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Missed Opportunities? Beneficial Uses of Illicit Drugs
Published in Ross Coomber, The Control of Drugs and Drug Users, 2020
Lester Grinspoon, James B. Bakalar
The greatest advantage of cannabis as a medicine is its unusual safety. The ratio of lethal dose to effective dose is estimated on the basis of extrapolation from animal data to be about 20,000:1 (compared to 3–50:1 for secobarbital and 4–10:1 for alcohol). Huge doses have been given to dogs without causing death, and there is no reliable evidence of death caused by cannabis in a human being. Cannabis also has the advantage of not disturbing any physiological functions or damaging any body organs when it is used in therapeutic doses. It produces little physical dependence or tolerance, and there has never been any evidence that medical use of cannabis leads to habitual use as an intoxicant.
Homicide
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Burkhard Madea, Musshoff Frank, Schmidt Peter
Whole blood cyanide levels are higher than plasma levels because of the concentration of cyanide in the red blood cells. Correlation of symptoms to whole blood levels is misleading because the effect of cyanide depends on the intracellular concentration at the cytochrome oxidase binding sites and the duration of poisoning. Peak whole blood cyanide concentrations lower than 0.2 mg/l usually do not cause symptoms, although poisoning has sometimes occurred at lower levels [2]. Whole blood cyanide levels in smokers may reach 0.4 mg/l without causing symptoms. At cyanide concentrations between 0.5 and 1.0 mg/l, untreated patients may be conscious, flushed and tachycardic. Stupor and agitation can appear with peak blood levels between 1.0 and 2.5 mg/l. Cyanide levels greater than 2.5 mg/l are associated with coma and are potentially fatal without treatment. According to Baselt and Cravey [18], the minimal lethal dose has been estimated to be 100 mg for HCN, 150 mg for sodium cyanide and 200 mg for potassium cyanide. Nevertheless, factors such as age, body mass, state of health, and mode of ingestion may influence these values, and survival after the ingestion of larger quantities has been reported. In this respect, 37 mg of HCN has been fatal, whereas recovery has been reported after the ingestion of 300 mg [7]. The blood cyanide concentrations in 32 fatal cases ranged between 0.4 and 230 mg/l (mean 37 mg/l) [137]. In comparison with these published data, the blood cyanide levels in our cases (3.0–80.9 mg/l) provided sufficient evidence to determine that death was due to cyanide toxicity.
Sedative and Hypnotic Drugs
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Arup Kumar Misra, Pramod Kumar Sharma
Barbiturate poisoning varies with its lethal dose. Severe poisoning with barbiturate happens when the dose is more than the 10 times of its therapeutic dose for hypnosis. If other depressant drugs or another sedative–hypnotics drugs are given concomitantly then the quantity of drug to be lethal is lowered. Barbiturate poisoning is most commonly seen in children due to accidental poisonings, suicidal bid, and drug abusers (Eugene et al., 1952). The patient is comatose with respiratory system affected early in severe barbiturate poisoning. Rapid and shallow or slow breathing pattern are characteristic of barbiturate poisoning. The lethal dose decreases the cardiac contractility leading to fall of blood pressure due to the depressive effect on the cardiovascular system. The medullary vasomotor centers and sympathetic ganglia are depressed by barbiturates leading to hypoxia (Eugene et al., 1952). Severe barbiturate poisoning may cause to kidney failure and pulmonary complications like atelectasis, edema, and bronchopneumonia. Management of barbiturate poisoning consists of supportive procedures like maintaining airway, breathing, and circulation. Forced diuresis, urine alkalinization, and maintaining of hydration will increase the renal excretion of barbiturate. In barbiturate poisoning, use of CNS stimulants are contraindicated (Santos and Olmedo, 2017).
