MARKING NUT

Latin name:         Semecarpus anacardium Linn.

Family:                 Anacardiaceae

Common name:   Bhilwa, Godambi, Bhilanean

English name:      Marking nut

Medicinal Use:     Antidiabetic, Antiarthritic, Anti-inflammatory

Active Principles: The juice contains

·      Semecarpol

·      Bhilawanol

Uses:

·      Laundry marker.

·      Quack remedy for assorted ailments.

·      Ink Preparation: Used During Voting / Election to mark on nail.

·      Ink Used in Postal Stamps.

The fruit of this plant is known as Bhilawan or the marking nut because its juice is used by dhobis (washermen) as marking ink on clothes. The nut is black, roughly cone shaped, and has a thick pericarp. The contained juice is brown, oily, and acrid. Its active principles are Semecarpol and bhilawanol.

Symptoms and signs:

When the juice is applied to skin, it causes irritation and painful blisters containing acrid serum which causes an eczematous eruption on any part of the skin with which it comes into contact. The lesion resembles a bruise which may later ulcerate and slough. Internally administered, the juice is much less irritant. Taken in larger doses, it causes blisters in the mouth and throat and severe gastroenteritis, followed in some cases by dyspnoea, cyanosis, tachycardia, coma, and death

Fatal dose: The fatal dose is about 5 to 10 Gms

Fatal period: Death may result within 12 to 24 hours.

Treatment:

This is symptomatic. When applied externally, the parts should be washed with warm water and bland liniments applied.

Postmortem appearances:

The findings confirm the clinical features.

The blister fluid should be preserved in rectified spirit and sent to a forensic science laboratory for analysis, if necessary.

Medicolegal aspects:

The juice is used as an abortifacient by application to the os uteri by means of an abortion stick. It is applied to the genitals as a punishment for adultery. It is used by malingerers to produce an artificial bruise to support a false charge; its presence, however, can be detected by chemical analysis of the blister fluid. The juice may be instilled into the eyes to produce an irritant conjunctivitis. This is resorted to by personnel in army, navy or air force when they wish to leave the job or by inmates of jail to avoid work. Accidental poisoning may occur from internal administration by quacks. The juice, like vitriol, has been thrown on the face with evil intentions.

 ABRUS PRECATORIUS

This is also known as Indian liquorice, gunchi or rati. The plant is found all over India and though all its parts are poisonous, the seeds are commonly used as poison. They are of the size of a small pea, about 0.85 cm long and 0.65 cm broad, and have an average weight of 120 mg. They are tasteless, odourless, oval, and red in colour, with a black spot on one pole. The active principle is abrin, a toxalbumin, and its actions resemble those of viperine snake bite

Symptoms and signs:

When the seeds are swallowed raw or after cooking, they are not poisonous. Poisonous symptoms resembling viper bite follow if an extract is injected under the skin or into a wound. Such a method is used to poison cattle by means of sui.

Suis are fine needles prepared by decorticating the seeds and powdering them, followed by mixing the powder with opium, onion, dhatura and spirit or water to make into a paste, and the paste shaped into small sharp needles, which are allowed to harden by drying in the sun.

Human poisoning is characterised by a local painful swelling and ecchymosis, followed by necrosis. The patient suffers from vertigo, cardiac arrhythmia, convulsions and death. When ingested, there is nausea, vomiting, abdominal pain, diarrhoea, and collapse.

Fatal dose and fatal period:

The fatal dose is 1-2 seeds by mouth or 90-120 mg abrin by injection. The fatal period is 3-5 days.

Treatment:

This consists in dissecting out the sui and injection of anti-abrin. The rest of the treatment is symptomatic.

Postmortem appearances:

The injured site is swollen, inflamed and necrosed. Fragments of sui are usually found in the wound. Haemorrhagic patches are seen under mucous membranes. Internal organs are congested and haemorrhagic.

Medicolegal aspects:

Suis are used to kill cattle either to produce cheap hides or for revenge. Human poisoning by keeping a sui-spike between fingers and giving a slap or contaminating wounds thereby, is recorded. Malingerers use the powdered seeds to produce conjunctivitis. The use of abrus as an arrow poison is known.

