Barbiturate poisoning . In relation to the advance of civilization, barbiturate poisoning is observed more frequently every day, especially in paramedical personnel for self-poisoning purposes and in young subjects addicted to repeated ingestion of drugs in significant doses, which put them at risk their life and require specialized treatment in an area equipped with modern means, which allow the correct care of disorders of vital functions.
Summary
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- 1 Classification according to its mode of action
- 2 Predisposing and aggravating factors
- 3 Pathophysiology
- 4 Clinical picture
- 5 Diagnosis
- 6 Evolution
- 7 Forecast
- 8 Treatment
- 9 Complications
- 10 Source
Classification according to its mode of action
- Ultrashort: 0.3 h ( thiopental, metohexital, tiamilal)
- Short: 3 h (pentobarbital, cyclobarbital, secobarbital)
- Average: 3 to 6 h (butabarbital, amobarbital, approvebital)
- Prolonged: 6 to 12 h (barbital, mephobarbital, phenobarbital): this being the most frequently used as an anticonvulsant and hypnotic, it is the one that produces the most intentional or accidental poisonings in our environment.
The short and medium-acting ones are used as sedative-hypnotics: the ultra-short ones, as anesthetics , and the long-acting ones, mainly, as anticonvulsions. The speed of action is associated with increased fat solubility and implies a predominance of liver metabolism. All of them, with the exception of ultra-short-acting ones, are rapidly absorbed in the digestive tract. Those of short action are metabolized in the liver and those of long action are eliminated in greater proportion in the renal route.
Predisposing and aggravating factors
Different factors determine the severity of barbiturate poisoning and among them are the type of drug, the dose, the patient’s tolerance, age and previous health status. Short-acting barbiturates commonly produce situations of shock and respiratory failure, given their high fat solubility and easier distribution in the brain . Poisoning at extreme ages of life has a worse prognosis, as does concomitant liver or kidney disease , since these organs are the route of excretion of these drugs . The mellitus diabetes , the pregnancy , the alcoholism , the malnutrition and associated chronic diseases also exacerbate the prognosis.
Pathophysiology
Barbiturate poisoning occurs mostly from ingestion with a suicidal mood, although the accidental cause sometimes occurs in children. Criminal poisoning practically does not exist in our environment. Ingestion of the drug does not produce local irritation in the upper digestive segment and is absorbed in its entirety, absorption that is maximum when the stomach is empty or if a diet rich in fats has been ingested , which increase the solubility of the barbiturate. Barbiturates depress intestinal motility and, therefore, the absorption time of the ingested dose is lengthened. Once absorbed, they are evenly distributed throughout the tissues , especially the nervous system, and progressively depress brain function, leading to deep coma and even death .
The mechanism of action of barbiturates is not completely known. They are believed to act by stimulating the synaptic inhibitory system GABA (gamma butyric acid), preventing neurotransmission in the CNS. Its sedative and hypnotic action may be due to an inhibition of neuroconduction at the level of the ascending reticular substance, resulting in a decrease in impulses reaching the cerebral cortex.
Barbiturates are metabolized slowly, are conjugated in the liver, and are excreted by the kidney . The Phenobarbital has the characteristic of being less soluble and is not metabolized so widely. Almost 25% is excreted unchanged in the urine . These properties will be taken into account when evaluating the treatment methods to be used in the management of poisoning by these products.
Clinical picture
After ingestion of a toxic dose of barbiturates, it is common for an initial period to occur which is characterized by behavioral disorders such as euphoria, agitation, loquacity, inconsistencies, hallucinations, drunken gait, etc. This period is followed by progressive unconsciousness, which ranges from a sleeping, awake patient to a comatose patient with abolished reflexes, respiratory depression with cyanosis or circulatory failure, and shock. The pupils are normal, miotic, or mydriatic and with little response to light . The highest risk of death is due to depression of breathing, which causes alveolar hypoventilation. Depression of myocardial function is not uncommon, which together with peripheral vascular dilation and decreased venous return , produce hypotension and shock. Progressive coma with loss of the pharyngeal and laryngotracheal reflex predisposes to aspiration and bronchopneumonia. This, together with complications from decubitus that sometimes occurs, explains the high risk of death , if emergent medical actions are not carried out. The hypothermia is present only in the most severe forms. According to the degree of impairment of consciousness and vital signs, victims are classified into 5 groups or stages:
- Stage 0: stuporous, but responds to the verbal command.
- Stage 1: responds to painful stimuli, but not verbally.
- Stage 2: does not respond to stimuli, but maintains reflexes and vital signs are stable.
- Stage 3: does not respond to stimuli, is areflexic, but maintains stable vital signs.
- Stage 4: does not respond to stimuli, is arrefléxico and its vital signs are unstable.
Stage 4 shock results from drug-induced spinal depression and is an indication of imminent death if one does not proceed vigorously.
Diagnosis
The clinical diagnosis of barbiturate coma is made on the basis of a history of suicidal tendency in the patient, psychological or psychiatric disorders, findings of remains or drug packaging. Other causes of coma, especially metabolic, such as diabetic ketoacidosis, such as liver and uremic, should be excluded. All coma, whether neurological, infectious, traumatic, tumorous, or cerebrovascular, are included among the differential diagnoses. The demonstration of barbiturate in samples sent to the toxicology laboratory (gastric content, blood , urine ), is of great help to clarify the diagnosis. It should be remembered that associations of toxic doses of barbiturates with other psychotropic drugs and alcohol are frequent..
Evolution
In mild forms the patient evolves towards healing, even spontaneously. The evolution is also favorable when a timely and well-directed treatment is applied. Little by little the reflexes appear (first the corneal), then the sensitivity to pain manifests, and consciousness slowly recovers, after a transitory state of excitement. Sometimes ideation and speech disorders persist for several days. Toral restitution without sequelae is the usual one, except in those cases that have suffered brain damage secondary to hypoxia or in which complications arise, such as bronchopneumonia, pressure ulcers and others induced by the coma.
Forecast
The prognosis depends on the dose, the age and the state of health of the patient, and the rapid and timely application of life-support measures and purifying methods of the poison, with which mortality is significantly reduced.
Treatment
The treatment of barbiturate poisoning is based on: prevention, application of life support measures, purification of the poison , use of general measures and treatment of complications. Prevention is achieved with proper management and control over the use of these drugs. Measures include: prescription sales, proper dosing, and keeping medications out of the reach of children, psychiatric patients, and the elderly with disabilities. Gastric emptying measurements and the administration of activated carbon repeatedly during the first 24 h, associated with a cathartic, are indicated if the digestive tract has been the gateway. Due to the ability of barbiturates to slow down the digestive tract, the mentioned techniques can be indicated within the first 6 to 8 h of ingestion of the poison. In general, with the measures described, more than 95% of these poisonings are successfully treated.