Characteristics of emergency department presentations following ingestion of Taxus baccata (yew)
Published in Clinical Toxicology, 2023
Vanessa Alexandra Buetler, Alexandra Maria Braunshausen, Stefan Weiler, Jolanta Klukowska-Rötzler, Aristomenis K. Exadaktylos, Evangelia Liakoni
The toxicity of Taxus baccata is mediated by two major taxine alkaloids, taxine A and taxine B, that are mainly present in all parts of the plant with the exception of the berries [1,3–7]. The cardiotoxic effects are mostly induced by taxine B and presentations following ingestion can range between asymptomatic cases and life-threatening cardiotoxicity [5,8]. Ingestion of about 50–100 g yew leaves (corresponding to 0.6–1.3 g yew leaves/kg body weight, or 3–6.5 mg taxines/kg body weight, or more than 100 leaves) can be lethal [4,6,9]. However, the exact lethal dose is unknown. The amount of the taxines absorbed can vary with several factors, including the preparation of the material (higher if leaves minced or mashed before ingestion than with untreated leaves) as well as the season of the year (higher taxine concentrations in the plant during winter) [4,10]. First signs of intoxication can be non-specific, such as nausea, emesis and abdominal pain [4]. In severe intoxications, cardiotoxicity can occur, mediated through inhibition of sodium and calcium channels, with potentially fatal outcome [5,6,8,9]. The diagnosis is mainly based on the patient’s history or identification of leaves in the gastrointestinal tract, while detection of specific alkaloids with mass spectrometry can also be used for confirmation [1,6,11]. Treatment is focused on decontamination measures and supportive care, and there is no known antidote available [4,12].
Cannabis as a potential compound against various malignancies, legal aspects, advancement by exploiting nanotechnology and clinical trials
Published in Journal of Drug Targeting, 2022
Nazeer Hasan, Mohammad Imran, Afsana Sheikh, Suma Saad, Gaurav Chaudhary, Gaurav Kumar Jain, Prashant Kesharwani, Farhan J. Ahmad
In comparison with other medications, cannabinoids have a promising safety profile. Various studies suggested that, as compared to codeine, THC is more sedating but different from opioids [8,28,210,211]. The dependence risk on cannabis is reported to be 9% in long-term users [212], significantly less than heroin addiction rates, cocaine, alcohol, and prescribed anxiolytics [212]. However, cannabis in a moderate amount has shown to be safe without inducing any changes in heart rate, blood pressure, neurologic testing, or blood tests [213]. Unlike other controlled substances, patients do not seem to develop a tolerance for cannabinoids [213]. The strategy-‘start low, go slow, and stay low’ should be adopted to mitigate the associated adverse effects by evaluating the balance between efficacy and safety [214]. In the context of toxicity, in one of the studies, it was found that the approximate ratio of toxicology threshold (based upon lethal dose (LD50) in comparison to daily dose intake for THC was much higher than for many other agents, such as opioids that illustrate the safety of cannabis for medical use [215].
Nicotine intoxication by e-cigarette liquids: a study of case reports and pathophysiology
Published in Clinical Toxicology, 2020
Gerdinique C. Maessen, Anjali M. Wijnhoven, Rosalie L. Neijzen, Michelle C. Paulus, Dayna A. M. van Heel, Bart H. A. Bomers, Lucie E. Boersma, Burak Konya, Marcel A. G. van der Heyden
There is no consensus on the lethal dose of nicotine. In this study, we provide a clear overview of nicotine plasma concentrations in survivors versus patients that died. In our dataset, the lethal nicotine concentration is between 800 and 1600 µg L−1, which is 4.4- to 8.9-fold higher than the generally accepted lethal oral dose of 60 mg or less that would lead to a plasma concentration of approximately 180 µg L−1 [15]. This latter plasma concentration is an estimate, since there are individual differences in nicotine metabolism, due to genetic polymorphism and other interindividual differences [38]. For example, women generally metabolise nicotine more rapidly than men [51]. Nevertheless, this results in minor differences and does not explain the gap between ±180 µg L−1 and 800–1600 µg L−1. Thus, there is a mismatch between the lethal dose consistently stated in textbooks, databases and safety sheets (30–60 mg), and the lethal doses we found in cases of nicotine intoxication. Such discrepancy has been noticed before, but the 60 mg-value is still widely accepted [15]. Our data thus supports the suggestion of Mayer [15] that revision of the 60 mg lethal dose is necessary.