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Purpose of Review: This review provides an update on recently published literature on the rise of illicit fentanyls, risks for overdose, combinations with other substances, e.g. stimulants, consequences, and treatment., Recent Findings: Overdose due to illicit synthetic opioids (e.g. fentanyl and fentanyl analogs) continues to rise in the US both preceding and during the COVID-19 pandemic. Fentanyl-related overdose is rising in new geographic areas e.g. the western USA. Stimulant-related overdose is also increasing nationwide driven by methamphetamine and cocaine. Polysubstance use, e.g. the use of a stimulant along with an opioid is driving stimulant-related overdose. Other medical consequences of injection drug use are rising including HIV and hepatitis C infections. Medication approaches to treating opioid use disorder remain the standard of care and there are new promising pharmacological approaches to treating methamphetamine use disorder., Summary: A 'fourth wave' of high mortality involving methamphetamine and cocaine use has been gathering force in the USA. Availability and use of illicit fentanyls are still the major drivers of overdose deaths and the current rise in stimulant-related deaths appears entwined with the ongoing opioid epidemic., (Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc.)

This forensic case presents unique postmortem imaging of a "drug mule" with fatal intoxication due to cocaine leakage on postmortem computed and magnetic resonance (MR) tomography compared with autopsy.Imaging by postmortem computed and MR tomography was performed before autopsy, histology, and toxicology were commissioned. Forensic imaging revealed 91 hyperdense, uniformly shaped body packs with signs of leakage, which was confirmed by autopsy. Postmortem MR imaging displayed the rarely described hypointense appearance of the body packs in T1- and T2-weighted sequences. Toxicology stated the dosage of cocaine intoxication as lethal.This case provides an opportunity to image internal cocaine drug containers on postmortem computed and MR tomography. The cause of death could be determined based on imaging and the radiological morphology of these packs by both imaging methods.

Exposure to levamisole-adulterated cocaine can induce a distinct clinical syndrome characterized by retiform purpura and/or agranulocytosis accompanied by an unusual constellation of serologic abnormalities including antiphospholipid antibodies, lupus anticoagulants, and very high titers of antineutrophil cytoplasmic antibodies. Two recent case reports suggest that levamisole-adulterated cocaine may also lead to renal disease in the form of pauci-immune glomerulonephritis. To explore this possibility, we reviewed cases of pauci-immune glomerulonephritis between 2010 and 2012 at an inner city safety net hospital where the prevalence of levamisole in the cocaine supply is known to be high. We identified 3 female patients and 1 male patient who had biopsy-proven pauci-immune glomerulonephritis, used cocaine, and had serologic abnormalities characteristic of levamisole-induced autoimmunity. Each also had some other form of clinical disease known to be associated with levamisole, either neutropenia or cutaneous manifestations. One patient had diffuse alveolar hemorrhage. Three of the 4 patients were treated with short courses of prednisone and cyclophosphamide, 2 of whom experienced stable long-term improvement in their renal function despite ongoing cocaine use. The remaining 2 patients developed end-stage renal disease and became dialysis-dependent. This report supports emerging concern of more wide spread organ toxicity associated with the use of levamisole-adulterated cocaine.

Intracorporeal concealment of illicit drugs is a rare observation at coronial autopsy examinations. The article reports 5 cases of accidental drug overdoses at the Westmead Coronial Morgue, Sydney New South Wales, over a 6-year period with evidence of intracorporeal drug concealment known as body packing or body stuffing. Three different forms of anatomic concealment of drugs are illustrated, Case 2 involving therapeutic medication in the form of glass ampoules for parenteral injection not previously reported. Three deaths were the result of acute toxicity due to polydrug abuse rather than as a consequence of the body packing behavior and rupture of the drug packaging, with the intracorporeal drug concealments an adjunct finding at the autopsy examinations. The cause of death in Case 3 was the direct result of acute cocaine intoxication due to rupture of drug packages in the rectum and mucosal absorption. The article details forensic sociological aspects of drug concealment and subcultural group human behavior that can assist in providing information for the initiation of investigations.

