Intensive Care of Acute Poisoning - A. V. Hovenko 2010

Main types of acute poisoning and their treatment
Drug poisoning
Hypnotic drug poisoning

The group of hypnotics is primarily based on the following drugs:

I. Barbiturates of varying duration of action:

a) long-acting (8-12 h) - barbital (veronal), phenobarbital (luminal);

b) intermediate-acting (6-8 h) - cyclobarbital, barbamil (amobarbital sodium);

c) short-acting (4-6 h) - hexobarbital, pentobarbital sodium (nembutal).

II. Combination agents containing barbiturates (bellataminal, belloid, bellaspon).

III. Non-barbiturate hypnotics (noxiron, chloral hydrate, bromisoval).

IV. Quinazolone derivatives (methaqualone).

Poisoning with barbiturates and non-barbiturate hypnotics.

Barbiturates are a group of medicinal agents derived from barbituric acid that exhibit hypnotic, anticonvulsant, and narcotic effects due to their Central Nervous system (CNS) depressant action. Barbiturates are administered orally in powders and tablets, as well as intramuscularly, intravenously (primarily for anesthesia), and rectally.

Indications for use: irritability, insomnia, neurotic conditions, neurocirculatory dystonia, convulsions, spasmophilia, chorea, etc.

Barbiturates are also used in anesthesiology to prepare a patient for anesthesia — premedication with barbiturates enhances the effects of narcotic, local anesthetic, and analgesic agents. Prolonged use of barbiturates can lead to tolerance and dependence. Administration of barbiturates sometimes causes allergic reactions, as well as adverse effects such as anxiety and agitation.

MECHANISM OF ACTION. Poisoning with barbiturates and their derivatives occurs quite frequently and is the result of accidental overdoses or suicide attempts. Upon oral administration, absorption takes place in the digestive tract. Barbiturates are weak acids, poorly soluble in Water and highly soluble in fats. The concentration of unbound, physiologically active barbiturates increases in hypoproteinemia, acidosis, and hypothermia.

Toxic and fatal doses of these drugs exceed therapeutic doses several times over. For instance, 5-10 therapeutic doses of barbamil cause severe poisoning, 16 doses result in death, and the lethal dose of phenobarbital is 0.1 g/kg. The lethal concentration corresponds to 10 single therapeutic doses of any individual drug or their combination taken simultaneously.

Clinical presentation. The manifestations of barbiturate poisoning are characterized by four developmental stages:

I - somnolence (Sleep onset);

II - superficial coma;

III - deep coma;

IV - post-comatose period.

Stage of somnolence - characterized by drowsiness, weakness, apathy, slurred speech, and ataxia. Pupils are moderately constricted, and the light reflex is satisfactory. Hypersalivation is observed. Reflex activity is preserved; the patient responds to painful and loud auditory stimuli. Respiratory and circulatory Functions are unimpaired.

Mild poisoning may be limited solely to these manifestations. After 10-15 hours, the patient wakes up spontaneously without any medical intervention.

Stage of superficial coma - characterized by deep sleep with preserved Reflexes; consciousness is absent. Pupils are constricted; corneal, pupillary, and deep tendon reflexes are present but diminished. Pathological reflexes (such as Babinski or Rossolimo signs) and mild nuchal rigidity may appear.

Respiration is slowed, and intermittent cyanosis is noted. The pulse is somewhat accelerated, and Blood pressure remains within normal limits.

During this period, mechanical asphyxia may occur due to glossoptosis (posterior Displacement of the Tongue), aspiration of vomitus, or bronchorrhea.

As poisoning progresses, deep coma develops, characterized by areflexia (the pupillary reflex being the last to disappear), loss of Muscle tone, pupillary constriction (though pupils dilate in the event of asphyxia), cyanosis, cold extremities, and shallow, slowed breathing, occasionally presenting as Cheyne-Stokes respiration. Acute cardiovascular failure occurs. Potential complications include respiratory arrest, collapse-like reactions, and pulmonary edema (less commonly, cerebral edema).

The post-comatose period is characterized by impaired motor coordination. Psychomotor agitation, depressed consciousness, emotional lability, sometimes depression, and transient neurological symptoms are observed. Pronounced ptosis, convergence disorders, nystagmus, and diplopia are present.

