Clinical presentation and diagnostics
The symptoms of acute intoxication develop rapidly and affect major body systems. Diagnosis is based on identifying the characteristic triad of symptoms indicating severe nervous system impairment.
The main manifestations include:
- Comatose state — the patient does not respond to external stimuli.
- Slow, shallow breathing — a direct consequence of respiratory center depression.
- Bradycardia — a significant decrease in heart rate.
The most critical diagnostic sign is marked miosis (pronounced pupillary constriction). However, a serious clinical pitfall lies here: if asphyxia (acute oxygen deprivation) develops against the background of inadequate breathing, the pupils paradoxically dilate. This fact must be considered when examining critically ill patients.
Principles of emergency therapy
The logic of treating acute poisoning is strictly subordinated to two main directions. The success of resuscitation measures depends on how quickly and concurrently these tasks are performed:
- Removal of the poison from the body to prevent its further absorption.
- Restoration of vital functions, primarily adequate pulmonary ventilation, as respiratory arrest is the direct cause of death.
Detoxification: drug removal
To interrupt the entry of the toxin into the bloodstream, the gastrointestinal tract must be thoroughly cleansed. The procedure includes two stages:
1. Gastric lavage Performed using special solutions to neutralize the substance:
- Solution of potassium permanganate (at a concentration of 0.05%) — reacts with the drug, causing its chemical oxidation.
- Suspension of activated charcoal in warm water — ensures reliable adsorption of toxin molecules on its surface.
2. Bowel cleansing Immediately after completing gastric lavage, the patient is administered a saline laxative. This accelerates the evacuation of the poison remaining in the intestine and prevents its late absorption.
Respiratory restoration
Combating respiratory failure requires both pharmacological and mechanical intervention.
For specific therapy, a pharmacological antagonist is used — the drug naloxone. It is a direct opioid receptor blocker. Naloxone is administered intramuscularly or intravenously, which rapidly displaces the toxin from receptor binding and reverses respiratory center depression.
In cases where deep pulmonary depression is observed and drug support is insufficient, resuscitation measures are immediately initiated — the patient is transferred to mechanical ventilation (artificial lung ventilation).
Briefly: answers to topical questions
Which specific drugs are used as saline laxatives in morphine poisoning?
Sodium and magnesium sulfates, as well as Carlsbad salt, are used as saline laxatives in morphine poisoning.
- Sodium sulfate (Na2SO4 · 10H2O) — also known as Glauber's salt.
- Magnesium sulfate (MgSO4 · 7H2O) — administered orally at a dosage of 15–20 g.
- Carlsbad salt — can be natural or artificial; it is a mixture of sodium and potassium sulfates, as well as sodium bicarbonate and sodium chloride.
These drugs are administered after gastric lavage to rapidly cleanse the intestine and reduce toxin absorption.
What is the pathogenetic mechanism of bradycardia development in acute morphine poisoning?
The pathogenetic mechanism of bradycardia in acute morphine poisoning consists of increased tone of the vagus nerve (n. vagus) centers.
This leads to a pronounced decrease in heart rate. This symptom is part of the classic clinical picture of acute drug intoxication, along with coma, slow shallow breathing, and marked pupillary constriction (miosis).
Is it advisable to use respiratory analeptics to restore breathing in morphine poisoning?
The use of respiratory analeptics is advisable exclusively in mild cases of narcotic analgesic poisoning.
In severe morphine poisoning, centrally acting stimulants are strictly contraindicated. In profound depression, respiration is not restored, but neuronal stimulation increases the brain's oxygen demand. Under conditions of hypoxia, stimulating neuronal metabolism only exacerbates their damage. To restore breathing in severe poisoning, the pharmacological antagonist naloxone (intramuscularly or intravenously) and mechanical ventilation are used.
Symptom triad of poisoning: Coma, Slow breathing, Bradycardia (CSB). And remember the "pinpoint" pupils as long as there is no asphyxia!
Class and exam questions
Why are the pupils initially constricted and then potentially dilated in morphine poisoning?
Marked miosis is a classic diagnostic sign of the drug's effect. But if respiratory depression leads to asphyxia (oxygen deprivation), the pupils compensatorily dilate.
Why use specifically potassium permanganate during gastric lavage?
A weak (0.05%) potassium permanganate solution causes direct chemical oxidation of the drug, depriving it of its toxic properties.
Which drug is the antidote and how is it administered?
Naloxone acts as the pharmacological antagonist — an opioid receptor blocker. It is administered intramuscularly or intravenously.
What to do if antidote administration does not restore breathing?
In cases of profound respiratory depression and ineffectiveness of conservative measures, resuscitation measures must be started immediately by transferring the patient to mechanical ventilation.
What else to study on this topic
- Mechanism of coma development in opioid intoxication
- Pathogenesis of morphine-induced respiratory center depression
- Chemical interaction between potassium permanganate and alkaloids
- Pharmacodynamics of naloxone as a receptor blocker
- Specifics of saline laxative action in poisoning
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