Although cocaine is a widely abused illicit substance that is known to cause death, deaths due to its use appear to occur in a minority of those who use it. This report was designed to review drug-related deaths due to cocaine, and the concomitant use of other drugs/medications. A retrospective review of drug deaths at the Bexar County Medical Examiner's Office in San Antonio, Texas, was undertaken for cases where cocaine was one of the drugs implicated in causing death. Analysis was performed comparing the concentrations of cocaine and benzoylecgonine present and the absence or presence of other drugs. The data obtained showed that cocaine was toxic over a large range with deaths occurring at concentrations ranging from 0.01 to 78 mg/L. Analyses also indicated an increased lethality when cocaine is used in combination with ethanol, heroin, opiates, and antidepressant/antipsychotic medications, which is consistent with previous reports and research. Antihistamine data showed that there may be relationship between increased toxicity and co-ingestion, although more research is necessary.

Background and Objectives: Historically, the duty of the medical examiner in assigning cause and manner of death in drug-related death cases has been fraught with controversial challenges. The lack of standardization in certifying drug-related deaths may involve differences among practicing forensic pathologists in their approach to such cases. The central objectives of the present study include characterization of current drug death patterns and the variability among medical examiners with respect to autopsy performance and death certification practices in one county medical examiner's office., Materials and Methods: Death certificates, scene information/investigative reports, autopsy reports, and toxicological laboratory results for each of the 100 cases of drug-related death occurring in 2002 in Fulton County, Georgia were reviewed. Comparison of overall autopsy rates and autopsy rates in drug-related death cases for each medical examiner individually and for the group collectively was performed. In examining cocaine-related deaths (most common), statistical analysis was performed for comparison of drug concentrations (cocaine and benzoylecgonine) between deaths certified as cocaine toxicity (poisoning) versus cocaine-complicating disease or causing an adverse event such as cerebral hemorrhage., Results: Causes of accidental drug deaths included cocaine 40%, mixed drug intoxication 37%, opioids 10%, ethanol 7%, and prescription medication (nonopioid) 5%. Overall total autopsy rates in 2002 for each of the 6 independent medical examiners ranged from 51% to 69% (mean 64%), whereas autopsy rates in drug-related death ranged from 55% to 91% (mean 81%). In review of the subset of 40 cocaine-related deaths, 25% were certified as cocaine toxicity (poisoning), with the remaining 75% certified as cocaine-complicating disease or causing and adverse event. Autopsy rates in cocaine-related deaths were as follows: cocaine toxicity 80%, cocaine-complicating disease 77.3%, and cocaine causing adverse event 62.5%. Thirty-eight percent of cocaine-related deaths were considered to be of "low suspicion" for drug involvement at the time the death was reported to the medical examiner with the remaining 62% being of "high suspicion". Autopsy rates were somewhat lower in the low suspicion group (67%) versus the high suspicion group (72%). Comparison of drug levels between cocaine-related death certification groups was performed. No statistically significant difference was shown in drug levels (cocaine, P > 0.3; benzoylecgonine, P > 0.2) between deaths certified as cocaine toxicity versus those certified as cocaine-complicating disease or causing adverse event., Conclusions: In Fulton County, accidental drug deaths in 2002 most often involved cocaine either alone or in combination with opiates and/or alcohol. Cocaine, opiates, or both were involved in greater than three-fourths (77%) of all drug-related deaths. The majority of all decedents were black (57%) and male (76%) with an average age of 42.2 years. Cocaine and ethanol were more frequently detected in black decedents, whereas opiates and polydrug abuse were more common in white decedents throughout the period studied. Preliminary investigation showed a high index of suspicion for the specific drug involved in virtually all opiate and alcohol cases, and in 62% of cocaine-related cases. Overall, the 100 accidental drug deaths in 2002 accounted for 7.5% of all deaths investigated and certified by the Fulton County Medical Examiner's Office. Our study provides further evidence to support the lack of correlation between serum drug levels and the mechanism of drug toxicity in cocaine-related deaths. No statistically significant differences were shown in parent cocaine or benzoylecgonine concentrations between those cases certified as toxicities or poisonings versus those cases certified as aggravating underlying disease or causing an adverse event. In addition, 62% of the cocaine-related death cases were considered initially to be of high suspicion for drug-related death, thus emphasizing the strong importance of scene information/investigative reports in evaluating drug-death cases and in formulating plans of action to handle each individual case. Among the drug-death cases handled by 6 staff medical examiners at the Fulton County Medical Examiner's Office, variation existed in autopsy performance and death certification practices. These issues are discussed in the context of the National Association of Medical Examiners' (NAME) Position Paper on Cocaine, NAME Forensic Autopsy Performance Standards, and other relevant literature. Most variations relate to completeness of the cause-of-death statement (whether or not comorbid conditions are included) rather than classification of manner of death within the office. However, specific wording in the cause of death may have significant ramifications regarding drug-related mortality statistics processed by the vital statistics system, with possible under-representation of drug-related deaths in single-cause mortality data.