Forensic Significance:

·      Juice is used as an abortifacient.

·      Malingering: production of artificial bruise or conjunctivitis with the juice.

·      Accidental poisoning due to quackery.

CORROSIVES

By corrosion is meant dissolution or gradual wearing away by chemical action. The corrosive poisons are classified as follows:

(1) Mineral acids-         

A.   Sulphuric acid

B.    Nitric acid

C.   Hydrochloric acid

2) Organic acids-

A.   Oxalic acid

B.    Carbolic acid

C.   Acetic acid

D.   Salicylic acid

3) Vegetable acid-

A.   Hydrocyanic acid

4) Alkalis-

B.    Caustic potash and soda

C.   Ammonium hydroxide

Action is characterized by:

·        Extraction of water from the tissues

·        Coagulation of cellular proteins, and

·        Conversion of haemoglobin into haematin

Sulphuric acid:

Sulphuric Acid is a heavy, oily, colourless, odourless, nonfuming liquid. It is hygroscopic i.e., it has great affin­ity for water with which it reacts violently, giv­ing off intense heat.

Uses:

1.   Industrial chemical (95 to 98% solution)

2.   Storage batteries and accumulators (30 to 35% solution)

3.   Drain cleaner (8 to 10% solution)

Usual Fatal Dose:

20 to 30 ml of conc. sulfu­ric acid. Deaths have been reported with in­gestion of as little as 3.5 ml.

Toxicokinetics:

Systemic absorption of sul­furic acid is negligible.

Mode of Action:

Produces coagulation necro­sis of tissues on contact.

Clinical features

1.    Burning pain from the mouth to the stom­ach. Abdominal pain is often severe.

2.    Intense thirst. However, attempts at drink­ing water usually provoke retching.

3.   Vomiting: The vomits is brownish or blackish in colour (due to altered blood), and may contain shreds of the charred wall of the stomach.

4.   If there is coincidental damage to the lar­ynx during swallowing or due to regurtitation, there may be dysphonia, dys­phagia, and dyspnoea.

5.   Tongue is usually swollen, and blackish or brownish in colour. Teeth become chalky white. There may be constant drooling of saliva which is indicative of oesophageal injury.

6.   There is often acid spillage while swallow­ing with consequent corrosion of the skin of the face (especially around the mouth), neck and chest. Burnt skin appears dark brown or black.

7.    Features of generalised shock are usually apparent.

8.   If perforation of stomach occurs, a severe form of chemical peritonitis can result. Rarely, perforation of duodenum occurs.²

9.   If the patient recovers, there are usually long term sequelae such as stricture forma­tion which may lead to pyloric obstruction, antralstenosis, or an hour-glass deformity of the stomach. The oesophagus may also be involved resulting in stenosis. There are indications of increased propensity for car­cinomas.

10. Contact of the acid with the eyes can cause severe injury including conjunctivitis, pe­riorbital oedema, corneal oedema and ul­ceration, necrotising keratitis, and iridocy­clitis.

Diagnosis:

1.   Litmus test: The pH of the saliva can be tested with a litmus paper to determine whether the chemical ingested is an acid or an alkali.

2.  Fresh stains in clothing may be tested by adding a few drops of sodium carbonate. Production of effervescence (bubbles) is indicative of an acid stain.

Treatment:

1.  Respiratory distress due to laryngeal oedema should be treated with 100 % oxy­gen and cricothyroidotomy.

2.  Some authorities recommend administra­tion of water or milk if the patient is seen within 30 minutes of ingestion (120-240 ml in an adult, 60-120 ml in a child). But no attempt must be made at neutralization with alkalis, since the resulting exothermic re­action can cause more harm than benefit.

3.  Remove all contaminated clothes and ini­gate exposed skin copiously with saline.

4.  Eye injury should be dealt with by retrac­tion of eyelids and prolonged inigation for at least 15 to 30 minutes with nonnal sa­line or lactated Ringer's solution, or tap water if nothing else is available. Anaes­thetic agents and lid retractors may be nec­essary.

