Origin and Chemical Properties
The source of this alkaloid is the South American plant — the coca shrub (Erythroxylon coca). Chemically, the substance is an ester of benzoic acid and methylecgonine.
In pharmacological practice, the drug is obtained either by direct extraction from plant material or by a semisynthetic method using ecgonine as a base. For medical purposes, the soluble form, cocaine hydrochloride, is traditionally used.
Pharmacokinetics and Local Effects in Ophthalmology
The substance is characterized by high anesthetic activity. Its main pharmacokinetic feature is the ability to cross mucous membranes into the systemic circulation extremely rapidly. This property causes a pronounced resorptive effect, often accompanied by severe toxic and adverse effects, making the drug hazardous for widespread use.
The drug is rarely used in ophthalmology. It is instilled directly into the conjunctival sac, providing local anesthesia lasting about one hour.
Local effects on the eye:
- Marked vasoconstriction of scleral blood vessels.
- Pupil dilation (mydriasis).
- Alteration of intraocular pressure (IOP): in most cases, it decreases, but susceptible patients may experience a sharp and dangerous spike in IOP.
- Specific complication: prolonged use leads to severe corneal epithelial ulceration.
Systemic Effects and Toxicity
Following absorption into the systemic circulation, the drug exerts a powerful stimulating effect on the central nervous system.
Psychotropic effects include euphoria, marked psychomotor agitation, and a notable decrease in hunger, anxiety, and physical fatigue.
The substance actively affects structures of the medulla oblongata, stimulating several vital centers:
- Respiratory center.
- Vasomotor center.
- Vomiting center.
Cardiovascular effects manifest as tachycardia, systemic vasoconstriction, and elevated blood pressure. This symptom complex is mediated by two main mechanisms: direct stimulation of the vasomotor center and potentiation of sympathetic influences (amplification of adrenergic excitation).
Toxic effects: in high doses, the drug causes seizures. As intoxication progresses, the excitation phase is replaced by CNS depression. There is a critical risk of mortality due to respiratory arrest, caused by direct paralytic depression of the respiratory center.
Emergency Care for Overdose
Treatment of acute poisoning requires immediate action aimed at removing the toxin, preventing its further absorption, and stabilizing the patient's condition.
Decontamination (removal of the poison):
- If contact occurs with mucous membranes, rinse them thoroughly with isotonic sodium chloride solution.
- If ingested, perform gastric lavage with a weak potassium permanganate solution (0.05–0.1%), followed by administration of enterosorbents and saline laxatives.
Limiting systemic absorption:
- If the drug was administered by injection, a tourniquet must be applied immediately proximal to the injection site.
Symptomatic treatment:
- Intravenous diazepam is administered to manage psychomotor agitation and seizures.
- If signs of respiratory depression develop, the patient is transitioned to mechanical ventilation.
Drug Dependence (Cocaine Abuse)
Chronic abuse (cocaine dependence) develops due to its specific psychotropic properties. The substance appeals to addicts because it induces euphoria (eliminating negative emotions and sharply elevating mood) while masking fatigue and temporarily increasing performance.
Routes of administration: chronic use can be intranasal (inhaling the powder), by chewing coca leaves, or via intravenous injection.
Withdrawal syndrome: abrupt cessation of the drug leads to a severe state characterized by deep depression, profound physical and mental exhaustion, and a distressing psychological background. As a result, profound psychological dependence develops, requiring specialized long-term care to overcome.