This case report describes an acute overdose in a female patient with the serotonin mixed agonist-antagonist m-chlorophenylpiperazine (mCPP), a new synthetic drug that is also a metabolite of the antidepressant trazodone. Following ingestion of three multi-coloured tablets, she developed anxiety, agitation, drowsiness, flushing, visual disturbances and tachycardia. The mCPP concentration was 320 ng/mL in plasma and 2300 ng/mL in urine. Amphetamine (40 ng/mL), benzoylecgonine (47 ng/mL) and alcohol (0.7 g/L) were also detected in plasma. The concentration of mCPP in plasma was approximately six times higher than the usual concentration measured in patients under trazodone treatment (26-108 ng/mL, average 56 ng/mL). However, one should be careful to link the observed symptoms to the use of mCPP only as the other drugs that have also been taken or an interaction between the drugs could also have played a role.

Testing for the presence of cocaine (COC) is common in postmortem and clinical laboratories. COC use may be detected by screening urine specimens for COC metabolite. In the forensic arena, screening positive results are confirmed by a more specific and sensitive technique, such as gas chromatography-mass spectrometry. This article reports the case of an individual who died of COC intoxication but whose immunoassay screen (EMIT) for COC metabolite was negative. Gas chromatography-mass spectrometry analysis of the urine detected benzoylecgonine (BE) at a concentration of 75 ng/mL and COC at 55 ng/mL. These concentrations explain the negative screening result since the cutoff concentration of the assay was 300 ng/mL for BE. The reported cross reactivity with COC was 25,000 ng/mL. However, heart blood concentrations of COC and BE were 18,330 and 8640 ng/mL, respectively. The results from this case provide evidence that an EMIT test alone may fail to detect COC use. Individuals utilizing results of drug screening by immunoassay must be aware of the limitations of this testing methodology.

Cocaine use during pregnancy is difficult to ascertain, and maternal reports are likely to be inaccurate. Presently, the dose-response characteristics between maternal cocaine use and fetal exposure and adverse effects are unknown. Clinically, some babies are harmed, whereas others are not adversely affected. Taking advantage of the fact that cocaine and its metabolite benzoylecgonine (BE) accumulate and can be detected months after exposure in maternal and neonatal hair, an analytical test for cocaine and BE was developed by the authors. The aim of this study was to describe the characteristics of maternal and neonatal hair cocaine as biomarkers of fetal exposure. Of nearly 10,000 cases, all mother-child pairs in whom at least one had cocaine and/or BE detected in hair were identified. The relationship between maternal and neonatal levels was studied. When available, these data were also compared with meconium levels of cocaine. Median cocaine concentration was 10-fold higher in hair of the mothers compared with the neonates (3.56 ng/mg vs 0.31 ng/mg of hair). Infants' cocaine in hair was positively correlated with maternal cocaine and BE in hair (r2 = 0.41 and r2 = 0.22, respectively, P < 0.001 for both correlations). Infants' BE was also correlated with maternal cocaine and BE concentrations in hair (r2 = 0.50 and r2 = 0.27, P < 0.001 for both correlations). Thirty-nine (40%) babies had negative cocaine and BE results despite their mothers being positive. Mothers whose infants were cocaine-positive had a median hair cocaine concentration of 7.34 ng/mg, significantly higher than those whose infants were negative (1.25 ng/mg). Maternal cocaine levels below 0.24 ng/mg may serve as a relative threshold for detectable fetal exposure during the third trimester of pregnancy. Fetal hair grows in the last trimester. Hence, a positive neonatal hair indicates maternal use after pregnancy became known, a strong indicator of maternal addiction. Transplacental exposure to cocaine of babies of addicted mothers is highly variable. The dose-response relationship of both cocaine and BE between maternal and neonatal hair suggests that the placenta protects some fetuses but not others. More research is needed to understand the mechanisms leading to placental defense against cocaine.

