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Acute Morphine Poisoning

Morphinum

For medical students2 min readUpdated 2026-10-10

Acute morphine poisoning is a life-threatening condition characterized by profound central nervous system depression, up to and including coma. The primary cause of mortality is complete respiratory arrest, making emergency management critically dependent on immediate toxin removal and administration of specific pharmacological antagonists.

Pathognomonic signMarked pupillary constriction (miosis) — the primary diagnostic marker of poisoning.
Cause of deathSevere untreated intoxication inevitably leads to fatal respiratory arrest.
AntidoteNaloxone — an opioid receptor blocker that rapidly restores respiratory function.
Toxin oxidation0.05% potassium permanganate solution reliably degrades morphine during gastric lavage.

Clinical Presentation and Diagnosis

Symptoms of acute intoxication develop rapidly and affect vital organ systems. Diagnosis relies on identifying a characteristic triad of symptoms indicating profound nervous system depression.

Key manifestations include:

An essential diagnostic sign is marked miosis (pronounced pupillary constriction). However, a serious clinical trap exists here: if asphyxia (acute oxygen deprivation) develops against the background of inadequate ventilation, the pupils paradoxically dilate. This fact must be considered when examining critically ill patients.

Principles of Emergency Therapy

The management of acute poisoning is strictly guided by two main objectives. The success of resuscitation depends on how rapidly and concurrently these tasks are performed:

  1. Removal of the toxin from the body to prevent its further absorption.
  2. Restoration of vital functions, primarily adequate pulmonary ventilation, as respiratory arrest is the direct cause of death.

Detoxification: Toxin Elimination

To halt toxin entry into the bloodstream, the gastrointestinal tract must be thoroughly cleansed. The procedure includes two stages:

1. Gastric Lavage Performed using specialized solutions to neutralize the substance:

2. Bowel Cleansing Immediately after gastric lavage is completed, a saline laxative is administered to the patient. This accelerates the evacuation of residual toxin from the intestines and prevents its delayed absorption.

Restoration of Respiration

Combating respiratory failure requires both pharmacological and mechanical interventions.

For specific therapy, the pharmacological antagonist naloxone is used. It acts as a direct opioid receptor blocker. Naloxone is administered intramuscularly or intravenously, allowing rapid displacement of the toxin from its receptors and reversal of respiratory center depression.

In cases of profound pulmonary depression where medical support is insufficient, immediate resuscitative measures are initiated — the patient is placed on mechanical ventilation (MV).

Mnemonic

Poisoning triad: Coma, Slow breathing, Bradycardia (CSB). And remember the "pinpoint" pupils, unless asphyxia sets in!

Frequently asked questions

What 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 (Na2Na2SO4 · 10H2O) — also known as Glauber's salt.
  • Magnesium sulfate (MgSO4 · 7H2O) — administered orally at a dose of 15–20 g.
  • Carlsbad salt — natural or artificial, consisting of a mixture of sodium and potassium sulfates, sodium bicarbonate, and sodium chloride.

These agents are administered after gastric lavage to rapidly cleanse the intestine and reduce toxin absorption.

What is the pathogenetic mechanism of bradycardia in acute morphine poisoning?

The pathogenetic mechanism of bradycardia in acute morphine poisoning involves increased tone of the vagus nerve centers (n. vagus).

This leads to a pronounced reduction in heart rate. This sign is part of the classic clinical picture of acute intoxication, alongside a comatose state, slow shallow breathing, and marked miosis.

Is it appropriate to use respiratory analeptics to restore breathing in morphine poisoning?

The use of respiratory analeptics is appropriate exclusively in mild cases of narcotic analgesic poisoning.

In severe morphine poisonings, centrally acting stimulants are strictly contraindicated. In profound depression, breathing is not restored, yet neural stimulation increases the brain's oxygen demand. Under hypoxic conditions, stimulating neuronal metabolism only exacerbates their injury. To restore breathing in severe poisoning, the pharmacological antagonist naloxone (intramuscularly or intravenously) and mechanical ventilation (MV) are used.

Why are pupils initially constricted in morphine poisoning, but may later dilate?

Marked miosis is a classic diagnostic sign of the drug's effect. However, if respiratory depression leads to asphyxia (oxygen deprivation), the pupils dilate compensatorily.

Why use potassium permanganate specifically during gastric lavage?

A weak (0.05%) solution of potassium permanganate induces direct chemical oxidation of the drug, abolishing its toxic properties.

What is the antidote and how is it administered?

The pharmacological antagonist is naloxone, an opioid receptor blocker. It is administered intramuscularly or intravenously.

What should be done if antidote administration does not restore breathing?

In cases of profound respiratory depression where conservative measures fail, immediate resuscitative measures must be initiated by placing the patient on mechanical ventilation (MV).

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