Complications at this stage manifest as mental disorders, Pneumonia, and tissue trophic disturbances.

First aid and Treatment: treatment for barbiturate poisoning requires simultaneous Structure/175.html">Implementation of the following measures: eliminating unabsorbed and absorbed poison, maintaining normal respiration and Circulation, and preventing potential complications of the coma.

1. One of the primary objectives in treating barbiturate poisoning is to restore adequate respiration and eliminate or prevent Hypoxia. To this end, airway patency must be ensured. In the case of laryngospasm or laryngeal edema, endotracheal intubation or conicotomy should be performed. In severe cases with signs of respiratory failure, artificial respiration is administered and the patient is placed on mechanical ventilation.

NB! Analeptics (cardiamine, bemegride, caffeine) are contraindicated in deep barbiturate coma, as they trigger The phenomenon of Brain Cell oxygen "stealing" and thereby worsen brain damage due to hypoxia!

2. Gastric lavage should be performed as early as possible using a large-bore tube, followed by the administration of activated charcoal and a laxative to remove unabsorbed drug, along with a cleansing enema (gastric lavage is not recommended if 6 hours or more have elapsed since poisoning, as sphincters may relax and allow barbiturates to enter the intestine).

NB! In comatose patients, gastric lavage is performed after endotracheal intubation to prevent aspiration syndrome!

3. Implementation of Forced diuresis combined with blood alkalinization.

4. In severe cases of poisoning accompanied by renal impairment, as well as high serum barbiturate concentrations (exceeding 0.1%), hemodialysis is the most appropriate Procedure; if unavailable, peritoneal dialysis and detoxification hemoperfusion should be used.

5. Symptomatic treatment:

- maintenance of cardiovascular function: infusion of plasma expanders, crystalloids, and glucose solutions, administration of Hormones, sympathomimetics (dopamine, dobutamine), and other agents;

- correction of hypoxic CNS injuries: B Vitamins: B1 — 2–4 ml of a 2.5% solution, B6 — 8–10 ml of a 5% solution, B12 — up to 800 mcg per day; ascorbic acid — up to 10 ml of a 5% solution; cytochrome C.

Poisoning by combination drugs (Bellaspon, Bellataminal). Drugs of this group have a similar composition, which includes barbiturates along with belladonna and ergot Alkaloids (ergotoxin).

Indications for use: therapeutic doses reduce the excitability of the body's central and peripheral adrenergic and cholinergic systems and exert a sedative effect on the CNS. They are used for increased irritability, insomnia, neuroses, neurodermatitis, and autonomic dystonia.

Mechanism of action: the toxic dose is 20–30 tablets of any combination drug. The lethal dose is 30–50 tablets of the combination drug.

Poisoning is dominated by the intoxication mechanisms of barbiturates due to their higher concentration in the tablets and prolonged effect on the body, unlike atropine, whose action ceases quite rapidly.

The Toxic Effect of belladonna alkaloids manifests as CNS excitation or depression (psychosis, coma) and blockade of peripheral parasympathetic nerve function.

Toxic doses of ergot alkaloids (3 mg) stimulate brain structures responsible for thermoregulation and vagal function. Conversely, ergot alkaloids depress brain structures that regulate vasomotor reactions. Vasoconstriction occurs initially in the poisoning process, followed by alpha-adrenoreceptor blockade. Consequently, blood pressure first rises and then falls.

Pathogenesis of poisoning: three phases of intoxication are distinguished:

1) depression — resulting from the hypnotic effect of barbiturates;

2) excitation with psychosis — resulting from the action of atropine and ergotoxin;

3) barbiturate coma against the Background of atropine poisoning, largely associated with the differing absorption rates of alkaloids and barbiturates.

The first Two phases of poisoning are primarily driven by the action of alkaloids (belladonna, ergot), while the third is driven by barbiturates. However, in the final phase of intoxication, all three substances act synergistically.

Clinical presentation: the first signs of poisoning appear 20 minutes after ingesting toxic doses of the drugs. There are IV degrees of poisoning severity.

Degree I poisoning — mild (develops after ingesting 2–5 tablets). It is characterized by lethargy, drowsiness, impaired motor coordination, dry Skin, slight skin hyperemia, and thirst. Hypersalivation and conjunctival injection are sometimes observed. Miosis develops. Sleep lasting 6–10 hours may occur.