Toxicologic analysis is an integral component in the investigation of suicide and requires correlation with a detailed scene inspection, with an extensive exploration into the decedent's medical and social background to uncover suicidal ideation or intent and a postmortem examination of the body. In this review, the authors analyzed 2864 cases classified as suicide upon autopsy and toxicologic examinations between 1993 and 2002 in the Kentucky Division of Medical Examiner's Services. Blood and urine were collected in 95.0% and 72.3% of cases, respectively. A total of 32.5% of the victims had negative blood toxicologic results, and 52.7% of urine toxicology screens yielded no drugs. Analysis of the data indicated that 3 times as many women had taken antidepressants and more than twice as many had consumed opioids. Drug toxicity ("overdose") ranked as the third (9.9%) leading cause of suicide after firearm injury (67.5%) and hanging (13.7%). Women succumbed to drug toxicity more than men (27.5% versus 5.9%). Of the overdose deaths, 66.5% had a negative blood alcohol concentration (BAC), while antidepressants, opioids, and benzodiazepines were detected in blood in 54.4%, 37.4%, and 29.2% of the subjects, respectively. The collection of these data serves the goals of public health and clinicians in devising strategies for suicide prevention.

Accidental ingestion of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) was detected in an infant admitted at the Pediatric Emergency Department by drug testing in urine. Concentrations of MDMA and its principal metabolite 4-hydroxy-3-methoxymethamphetamine (HMMA) in the infant's hydrolyzed urine were 11.7 mg/L and 34.4 mg/L, respectively. Apparent febrile convulsions and cardiovascular side effects resolved within 1 day after treatment with benzodiazepines. Chronic exposure to cocaine was evidenced by segmental hair analysis. Continuous maternal denial of the presence of any drug in the household made diagnosis of accidental ingestion of MDMA and chronic exposure to cocaine problematic. Periodic clinical and laboratory follow-ups were requested to check eventual long-term effects of exposure to illicit drugs and discontinuation of the child from exposure to dangerous environments.

The determination that cocaine is directly responsible for the immediate cause of death should be considered only when there is a reasonably complete understanding of the circumstances or facts surrounding the death. Another, more obvious and immediate cause of death must be absent, or, at least cocaine must be shown to be a significant contributing factor in the chain of medical findings that lead directly to the immediate cause of death. Not all death investigation requires the sequential steps described in this paper, but these steps must be considered early on in the investigation whenever there is scene, investigational, medical or a historical basis to believe that cocaine is directly related to the cause of death. A relatively high profile death when cocaine is known to be involved, or a death involving unusual behavior on the part of the deceased with police involvement are examples where these considerations may well apply. Information needs to be obtained as soon as possible to have the highest chance of successfully documenting the toxicologic basis for the diagnosis. These facts would include, but would not necessarily be limited to, a scene investigation (whenever possible), a careful review of the investigative reports from all involved agencies, the initial core temperature of the body as well as that of the environment at the time of the collapse or death, the past medical history of the individual, and the results of a complete forensic autopsy and toxicologic studies. Knowledge of and an understanding of the current relevant forensic literature on this subject should be available to the reviewer prior to any interpretation of the significance of cocaine upon a specific death.

The National Association of Medical Examiners Committee on Cocaine-related Deaths recommends that the following guidelines be applied in the process of documenting, interpreting, and certifying potential cocaine-related fatalities. The committee cautions that the investigation of any drug-related death requires a complete investigation of the circumstances of death, the death scene, and past medical history. It is also necessary to have the results of the forensic toxicological analysis and those of a complete forensic autopsy examination prior to formulating an opinion as to the cause and manner of death. Cocaine should be considered the underlying cause of the death when 1 or more of the following is true: (1). the circumstances surrounding the death can be associated with an acute cocaine exposure and there are no supervening causes of death; (2). the immediate cause of death is directly due to a readily identifiable mechanism or disease such as a gunshot wound or a stroke, yet the acute use of cocaine was the direct underlying cause of the trauma or the disease process; and (3). chronic cocaine use leads to a disease that results in an ultimately fatal pathologic process leading to organ injury and death. The committee further cautions that reported drug levels may not directly relate to the toxic or lethal effects of the drug upon the patient. These guidelines are intended for use by practicing medical examiners and physicians who certify drug deaths, as well as providing education tools for students.

