Spinal And Cardiac Poisons

Spinal and Cardiac poisons poisons are important topics for Forensic Medicine and Toxicology (FMT) preparation.

Read this blog post thoroughly to understand everything you need to know about this topic and elevate your NEET PG Forensic Medicine preparation

Spinal Poisons

1. Strychnine Poisoning 

• Caused by Strychnine derived from Strychnos nuxvomica (Kuchila)
  • It is used to kill dogs, hence called Dog-buttons.
  • Seeds shape is concavo-convex.
  • It is odorless and bitter in taste.
  • Fatal dose: One crushed seed
  • Tests to identify Strychnine is.
    • Wenzel test
    • Sonenshein test 
  • Strychnine is excitatory in action. 

• Active Principles
  • Strychnine: It is a more potent than one
  • Brucine: These two are alkaloids
  • Loganin: It is a glucoside.

Mechanism of Action

• Acts on the anterior horn cell of the spinal cord (Renshaw cells)
• Complete blockade of the Ventral horn of motor neurons and postganglionic receptor site.
• Effects of glycine (inhibitory neurotransmitter) are inhibited in the spinal cord and brainstem.
  • Thus, the overall effect is excitatory. 
  • Thus, this disease mimics the mechanisms of Tetanus.
• Two phases are present
  • Convulsion
    • Convulsion phase is increased in this poisoning. 
    • There may be 5-6 convulsions simultaneously.
    • Clonic convulsions are seen.
  • Relaxation 
    • Normally duration of the relaxation phase is more compared to the convulsion phase.
    • But in this poisoning, the convulsion phase is elevated.
• Cause of death is respiratory muscle spasm - Asphyxia. 
• Consciousness will be retained.

Differentiation between Tetanus and Strychnine poisoning 

• In Strychnine Poisoning
  • All muscles are affected at the same time.
  • External stimuli increase the convulsions.
• In tetanus, there will be sequential muscle spasms.

Clinical Features 

• Tonus
  • Opisthotonus
    • Hyperextension of back.
    • Most characteristic feature.
  • Emprosthotonus
    • Hyperflexion of back.
  • Pleurothotonus
    • Lateral bending 
• Spasm
  • Risus Sadonicus
    • Spasm of facial muscles.

Tests

• Wenzel test
• Sonneschin test

Treatment

• Avoid gastric lavage as there will be convulsions. (Gastric lavage is Contraindicated in Convulsions).
• Controlling seizures
• Keeping patients away from convulsion-triggering stimuli
• Acidification of the urine 
• Antidote (to control seizures)
  • Phenobarbitone
  • Diazepam 

Postmortem Findings 

• Rigor mortis
  • Mnemonic: ST Ea L
  • ST-Strychnine, Ea- Early, L- Long duration 
  • Early in onset and long duration 
• Postmortem Caloricity
  • Body temperature increases after death due to increased muscle action.
• Putrefaction
  • Rate of putrefaction is decreased. 
• Brain and spinal cord are to be preserved.

2. Gelsemium Poisoning

• It is inhibitory in action.

Cardiac Poisons

Mnemonic: Queen D O N A C

• Caused by 
  • Quinine
  • Digitalis
  • Oleander (yellow, white/pink)
  • Nicotina tabacum
  • Aconite
  • Cerebra odellum

1. Aconite Poisoning

• It is also called blue rocket/ monks hood/ meetha zeher

• Roots are conical in shape and tapered at the end with longitudinal ridges.
• All parts are poisonous.
• Roots and seeds are the most poisonous part.
• Roots of Aconite are generally mistaken as Horseradish root

Active Principles

• Aconitine
• Pseudaconitine
• Aconin

Mechanism of Action

• Mainly acts on sodium channel (AcoNite, Na+ channel action).
• Binds to voltage-dependent sodium channels and prolongs the action leading to
  • Excitation of sensory nerves
    • Sensory nerves are predominantly affected than motor nerves.
  • Paralyze the motor ganglia of the heart.
  • Respiratory center is slowed.
  • Tachycardia followed by Bradycardia is observed.
• Cause of death is due to Cardiac arrhythmia (mostly Ventricular arrhythmia)
• Hyperkalemia is also seen. 

Signs and Symptoms

• Tingling and numbness of mouth and throat (most characteristic symptom)
• Sweet taste 
• Numbness and paranesthesia of face, perioral area, and progress to all over the body.
• Weakness of four limbs
• Twitching of muscles
• Hippus sign: Alternate contraction and dilation of the pupil.
• Xanthopsia: Visual illusion of yellow color around objects.
• Hypotension, tachycardia, ventricular ectopic, cardiac arrhythmia with AV block

Fatal Dose: 1-2 gms of the root is fatal.

Treatment

• Gastric lavage with warm saline.
• Atropine for AV block.
• Supportive treatment 
• Correction of hyperkalemia 

Medicolegal Importance

• Accidental poisoning by horseradish root 
• One of the ideal homicidal poisonings.
• It mimics natural cardiac arrhythmia.
• Destroyed by putrefaction. 

2. Oleander Poisoning

A. Yellow Oleander

• Also called Cerbera Thevetia or peela kaner.
• All parts of the plant are poisonous.
• Active Principles
  • Cerberin
  • Thevetin A and B
  • Neriifolin

B. Pink Oleander

• It is termed as Nerium odorum or white oleander.

• Active Principles
  • Oleandrin
  • Nerin
  • Folinerin
  • Rosagenin

Mechanism of Action of Oleander poisoning

• Action is like digitalis.
• Inhibition of Sodium-Potassium ATPase channel leading to
  • Brady/Tachycardia
  • AV block
  • Hyperkalemia 

Treatment of Oleander Poisoning 

• Gastric lavage with warm saline
• Antidote: Digibind (same as that of Digitalis)
  • Digibind binds to the Fab end of the antibody.
• For AV block - Atropine
• For hyperkalemia - Dextrose and Insulin 

3. Digitalis Poisoning

• Digitalis purpurea is also called purple Fox glove.

Mechanism of action

• Inhibition of Sodium-potassium ATPase channel

Treatment 

• Treatment is same as Oleander poisoning.

4. Cerebra Odellum

• Also called are Suicidal tree.

Active Principles

• Cerberin
• Cerebroside
• Odolin
• Odolotoxin

Treatment

• BHIST regime

5. Nicotine 

• Most common substance abuse in India

And that is everything you need to know about Spinal and Cardiac Poisons for your FMT paper. For more informative and interesting blog posts to upgrade your NEET PG preparation, download the PrepLadder App and keep following our blog.