Regular use of even therapeutic doses of barbiturates most likely leads to the development of tolerance and dependence. While tolerance to sedative and intoxicating effects develops, the lethal dose is not increased in the same way. As a result, acute barbiturate poisoning can occur at any time during chronic intoxication. Abrupt withdrawal from barbiturates can be life-threatening, unlike opioid withdrawal. Withdrawal symptoms are similar to those of alcohol withdrawal. The individual becomes restless, anxious, anxious and weak, complaining of abdominal cramps, nausea and vomiting. Symptoms peak on the second and third day, when cramps may occur. Up to 75% of subjects may have one or more seizures and about 66% may develop delirium for several days. Delirium is similar to what is sometimes seen during alcohol withdrawal (delirium tremens) and involves anxiety, disorientation and visual hallucinations. During delirium, restlessness and hyperthermia can lead to exhaustion, cardiovascular collapse and death. However, this is not inevitable and symptoms may disappear over time (usually after about eight days).
Recently, such controversy has raged over barbiturates that the dispute has been dubbed „the battle of the barbiturates.“ E. Number of patients taking barbiturates, 17 (41.5%) If chronic barbiturate poisoning is indeed not very rare, why does it seem relatively unknown and diagnosed? Morgan (1953) believes the condition is common but not well recognized because it is unknown, just like bromide psychosis a quarter of a century ago. Sometimes the state resembles long-standing alcoholism or, as Willcox (1934a) and Purvis-Stewart pointed out many years ago, it can mimic a large number of neurological diseases. Again, generally known, however, mild chronic barbiturate poisoning can be diagnosed more often; In a London university hospital, the „interesting psychiatric syndromes“ resulting from the prolonged use of barbiturates as sedatives and hypnotics became known as „chronic subclinical barbiturate poisoning“ (Strauss). As long as the addict is able to satisfy his drug demand, he may feel comfortable despite his symptoms, although „persistent symptoms, especially those accompanied by a drug request“ (Hunter and Greenberg) can arouse suspicion. If this request is not met, the addict may suffer from symptoms such as anxiety, depression, insomnia; It can be assumed that these temporary withdrawal symptoms show an exacerbation of its original symptoms, so more barbiturates can be prescribed more frequently and in increasing doses. A vicious circle can set in this way, so that an original.“ a mild psychiatric disorder turns into a serious condition“ (Hunter, 1957), which in rare cases is known to have led to a leukotomy (Hunter) or several such surgeries. „Patients with chronic states of tension“ – as Sargant (1958) writes – may remain tense and anxious for many years to come because they suffer more from a state of chronic barbiturate tension self-induced or induced by a doctor than from a persistent anxious neurosis itself. I now see patients who have undergone one, two or even three leucotomies for prolonged chronic tension and then turned out to be cases of chronic barbiturate addiction. Surveys of N.H.S.
prescriptions in Scotland and the United Kingdom in 1949 and 1951 respectively showed that sedatives and hypnotics accounted for about 15% of all prescribed drugs, with barbiturates alone accounting for 9.4% in the 1949 sample (Dunlop et al. 1952) of more than 17,000 N.H.S. prescriptions. In England and Wales, analyses of monthly samples of more than 100,000 NHS prescriptions carried out regularly by the Department of Health were carried out; Such a sample represents less than 1% of the total monthly number of N.H.S. revenues, but is considered fairly reliable (Davis), and the N.H.S. processes revenues for more than 90% of the population. In January 1953, barbiturates accounted for 6.30% of all prescriptions, while other sedatives and hypnotics accounted for 2.53% (Table 7). In October 1954, 8.8% of prescriptions were for barbiturates or preparations containing barbiturates, with barbiturates being the only or most important therapeutic agent in 6.4% (Brooke). In October 1955, out of 106,000 prescriptions, more than 10,000 (9.6%) were barbiturates or preparations containing barbiturates (Davis).