Objective: To provide current information on general and specific interventions for overdoses likely to require intensive care., Design: Review of literature relevant to selected interventions for general management of overdoses and specific poisons., Results: The benefit of interventions to decrease absorption or enhance elimination of toxins is limited to a relatively small number of specific agents. Antidotes and certain interventions may be helpful in preventing or treating toxicity in specific poisonings when used appropriately. Intensive supportive care is also necessary to achieve good outcomes., Conclusion: Knowledge of the indications and limitations of current interventions for poisonings and overdoses is important for care of the critically ill poisoned patient.

Objective: Cocaine, which first made its appearance >1,000 yrs ago, is now widely used throughout the world. The physiologic responses to cocaine may cause severe pathologic effects. This review highlights the many critical care challenges resulting from these effects., Design: Historical vignettes, epidemiologic factors, modes of preparation and delivery, and the physiologic and pharmacologic effects of these agents are presented., Setting: Cocaine causes intense vasoconstriction, which potentially causes damage to all organ systems. Examples of these toxicities are presented., Patients: The adverse multisystem responses to cocaine exposure produce organ failure, which challenges diagnostic accuracy and therapeutic intervention. Organ system failure involves the brain, heart, lung, kidneys, gastrointestinal tract, musculature, and other organs. These harmful effects are additive to preexisting organ dysfunction., Intervention: Recognition of associated cocaine injury alerts the physician that organ dysfunction is more likely to occur and to be more severe. Such anticipation helps plan for therapy in the critical care setting., Results and Conclusions: Cocaine use is an expanding health hazard, despite intense governmental efforts to contain its distribution and use. Recognition of the signs and symptoms of cocaine toxicity help anticipate the subsequent organ dysfunction and implement earlier organ system support.

Diphenhydramine (DPH)-related deaths in adults are extremely rare, and detailed autopsy studies are rarer still. Toxicologic and anatomic findings in 4 cases of suicidal DPH overdose are described and compared with findings in a database of cocaine- and heroin-related deaths. Blood DPH levels were many times higher than those considered therapeutic (5000-35,000 ng/ml versus 50-100 ng/ml). Marked pulmonary edema with visceral congestion was a constant finding. Mean lung-body weight ratios for DPH, cocaine, heroin, and trauma controls were 0.015, 0.015, 0.019, and 0.013, respectively. When normalized for body weight in this fashion, edema in DPH-related deaths was comparable to that in cocaine-related deaths. Cardiac enlargement was apparent in 3 of the 4 DPH cases, 1 with marked myocardial fibrosis. The finding of increased heart size suggests that preexisting heart disease may provide the necessary substrate for lethal cases of DPH toxicity. Pulmonary edema in these cases remains unexplained, with edema in cases of heroin-related toxicity significantly worse than that produced by cocaine or DPH (p < .0001). Because DPH and cocaine can exert similar effects on the heart, a common mechanism may produce pulmonary edema in both. A different mechanism may account for heroin-related edema.

A case report of an 11-month-old infant with cocaine intoxication and intussusception is presented. We present this case because there are no prior reports in the literature of cocaine intoxication associated with intussusception. The diagnosis was not initially considered in this patient. We feel the association is biologically plausible and alert physicians to consider intussusception in the differential diagnosis of the cocaine-exposed child with vomiting and abdominal pain.

Objective: To relate the clinical presentation of acute cocaine intoxication in the third trimester to preeclampsia and eclampsia., Methods: Eleven women presented to Long Beach Memorial Women's Hospital and the University of California, Irvine Medical Center with hypertension and clinical symptoms of headache, blurred vision, abdominal pain, or seizures in the third trimester of pregnancy. Each had a positive urine drug screen for cocaine. The laboratory evaluation for preeclampsia included a complete blood count, platelet count, uric acid, aspartate aminotransferase, alanine aminotransferase, creatinine, and urine for protein content., Results: All women had a diastolic blood pressure of at least 90 mmHg, which returned to the normal range 45-90 minutes after admission. Each presented with one or more symptoms associated with preeclampsia, which ultimately improved as the drug wore off. In addition, all laboratory evaluations for preeclampsia were negative., Conclusion: If a patient presents in the third trimester with hypertension and clinical symptoms of preeclampsia that rapidly improve shortly after admission, cocaine intoxication should be considered as the possible source.

