Strychnine poisoning

Introduction

Strychnine poisoning is a rare but severe toxicological condition resulting from exposure to the alkaloid strychnine. This compound, derived from the seeds of the Strychnos nux-vomica tree, has historically been used as a pesticide, particularly for killing rodents. Despite its limited use today, due to the availability of safer alternatives, strychnine remains a potent poison with significant clinical implications. The pathophysiology of strychnine poisoning involves the disruption of normal neurotransmission, leading to severe neurological and muscular symptoms.

Chemical Properties and Mechanism of Action

Strychnine is a highly toxic, colorless crystalline alkaloid with the chemical formula C21H22N2O2. It acts as a competitive antagonist of the inhibitory neurotransmitter glycine at the glycine receptor, predominantly in the spinal cord. This antagonism results in the unchecked excitatory neurotransmission, leading to increased neuronal firing and severe muscle contractions.

The glycine receptor is a chloride channel that, when activated by glycine, allows chloride ions to enter the neuron, causing hyperpolarization and inhibition of neuronal firing. Strychnine binds to this receptor, preventing glycine from exerting its inhibitory effect, thus leading to a state of hyperexcitability.

Clinical Presentation

The onset of symptoms following strychnine ingestion is rapid, typically occurring within 15 to 60 minutes. The hallmark of strychnine poisoning is the presence of severe, painful muscle spasms and convulsions. These spasms are often triggered by minimal stimuli such as noise, touch, or light.

Neurological Symptoms

The neurological manifestations of strychnine poisoning are primarily due to the loss of glycine-mediated inhibition in the central nervous system. Patients may experience heightened reflexes, opisthotonos (a condition characterized by severe hyperextension and spasticity), and risus sardonicus (a sustained spasm of the facial muscles resulting in a characteristic grimace).

Musculoskeletal Symptoms

Muscle rigidity and convulsions are prominent features. The convulsions are typically generalized and may resemble tetanus due to the similar pathophysiological mechanism of glycine receptor inhibition. Unlike epileptic seizures, these convulsions do not originate from the cerebral cortex and are not associated with loss of consciousness.

Autonomic Symptoms

Autonomic instability is common, with symptoms including tachycardia, hypertension, and hyperthermia. These symptoms result from excessive sympathetic nervous system activity due to the lack of inhibitory control.

Diagnosis

The diagnosis of strychnine poisoning is primarily clinical, based on the characteristic presentation of muscle spasms and convulsions. A detailed history, including potential exposure to strychnine-containing substances, is crucial. Laboratory tests may reveal metabolic acidosis and rhabdomyolysis due to prolonged muscle activity.

Confirmation of strychnine exposure can be achieved through toxicological analysis of blood, urine, or gastric contents. High-performance liquid chromatography (HPLC) and gas chromatography-mass spectrometry (GC-MS) are commonly used analytical techniques for detecting strychnine.

Treatment

Management of strychnine poisoning is primarily supportive, focusing on controlling convulsions and maintaining adequate ventilation. Benzodiazepines such as diazepam or lorazepam are the first-line agents for controlling muscle spasms and seizures. In severe cases, barbiturates or propofol may be required for sedation and muscle relaxation.

Airway Management

Ensuring a patent airway is critical, as muscle spasms can compromise ventilation. In cases of severe poisoning, endotracheal intubation and mechanical ventilation may be necessary.

Decontamination

Gastric decontamination with activated charcoal can be considered if the patient presents within an hour of ingestion. However, the risk of aspiration due to convulsions must be carefully weighed against the potential benefits.

Supportive Care

Supportive care includes monitoring and managing complications such as rhabdomyolysis, metabolic acidosis, and renal failure. Intravenous fluids and electrolyte replacement are essential components of supportive care.

Prognosis

The prognosis of strychnine poisoning largely depends on the dose ingested and the timeliness of medical intervention. With prompt and appropriate treatment, the mortality rate is significantly reduced. However, severe cases can result in complications such as acute respiratory distress syndrome and renal failure.

Epidemiology

Strychnine poisoning is rare in developed countries due to strict regulations on its use and availability. However, it remains a concern in regions where strychnine is still used as a pesticide. Accidental ingestion, intentional self-harm, and occupational exposure are the most common scenarios leading to poisoning.

Historical Context

Historically, strychnine was used not only as a pesticide but also in small doses as a medicinal tonic and performance enhancer. Its use in medicine has been largely abandoned due to the high risk of toxicity and the availability of safer alternatives.

Prevention

Preventing strychnine poisoning involves strict regulation and control of its use and distribution. Public education on the dangers of strychnine and the importance of using safer alternatives for pest control is crucial. In occupational settings, appropriate protective measures and training are essential to minimize the risk of exposure.