In this study we described acute medical problems in patients with blood-test confirmed cocaine use. Most patients were men who chronically abused cocaine and had no employment. Of note, 53% of the patients were over 30 years old in line with increases in age of patients with cocaine-related health problems in other European countries
]. The patients who abused more than one drug did so most commonly by combining cocaine with ethanol, opioids or cannabis, as reported by others
]. We found that such polydrug use lead to significantly more severe intoxications compared with the use of cocaine alone. Co-use of ethanol was predominant in the present and in the previously studied series of cocaine intoxications
]. Ethanol co-use with cocaine forms cocaethylene but also increases the plasma levels of cocaine, cocaine-induced subjective and also its cardiostimulant effects
]. Ethanol may therefore increase the toxicity of cocaine
] consistent with our findings. In accordance with data from the US
], most visits occurred during night time. In our study, cocaine was mostly abused nasally or intravenously while predominantly intravenous and inhalational use was reported in the US
] and mainly nasal administration was documented in Spain
]. It is possible that intravenous drug use is overrepresented in our sample because it may lead to increased utilization of the ED due to more severe complications. Severe toxicity was more frequent with injection drug use compared to other routes of administration but this association was not statistically significant in the present study. In our study and in line with the work by others
], co-use of other stimulants such as amphetamines or methylphenidate was hardly ever reported and amphetamines were only sporadically detected in the blood. In a recent analysis of exposures reported to the Swiss Toxicological Information Centre, co-use of amphetamines was noted in about 10% of the cocaine user
]. Use of GHB was very rarely reported in our study whereas 15% of GHB users who presented to an ED in Zurich reported co-ingestion of cocaine
]. In Spain, co-use of GHB in patients with cocaine intoxication was reported in only 6% of patients
]. Use of methylphenidate was not reported in our study in accordance with an analysis of a small number of methylphenidate users presenting to the Basel ED
] who did not co-use cocaine. In contrast, cocaine users with opioid substitution therapy in the Basel area indicate that they misuse methylphenidate orally, nasally, or intravenously as a substitute for cocaine
]. Thus, methylphenidate co-use may have gone undetected because, contrary to other amphetamines, it was not detected by the blood screening test. Taken together, the data indicate that cocaine is not typically combined with other stimulants but rather co-used with sedating drugs including opioids, ethanol, or cannabis.
Chief complaints associated with acute cocaine toxicity were mainly neuropsychiatric or cardiovascular. The most commonly reported symptoms included anxiety, restlessness, agitation, chest pain and palpitations similar to previous studies
]. Sixty-four percent of the patients presented with psychiatric symptoms similar to the 55-61% reported by recent previous studies
] but higher than the 31-37% reported by earlier studies
]. Loss of consciousness occurred in the multidrug user group, mainly due to concomitant use of ethanol or opioids. Hypertension and tachycardia were the main clinical signs regardless whether cocaine was used alone or in combination with other substances. Twenty-one percent of the patients reported chest pain. Percentages of patients reporting chest pain ranged from 11-39% in other case-series
]. Two (1%) patients suffered from cocaine-related acute MI. MI similarly occurred in 1% of the patients presenting with cocaine toxicity and in 6%
] of those with cocaine-associated chest pain in other studies
]. Cardiovascular problems including myocardial infarction and arrhythmias are well-known medical complications of cocaine use
]. Cocaine use has been observed in about 25% of 18–45 year-old patients with myocardial infarctions in
]. Myocardial infarction may result from vasospasms
] and excessive sympathetic activation. However, most cardiac deaths occur in patients with chronic cocaine use
] and may involve structural cardiovascular disease including myocardial hypertrophy and microangiopathy
]. In the presents study, both cases of cocaine-induced myocardial infarction occurred in chronic cocaine users. Stenting of significant coronary artery stenosis was performed in one while no coronary flow limitation was detected in the other. Similar to acute MI, cocaine use is an important risk factor for ischemic or hemorrhagic stroke in younger patients without classical cardiovascular risk factors
]. In the present study, there was one patient with cocaine-induced ischemic stroke without other known risk factors except for tobacco smoking. Potential mechanisms of cocaine-induced ischemic or hemorrhagic stroke include arterial hypertension, vasospasm, disruption of cerebrovascular autoregulation, and enhanced platelet aggregation
]. Other severe neurological complications in our study included 3 cases of self-limited seizures (2%). In all cases the patients had used other substances in addition to cocaine (heroin in 2 cases and ethanol in 1 case). Furthermore, one patient had a known history of seizures. Self-limited seizures were reported in 3-4% of patients in previous studies
In our study, the management of patients included administration of intravenous fluids and benzodiazepines to control central and peripheral manifestations of sympathetic toxicity. The majority of patients including most patients with severe acute intoxications could be discharged home after less than 24 hours of observation in the ED as shown previously
]. However, a significant number of patients needed psychiatric evaluation and referral.
This study has several limitations. As in all retrospective studies, there was some missing data and the initial patient histories and clinical data were not recorded in a standardized manner. In addition, it is possible that a few patients with positive drug tests for cocaine and use before 12 h prior to presentation were misclassified as acute intoxications. Similarly, acute co-use of cannabis was likely overestimated based on positive blood tests. In contrast, there was no screen for GHB in all patients and co-use of GHB may have gone undetected. As in all such studies, data from only one large ED may not be representative and reflect local drug using trends. Additionally, severe toxicity may have been overrepresented because we act as referral center for the Basel area including parts of France and Germany.
Our study has also several strengths. We had detailed patient and clinical data documentations in contrast to studies based on coded diagnoses or analyses of poison center data. In addition, the exposure to cocaine was confirmed in the blood for all patients and confirmative blood tests results for co-used ethanol and illicit drugs were also available for the majority of patients.