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.

Computed tomography of a man with cocaine-induced hepatic necrosis demonstrated a narrow peripheral zone of decreased attenuation that showed widening on follow-up examination 4 days later. The patient died of fulminant hepatic necrosis 10 days after presentation.

Acute crack cocaine intoxication has become a significant problem in both adolescent and adult patients. Recently, cases of cocaine toxicity in infants and toddlers have been described. We report a four-year-old child with acute hemorrhagic diarrhea and shock after intoxication by crack cocaine. Acute cocaine intoxication should be considered in the differential for hemorrhagic diarrhea and shock. The gastrointestinal decontamination following cocaine ingestion is discussed.

We retrospectively studied 474 patients seen at Hennepin County Medical Center because of medical complications related to acute cocaine intoxication. Of the 474, 403 had no history of seizures. Seizures within 90 minutes of cocaine use was the primary diagnosis in 32 (7.9%) of the 403. The majority of seizures were single, generalized, induced by intravenous or "crack" cocaine, and not associated with any lasting neurologic deficits. Most that were focal, multiple, or induced by nasal cocaine were associated with an acute intracerebral complication or concurrent use of other drugs. Of 71 patients with a history of non-cocaine-related seizures, 12 (16.9%) presented with cocaine-induced seizures; most of these were multiple, of the same type as those in their history, and induced by even nasal cocaine. In the 44 cocaine-induced seizure patients, a pattern of habitual cocaine abuse was associated with diffuse brain atrophy on CT and diffuse slowing on EEG.

We report the symptomatology, clinical, and laboratory findings in four patients following oral ingestion of crack cocaine. All of the patients had a positive urine test for cocaine metabolites measured by gas chromatography-mass spectroscopy. Retrospective analysis of the four patients revealed alterations in function of the cardiovascular system (4), the autonomic nervous system (4), the central nervous system (3), and the gastrointestinal system (1). Three patients ingested crack cocaine as a direct result of confrontation with law enforcement officers. The symptomatologies of acute toxicity from oral ingestion of crack cocaine are related to its effect on the cardiovascular system and the brain. Cocaine toxicity should be considered in patients with acute and unexplained cardiovascular, central nervous system, or gastrointestinal complaints. Law enforcement personnel should be made aware of the signs and symptoms of cocaine intoxication and be made aware of the propensity to ingest the evidence.

A case of a nine-month-old male who ingested cocaine is presented. The rarity of this type of ingestion, as well as the caretaker's denial of the presence of cocaine in the household, made rapid diagnosis of this infant's malady difficult. We present this case to alert physicians to the presentation and treatment of cocaine-intoxicated infants.

A 29-year-old homosexual man died as a result of cocaine inserted into his rectum by his sexual partner. The apparent purpose of this form of drug abuse is to relax the anal sphincter muscles. However, as in this case, cocaine administered in this fashion has a high potential for toxicity. The possible legal and medical ramifications of death resulting from this practice are discussed.

The deleterious effects of cocaine have been described in the adult population and in the neonate. Documentation of adverse effects in pregnant patients has been limited. We report the first known fatal vaginal administration of cocaine.

We report seven fatalities resulting from the ingestion of illicit drugs packaged in condoms, rubber balloons, or plastic bags which were observed in the last 4 years at the Office of the Chief Medical Examiner, State of Maryland. All the victims, with the exception of one, were men ranging in age from 19 to 37 years. There was no racial predominance. No drug paraphernalia was found at any scene. In two cases, seizure-like activity was documented. One victim had recently returned from Nigeria; therefore, Lassa fever was initially suspected. Two of the victims were "body packer" contrabanders who had just arrived from Africa. They used body cavities to hide large amounts of heroin to avoid U.S. Customs. The other five cases were "mini-packers," small-time illicit drug dealers who had swallowed a single bag of cocaine to avoid police detection. The possible mechanism of leaking or rupture of the latex container is discussed.