The estimated cost of barbiturates for home service only in the N.H.S. At that time, there were more than 1/2 million pounds a year, which is not much less than a billion billion doses of a barbiturate or 100,000 pounds in weight (Davis). Willcox (1934b) went so far as to say that, in his experience, „most deaths from barbiturate poisoning occur in people who have taken the drugs in repeated daily doses“ and that barbiturates „have almost never been used as a means of suicide, except by individuals accustomed to their daily use and daily effects.“ Is the amount of barbiturates prescribed also the amount taken? Camps (1961), a pathologist with the Ministry of the Interior, noted that „fantastic amounts“ were found in the homes of people who had committed suicide; „There`s nothing like having 1,000g of fast-acting barbiturate in a household.“ He estimated that at least 10% of them were unused in people`s homes, and he had no doubt that promiscuity orders were an incentive to take overdoses. Locket (1957a) also noted that many patients keep a large amount „in stock“ and carelessly leave the tablets within reach of young children. In 1952 (b), the Lancet had stated that such revenues generally applied to large quantities; The average sizes of current barbiturate prescriptions are estimated in Table 8. Barbiturates injected into a vein create an almost immediate feeling of heat and drowsiness. In addition to the usual dangers of injection (hepatitis, HIV, etc.), barbiturate injectors have an increased risk of overdose, gangrene and skin abscesses. Barbiturates in case of overdose with other sedatives of the CNS (central nervous system) (e.g. alcohol, opiates, benzodiazepines) are even more dangerous due to the CNS additive and the respiratory calming effect. In benzodiazepines, not only do they have additive effects, but barbiturates also increase the binding affinity of the benzodiazepine binding site, resulting in exaggerated effects of benzodiazepines. (e.g.
If a benzodiazepine increases the frequency of opening the channels by 300%, and a barbiturate increases the duration of their opening by 300%, the combined action of the drugs increases the overall function of the channels by 900%, not by 600%. There is a small group of List II drugs for which physicians must write prescriptions according to the same stricter guidelines as for List I drugs (write the prescription entirely in letters, list the patient`s name, and include the name and initials, address, city, and telephone number of the licensed prescriber who issues the prescriptions, and the name and initials, address and place of the person to whom the order is issued). This group of drugs includes barbiturates amobarbital, butalbital, cyclobarbital and pentobarbital. NOTE: The doses indicated correspond only to the hypnotic use of these drugs. Maximum doses of barbiturates are not considered when used as anticonvulsants. A barbiturate[a] is a drug that acts as a sedative of the central nervous system. Barbiturates are effective as anxiolytics, hypnotics and anticonvulsants, but have the potential for physical and psychological dependence, as well as overdose potential among other possible side effects. They have been largely replaced by benzodiazepines („Z drugs“) in routine medical practice, particularly in the treatment of anxiety and insomnia, due to the significantly lower risk of addiction and overdose and the lack of an antidote to barbiturate overdose. Nevertheless, barbiturates are still used for various purposes: general anesthesia, epilepsy, treatment of acute migraine or cluster headaches, acute tension headaches, euthanasia, death penalty and assisted suicide.
[2] In this way, the anticonvulsant properties of barbiturates were discovered, with phenobarbital being the first truly effective drug for the treatment of epilepsy (Iváñez and Díez-Tejedor 1998). Table 2 shows examples of anticonvulsants commonly used in the treatment of epilepsy before and after the introduction of phenobarbital. The discovery of the anticonvulsant properties of phenytoin (the first drug to show that an antiepileptic drug does not need to be hypnotic) by Houston Merritt and Tracy Putnam (Boston City Hospital, USA) in 1938 broadened the spectrum of antiepileptic drugs (the first drug to show that an antiepileptic drug does not need to be hypnotic), in 1944 of trimehadion and in the late 1950s of carbamazepine, resulting in a reduction in the use of barbiturates in these applications. Some symptoms of an overdose usually include slowness, incoordination, difficulty thinking, slow speech, erroneous judgment, drowsiness, shallow breathing, falling, and, in severe cases, coma or death. The lethal dosage of barbiturates varies greatly with tolerance and from one individual to another. The lethal dose is highly variable in different members of the class, with superpotent barbiturates such as pentobarbital potentially fatal at much lower doses than low-acting barbiturates such as butalbital.
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