5.  The following measures are contraindi­cated: oral feeds, induction of vomiting, stomach wash, and use of activated char­coal.

6.  Administration of steroids has been shown to delay stricture formation (in animals) when given within 48 hours of acid ingestion, but the practice is generally not recommended because of increased risk of per­foration.⁴ Administer antibiotics only if in­fection occurs. Prophylactic use is not ad­visable unless corticosteroid therapy is be­ing undertaken.

7.  Since there is often severe pain, powerful analgesics such as morphine may have to be given.

8.  The use of flexible fibreoptic endoscopy is now standard practice in the first 24 to 48 hours of ingestion to assess the extent of oesophageal and gastric damage. If there are circumferential 2nd or 3rd degree bums, an exploratory laparotomy should be per­formed. If gastric necrosis is present, an oesophagogastrectomy may have to be done.

9.  Emergency laparotomy is mandatory if there are signs of perforation and peritoni­tis.

10. If the patient recovers, there may be long term sequelae such as stenosis and stricture formation. Follow-up is therefore es­sential to look for signs of obstruction ­nausea, anorexia, weight loss. Surgical pro­cedures such as dilatation, colonic bypass, and oesophagogastrostomy may have to be undertaken.

Autopsy Features:

1.  Conoded areas of skin and mucous mem­branes appear brownish or blackish. Teeth appear chalky white.

2.  Stomach mucosa shows the consistency of wet blotting paper, there may be inflammation, necrosis, or perforation of the g.i. tract.

Vitriolage:

 This means throwing of any corrosive; not necessarily sulphuric acid, on a person with malicious intent. These fluids are usually thrown on the face with the object of destroying vision or causing facial disfigurement and this result in grievous hurt. Sulphuric acid (oil of vitriol) is most commonly employed for this purpose and hence it is called vitriolage. Nitric and carbolic acids are sometimes used. The use of caustic soda, caustic potash, iodine and marking nut juice has also been recorded. Sulphuric acid produces severe chemical burns. They are characterised by discolouration and staining of skin and clothing (brown or black in sulphuric acid and yellow in nitric acid), trickle marks, absence of vesication and red line of demarcation, and the presence of the chemical substance in the stains. Immediate treatment consists in washing away the corrosive acid with large amount of water and soap or dilute solution of sodium or potassium bicarbonate. Later, a thick paste of magnesium oxide is applied. The raw surface may afterwards be covered with antibiotic ointment; when the eyes are involved, they should be washed at once with a large amount of water followed by irrigation with 1 % solution of sodium bicarbonate. A few drops of olive oil are then instilled into the eyes. Eye drops containing antibiotics and steroids are helpful.

 CASE STUDY:

The mass poisoning which took place in the French town of Pont-St. Esprit in 1951 has been widely presented in the lay and scientific press as an example of ergotism. While the poisoning was traced to bread, ergotism was not the cause of the syndrome, which was due to a toxic mercury compound used to disinfect grain to be planted as seed. Some sacks of grain treated with the fungicide were inadvertently ground into flour and baked into bread. Albert Hofmann arrived at this conclusion after visiting Pont-St. Esprit, and analyzing samples of the bread (which contained no ergot alkaloids) and autopsy samples of four of the victims who succumbed (Hofmann 1980; Hofmann 1991). On the other hand, Swedish toxicologist Bo Holmstedt insists the poisoning was in fact due to ergotism (Holmstedt 1978)

A 61-year-old chemist reportedly injected a solution of crushed castor beans (Ricinus communis) and acetone into an antecubital vein. This unwitnessed event occurred one day before he presented to the ED. Upon presentation he was asymptomatic except for an apparent infection at the injection site. Several hours later he developed vomiting, bloody diarrhea, acidosis, hypoglycemia, renal failure, hypotension and a decreasing level of consciousness. The patient was treated symptomatically, gradually worsened and died about 12 hours after presentation.

REFERENCES-

·        Parikh’s Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

·       Textbook of Forensic Medicine and Toxicology: V. V. Pillay.

·        Dr. Sally Lukose: Class Notes.