute cocaine intoxication in the conscious dog: Studies on the mechanism of lethality. J Pharmacol Exp Ther 1981;217:350-356. 48. Derlet RW, Albertson TE: Diazepam in the prevention of seizures and death in cocaine-intoxicated rats. Ann Emerg Meal1989;18:542-546.

22. Dusenberry SJ, Hicks M J, Mariani PJ: Labetalol treatment of cocaine toxicity (letter). Ann Emerg Med 1987;16:235.

49. Beerman R, Nunez D, Welti CV: Radiographic evaluation of the cocaine smuggler. Gastreintest Rafliel 1986;11:351-354.

23. Gay 6R, Loper KA: The use of labetalol in the management of cocaine crisis. Ann Emerg Med 1988;17:282-283.

50. Fainsinger MH: Unusual foreign bodies in bowel. JAMA 1977;237:2225-2226.

24. Spivey WH, Schoffstall JM, Kirkpatrick R, et al: Comparison of labetalol, diazepam, and haloperidol for the treatment of cocaine toxicity in a swine model (abstract). Ann Emerg Med 1990;19:183-184. 25. Sand IC, Brody SL, Wrenn KD, et al: Experience with esmolol for the treatment of cocaine-associated cardiovascular complications. Am J Emerg Meal1991;9:161-163. 26. Rowbotham MC, Hooker WD, Mendelson J, et al: Cocaine-calcium channel antagonist interactions. Psychopharmacology 1987;93:152-154.

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51. Hoffman RS, Chiang WK, Weisman RS, et al: Prospective evaluation of "crack-vial" ingestions. Vet Hum Toxico11990;32:164-167. 52. Hartoko TJ, Demey HE, DeSchepper AMA, et al: The body packer syndrome-Cocaine smuggling in the gastrointestinal tract. Kiln Wochensch 1988;66:1116-1120. 53. Diamont-Berger O, Gherardi R, Baud F, et al: Intracorporeal concealment of narcotics: Experience at the medico-judicial emergency centre of the HoteI-Dieu hospital: 100 cases. Presse Med1988;17:107-110.

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54.Marc B, Baud FJ, Aelion MJ, et al: The cocaine body-packer syndrome: Evaluation of a method of contrast study of the bowel. J Forens Sci1990;35:345-355. 55.Kerssehot E, Beaucourt L, Degryse H, et al: Roentgenographicar detection of cocaine smuggling in the alimentary tract. ForthschrRontgenstri 1985;42:295-298. 56. Gherardi R, Marc B, Alberti X, et al: A cocaine body packer with normal abdominal plain radiograms: Value of drug detection in urine and contrast study of the bowel. Am J ForensMed Pathol 1990;11:154-157.

Address for reprints: Charles V Pollack, Jr, MA, MD Department of Emergency Medicine Maricopa Medical Center 2601 East Roosevelt Phoenix, Arizona 85010

57. ShermanA, Zingier BM: Successful endoscopic retrieval of a cocaine packet from the stomach. GastrointestEndosc 1990;36:152-154. 58. Suarez CA, Arango A, Lester JL: Cocaine-condom ingestion: Surgical treatment. JAMA 1977;238:1391-1392. 59.Trent MS, Kim U: Cocaine packet ingestion: Surgical or medical management?Arch Surg 1987;122:1179-1181.

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