Calotropis gigantea

 

Botanical Name

Calotropis gigantea (Linn.) Ait. f  [1]

Synonyms

Asclepias gigantean, Willd, Sp. Pl. i.; Madorius, Rumph., Amboyn., vii. t. 14, f. l  [1] [2] [3] [4]

Family

Asclepiadaceae

Vernacular Names

Malaysia Remiga, rembiga
Indonesia Widuri
India Aak, akanda, arka, alarka (Sanskrit); Madar (Hindi) [4]

Description

The genus Calotropis comprises of six species all native to North Africa and Southwest Asia. Calotropis gigantea is a medium sized shrub or small tree that grows up to 4m high with a generally waxy appearance and copious milky sap. The stem is ash coloured, smooth, branching sometime almost from the base. The leaves are grey-green, opposite, alternating, waxy, thick and rounded-ovate. They measure 5–15cm x 4–10cm with a short pointed tip and a heart-shaped base partly clasping the stem; a stiff brush of hairs occur at the base of the midvein. The flowers are white with deep purple blotch at the base of each lobe and deep purple scales between the petals and the stamens; more or less tubular, 5-lobed, 2–3cm across, devoid of milky sap. They are grouped in umbels in which the outer flowers open first while the inner do not develop fully. The fruit is a grey-green bladdery pod, 8–12 cm long, rounded at the base but shortly pointed at the tip and containing numerous seeds. The seeds are brown, flattened, with a tuft of long white hair at one end. [2]

Distribution

This plant is chiefly found in waste lands in India, Sri Lanka, Southern China, Malaysia,  Singapore and Indonesia. It has spread to the South Pacific Islands and Northern Australia [1] [2].

Plant Use

Ornamental, medicinal [4] .

Toxic Parts

Whole plant

Leaves and Stalk – Calotropin and Calotropagenin

Latex – uscharin (0.45%); Calotoxin (0.15%) and Calactin (0.15%)

Roots – Calotropin, Calactin, Uscharidin and Frugoside [1] [2]

Toxin

C. gigantea contains a number of toxic cardenolides in the all parts including the roots. Cardenolides are C(23)-steroids with methyl groups at C-10 and C-13 and a five-membered lactone at c-17. They form the aglycone part of cardiac glycosides and have at least one double bond in the molecule. Some of the more popular cardenolides in medical practice include digitoxin and ouabain. The cardenolides in Calotropis gigentea include the following: calotropin, calactin, urcharidin and frugoside.[1]

Pathophysiology

Cardiac glycosides generally bind to a site on the cells membrane causing reversible inhibition of the sodium-potassium ATPase pump. This leads to increase intracellular sodium and decrease intracellular potassium.  In the myocytes the increase in intracellular sodium results in increase intracellular calcium leading to early depolarization, cardiac irritability and dysarrhythmias. Clinically, this is manifested in the form of after-contractions such as premature ventricular contractions. The inhibition of Na+-K+-ATPase in skeletal muscles results in increased extracellular potassium contributing to hyperkalaemia. There are also increases in vagal stimulation and decreases in sympathetic tones leading to bradycardia and heart block.

The latex contained a yet unidentified vesicant allergent which can cause direct irritant action on mucous membranes especially the eyes. The skin reaction is mainly due to allergy rather than direct irritant action.[2]

The plant also contains a significant amount of calcium oxalate crystals.

Risk Management

In Malaysia C. gigantea is grown in gardens of the Indian community for religious purposes. Children and household pets can be poisoned if the plant parts are being chewed or eaten. While cardiac glycoside poisoning is relatively rare, severe toxicity can lead to death. Life-threatening poisoning has been reported after ingestion of plant extracts and tea, use of contaminated herbal products, and deliberate ingestion of substantial quantities ofplant parts by adults. [1] [2] [3]

Clinical Findings

The effects of vesicant allergens include conjunctivitis when in contact with the eye to process to iridocyclitis. It can also result in allergic dermatitis in people sensitive to the latex.

Calcium oxalate causes painful burning sensation of the lips and mouth with inflammatory reaction, oedema and blistering. Hoarseness, dysphonia and dysphagia may ensue.

Effects of Cardiac glycosides on:

Cardiovascular System – Marked bradycardia with varying degree of heart block, ventricular dysarrhythmias, hypotension and asystole.

Nervous System – Fatigue, lethargy, malaise, headache, confusion, agitation and dizziness.

Gastro-intestinal System – Vomiting, cramping, abdominal pain and nausea shortly after ingestion which may continue for several hours preceding deterioration of myocardial contractility.

Mild to Moderate Toxicity – Acute poisoning leads to nausea, vomiting, abdominal pain, lethargy and bradycardia. In chronic toxicity the patient may present with bradycardia, malaise, nausea, anorexia, delirium and visual changes.

Severe Toxicity – In acute poisoning the patient may present with severe bradycardia, heart block, vomiting, and shock. Hyperkaleamia is a prominent feature in severe acute toxicity. Severe chronic toxicity causes dysarrhythmias and varying degree of heart block, but hyperkalaemia is uncommon. [1] [2] [3]

Management

Calcium oxalate toxicity is a self limiting process and the pain and oedema will subside spontaneously. Cool liquids or demulcents held in the mouth could provide some relieve. Analgesics may be used in severe cases. Calcium oxalate is insoluble and does not cause systemic oxalate poisoning.

Prehospital care should include Advance Life Support (ALS); focus should be on supporting the respiratory and cardiac function. Patients with protected airway and normal mental status should be given activated charcoal. Atropine should be considered if patient has clinically significant bradycardia. During transportation, the patient should receive oxygen and be on drip. There should also be continuous monitoring of the heart and pulse oximetry.

At the hospital the basic principles of care of toxicological emergency should be instituted i.e. providing general supportive care, preventing further exposure and absorption, administering antidote and treating complications as they arise.

Antidote: Sheep-derived digoxin antibody (Fab fragments) have been found to be effective for other cardiac glycoside poisoning. It’s used should be considered in life-threatening complications like ventricular dysarrhythmias, hyperkalaemia, high degree heart block and cardiac arrest not responding to conventional treatment.

Bradycardia can be treated with Atropine and cardiac pacing. The use of Phenytoin and Lidocaine should be considered if Fab fragments are not immediately available. Hyperkalaemia being the result of redistribution phenomenon can be treated using Glucose, Insulin, or Sodium bicarbonate to facilitate its redistribution intracellularly.

The treatment of cardenolide poisoning is largely supportive, but special attention should be paid to potassium balance, since cardenolides inhibit Na/K-ATPase (the Na/K pump), inhibiting the influx of potassium into the cells; the severity of toxicity, and therefore the prognosis, is related to the degree of hyperkalaemia that results. Fab fragments of antidigitoxin antibody are effective not only in poisoning with digoxin but with other cardiac glycosides too. Repeated doses of activated charcoal (50g 4-hourly) reduced mortality in one study from 8.0% to 2.5%, probably encouraging the intestinal secretion of the toxic cardenolides.[3]

Read More

  1) Botanical info

References

  1. Knight AP. A Guide to Poisonous House and Garden Plants. Colorado State University Fort Collins. p. 121–122.
  2. Lewis SN, Richard DS, Micheal JB. Handbook of Poisonous and Injurious Plants. Springer-Verlag Berlin; 2007.
  3. Gordon CC, Patrick M, Alimuddin Z. Manson’s Tropical Diseases. Saunders Elservier London; 2009. p. 608.
  4. Khare CP., Indian Medicinal Plants: An Illustrated Dictionary Springer, Berlin 2007 pg. 113