Stage II poisoning is moderately severe (developing after the ingestion of 6-15 tablets). The first clinical signs appear within 10-15 minutes, manifesting as vomiting and drowsiness, which are followed in 1.5-2 hours by a deep, unarousable sleep lasting 10-15 hours. This is subsequently followed by motor agitation and psychosis accompanied by delusions and hallucinations, along with impaired motor coordination. Within 1-6 hours, the victim falls asleep again. Spontaneous awakening occurs after 10-12 hours. Body Temperature may be low-grade fever (37.5 °C) or high (39 °C). Miosis gives way to mydriasis; divergent strabismus, dryness of the mucous membranes, and hyperemia of the face and trunk may be observed. Respiration accelerates to up to 50 breaths per minute, sometimes accompanied by snoring or becoming stridulous, and laryngospasm is possible. Hemodynamics are impaired. The pulse is accelerated up to 120 bpm, Heart sounds are muffled, and blood pressure drops to 80/50 mmHg.

Stage III poisoning is severe (occurring after the ingestion of 16-30 tablets) and is characterized by intense, brief psychomotor agitation, generalized epileptiform clonic-tonic seizures, psychosis, rapid loss of consciousness, a significant decrease in reflex activity, and progressive respiratory and circulatory impairment.

The pupils are significantly dilated, and the reaction to light is sluggish. The skin is hyperemic or markedly pale with a cyanotic tinge.

Hypersalivation in the absence of coughing leads to The Development of an aspiration-obstructive form of respiratory disorder; central types of respiratory disorders may also occur (tachypnea alternating with bradypnea, Cheyne-Stokes respiration). Dry and moist rales are auscultated in the Lungs.

Hemodynamic changes: pulse accelerated to 140-150 bpm, low volume, blood pressure decreased to 60/40 mmHg.

Neurological changes: a comatose state develops with hypo- or areflexia, decreased body temperature, and acidosis. Cutaneous reflexes are absent. Pathological reflexes appear (Babinski, Oppenheim). Meningeal syndromes may occasionally develop (nuchal rigidity, Kernig's and Brudzinski's signs).

Stage IV poisoning is extremely severe (developing after the ingestion of 30 or more tablets) and is classified as a deep coma.

Against the background of prodromal poisoning symptoms (vomiting, impaired motor coordination, dry Mouth, drowsiness), the victim is in a state of deep sleep or coma. Body temperature rises to 41 °C and then returns to normal. Pupils are dilated. Marked pallor or cyanosis of the skin develops. Severe respiratory and Circulatory Disorders occur.

Hemodynamic changes: blood pressure decreased to 60/0 mmHg, bradycardia.

Respiratory disorders: shallow, infrequent, periodic breathing. Numerous moist rales are heard in the lungs. Severe complications of poisoning include pulmonary edema, aseptic pneumonia, collapse, and hypoxic cerebral edema.

Deep coma lasting for several hours can lead to death due to impaired function of vital brain structures (respiratory arrest, drop in blood pressure). The mortality rate ranges from 0.7 to 2.5%.

Emergency Care and Intensive Therapy:

1. Gastric lavage via a tube followed by the administration of activated charcoal or another enterosorbent and a saline laxative solution (sodium sulfate, magnesium sulfate). In cases of extremely severe poisoning, gastric lavage is performed after cardiopulmonary resuscitation. If a comatose state develops, gastric lavage is performed following prior endotracheal intubation.

2. Forced diuresis. If available, extracorporeal hemodialysis or hemoperfusion.

3. The specific antidote for atropine is a 0.5% solution of galantamine hydrobromide, administered intramuscularly at 1 ml, and subcutaneously at 2 ml.

As an antidote, a 0.05% solution of neostigmine (Proserin) can be prescribed subcutaneously at 1 ml per administration.

4. Symptomatic therapy:

a) for hemodynamic disorders: strophanthine, dopamine, mesaton;

b) for delirium syndrome: chlorpromazine (aminazine) 2.5% solution 1-2 mg/kg per day;

c) for hypovolemia: crystalloid and colloid solutions.

5. If coma develops, the management strategy should be the same as that for barbiturate poisoning.

6. Measures aimed at eliminating pulmonary edema.