By Omer Bayazeid

Aconitine Poisoning

Aconitine: Acontine is a diterpenoid alkaloid

produced by plants of the Aconitum genus.

Various species of Aconitum have been used by different populations for centuries as poisons and medicines, with certain species still being used in Chinese and Japanese herbal medicines.

Aconitine Poisoning:

CASE HISTORY:

A healthy 25-year-old man went for an afternoon walk with four friends on an uninhabited island off the coast of Newfoundland, Canada. At 2:30 pm, he picked some wild flowers with purple and pink petals along with a few blackberries (Epetrium nigrum) and ate them. His friends were able to get a sample of the flowers from the same site. These flowers were later identified as A. napellus.

At around 5 pm, he complained of nausea and abdominal pain, vomited one half hour later, and collapsed suddenly at 6:15 pm. Resuscitation was attempted but was unsuccessful.

At autopsy, the nail beds were noted to be cyanosed. Internal examination showed severe congestion of all organs. Histologic examination revealed bilateral massive intrapulmonary hemorrhage and edema. Urine and blood were collected at the time of autopsy and were sent for toxicological analyses.

Urine screens for drugs of abuse including screens for cannabinoids, opiates, benzodiazepines, phencyclidine, barbiturates, amphetamines, and cocaine metabolites were negative. Analysis of the blood sample for both alcohol and digoxin was negative.

The case history indicated the ingestion of A. napellus and the possibility of aconitine poisoning.

A liquid chromatography tandem-mass spectrometry (LCMS⁄MS) method was, therefore, developed for the analysis of aconitine in the blood and urine samples.

These analyses confirmed the presence of aconitine which was in the postmortem femoral blood sample at a concentration of 3.6 lg⁄L and in the urine sample at a concentration of 149 lg⁄L. The cause of death was considered to be aconitinie poisoning secondary to ingestion of A. napellus.

For many thousands of years the toxicological properties of particular plants have been exploited for both medicinal and sometimes criminal purposes.

However, most cases of poisoning typically involve pharmaceuticals or drugs of abuse and routine toxicological analyses do not generally detect plant alkaloids.

Therefore, in recent years recorded cases of plant poisoning have become a rare occurrence and instances may be missed unless sufficient case history or scene evidence is available.

Aconitine:

Aconitum napellus (also known as aconite, Wolfsbane, Monkshood, etc) is native throughout Europe. It is a perennial plant and can grow up to 1 metre high with light green leaves and blue, mauve or white flowers.

Although now seldom found wild, it is thought to be one of the most poisonous plants in the United Kingdom and is still cultivated in domestic gardens.

It is also related to the other Aconitum plants of the Ranunculaceae family that are widely distributed across North America and northern Asia.

Various Aconitum species are also used in Chinese herbal products mainly for the treatment of musculoskeletal disorders, however, several cases of poisoning have been reported.

Case History:

A 60 year old male with personal problems had produced an aconite extract for oral ingestion by liquidising tissue from Aconitum napellus (possibly self-cultivated).

Shortly afterwards he became agitated, nauseous and began to vomit violently. An ambulance was called and he was taken to a nearby hospital

He remained conscious for a while and informed the staff of the ingestion of aconite and his intentions. He was treated supportively but died following cardio-respiratory arrest, approximately two hours after ingestion.

A post-mortem examination one day after death revealed no evidence of natural disease. Various plant tissues and books pertaining to plant pathology/toxicology were found at the original scene. Specimens of blood/serum and urine obtained at post mortem and taken upon admission (ante mortem), along with a sample of the apparent aconite extract (liquid), were submitted for toxicological analysis.

Chemical structure of aconitine.

A review by Chan of aconitine poisoning between 1955 and 1994 showed a total of 30 reported deaths, with 23 occurring in China.

However, there are very little published data regarding aconitine concentrations measured in biological fluid. Two recent papers presented extensive data for many Japanese Aconitum plant alkaloids.

In these non-fatal and fatal cases, although jesaconitine was determined to be the main alkaloid present, aconitine was also detected and concentrations of 1.7 ygI1 and 1.1 ygll were measured in the ante mortem serum and post mortem blood, respectively. I

n both instances poisoning was attributed to aconite ingestion. In the case presented here there was overwhelming clinical and circumstantial evidence of Aconitum napellus intoxication.

As this aconite species has a different alkaloid profile to that ingested in the Japanese cases, it was not appropriate to compare aconitine concentrations. Nevertheless, based on published information, the concentrations measured (particularly in the post mortem femoral blood; 10.8 ygn) supported aconite poisoning leading to cardiorespiratory arrest as the cause of death.

The additional presence of ethanol (166 mgldl) may have also exacerbated toxicity. Plant alkaloids are not usually identified during routine toxicology screening. However, as in this case, at high concentrations aconitine may be detectable during routine screening for chemically basic drugs, particularly when using HPLC-DAD or GC-MS.

Due to the vast numbers of possible alkaloids, difficulty in obtaining pure analytical standards andthe lack of comparative cases it is difficult to compile and maintain relevant data.

The only indication for potential plant poisoning will therefore probably be based upon evidence at the scene or witness statements. Provision of material in such cases is therefore vital in order to determine the relevant toxicological analyses required.

Thank you