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Water dropwort
Plant Name:
Water dropwort
Scientific Name:
Oenanthe aquatica, Oenanthe crocata, Oenanthe fistulosa, Oenanthe fluviatilis, Oenanthe javanica, Oenanthe javanica ssp. javanica, Oenanthe javanica ssp. stolonifera, Oenanthe lachenalii, Oenanthe laciniata, Oenanthe peucidanifolia, Oenanthe pimpinelloides, Oenanthe sarmentosa, Oenanthe silaifolia
Family:
Apiaceae
Toxins:
Oenanthotoxin
Poisoning Symptoms:
Drooling, frothing at the mouth, severe gastrointestinal upset (vomiting, diarrhea), anxiousness, confusion, loss of coordination, tremors, muscular weakness, severe seizures, rhabdomyolysis, cardiac dysrhythmias, renal failure, respiratory failure and death
Additional Information:
Water dropwort refers to a genus of plants in the carrot family (Apiaceae). Several species are extremely toxic, the most notable being O. crocata; a plant that most sources consider to be the most poisonous of all British plants. Most varieties grow in damp, marshy ground and can commonly be found in wet meadows, pastures and along the banks of streams and rivers.
Water dropwort is a spring flowering wetland plant, accordingly most cases of poisoning occur around this time. The plant grows to a height of between 3 and 5 feet with shiny green, serrated, lance shaped leaflets, growing off the rootstalk. At the end of the rootstalk, small white flowers grow from a compound umbel similar in appearance to many other species in the carrot family that grow in umbrella like clusters. The rootstalk is compartmentalized with numerous small chambers containing a highly poisonous brown or straw-colored liquid that is released when the stem is broken or cut. Unlike many toxic plants, grazing animals find Water dropwort to be quite palatable, especially the roots and green seed heads. The fact that this plant commonly grows in moist areas near a water source where grazing animals are likely to congregate makes it all the more dangerous.
The chief poison is oenanthotoxin, a central nervous system (CNS) poison, that acts as a noncompetitive gamma-aminobutyric acid antagonist severely disrupting normal CNS function. The toxin is most concentrated in the roots and rootstalk, although all parts of the plant contain a potentially lethal amount of the toxin. Other toxins in the plant include coniine, which is structurally similar to nicotine and acts as both an agonist and antagonist on nicotinic (cholinergic) receptors. Like oenanthotoxin, coniine plays a role in disrupting CNS function, initially acting as a stimulant and then as a severe CNS depressant resulting in coma and death; typically by way of respiratory failure.
The initial symptoms of ingestion may manifest in as little as 5 minutes or be delayed as long as an hour. Additionally death may occur in as little as 15 minutes or be delayed for hours or days as symptoms rapidly or slowly progress from bad to worse depending upon the amount ingested and the specific animals constitution; in most cases death will occur in under six hours. The specific quantity necessary to cause death varies with the season and age of the plant as well it depends upon which part of the plant was ingested; the roots being the most toxic. The dose needed to cause clinical signs and the lethal dose are nearly identical, a little more than 1 g/kg body weight. A piece of root roughly the size of a walnut is enough to cause the death of a cow; approximately 230 grams will kill a horse. However, the ingestion of even smaller amounts may result in a severe and potentially lethal intoxication. As little as 0.3% body weight for swine, 0.5% body weight for horses, 0.1% body weight for cattle, and 0.2%-0.5% body weight for sheep can be lethal. The initial symptoms of ingestion generally consist of drooling, frothing at the mouth, severe gastrointestinal upset (vomiting, diarrhea), anxiousness, confusion, and loss of coordination. As the intoxication progresses the symptoms will become more severe. In potentially lethally intoxicated animals the syndrome is typically very violent and includes tremors, muscular weakness, renal failure, severe seizures, rhabdomyolysis, cardiac dysrhythmias, respiratory failure and death. It is not uncommon for symptoms to progress so fast that death occurs as soon as 30 minutes after the initial onset of clinical signs.
First Aid:
The prognosis for animals that have ingested Water Dropwart will depend largely upon how much of the plant was ingested; but in general will be guarded to poor. The rapid onset of symptoms such as the abrupt onset of seizures will generally aid in identifying Water Dropwart ingestion; as it is likely the animal will still be in or around the area that it ingested the plant. This should make a differential diagnosis based upon the animals immediate environment rather straight forward. This, however, is not necessarily a positive as rapidly progressing symptoms are indicative of a large ingestion that will more often than not end in a fatality.
As is the case with many highly toxic plants there is no specific antidote and treatment is going to be symptomatic and supportive. The primary goal of treatment will be prompt airway management and seizure control, plus decontamination if achieved early and after stabilization. If the ingestion was recent (e.g. the animal was observed eating Water Hemlock and/or you find identifiable plant matter in the mouth) and CNS symptoms are not present the administration of an efficient emetic to induce vomiting, followed by the administration of activated medical charcoal is suggested; a cathartic to induce defecation may also prove beneficial. If vomiting is promptly produced before the toxin can be absorbed into the body, the patient is likely to recover.
The progression of symptoms is rapid and dramatic and once CNS symptoms such as convulsions develop, the likelihood of a positive outcome drops dramatically. If the animal is presenting with central nervous system disturbances such as clonic-tonic convulsions then those should be treated and stabilized prior to attempting to decontaminate the animal through emesis and activated charcoal administration. The administration of benzodiazepines such as lorazepam or diazepam (1 to 2 mg/kg), intravenously may be an effective frontline treatment for seizure control. If no improvement is seen it may be necessary administer a barbiturate such as intravenous sodium pentobarbital (given till improvement is seen and repeated as necessary). The anticonvulsant phenytoin (Dilantin) is not recommended as it has not been shown to be effective for seizure control following water hemlock poisoning. Treatment with high doses of benzodiazepines or barbiturates may cause respiratory depression and respiratory support including intubation and mechanical ventilation is required in these patients. Additionally, if the preceding procedures have failed to bring the seizures under control, then it may be necessary to anesthetize the animal with isoflurane gas. For cattle, injections of morphine have produced some positive results in reducing convulsions and easing their pain.
Further treatment for complications of rhabdomyolysis, metabolic acidosis, hyperthermia, and hypotension may be required. The management of rhabdomyolysis includes ensuring adequate hydration and urinary alkalinization; a complication of rhabdomyolysis is acute renal failure which may require management with hemodialysis. However, hemodialysis, hemoperfusion or other extracorporeal techniques do remove cicutoxin from the blood and are therefore not useful in enhancing elimination. Metabolic acidosis is treated by administering sodium bicarbonate. Low blood pressure is usually treated with intravenous fluid replacement, but the administration of dopamine or norepinephrine may be required to restore blood pressure. If the animal manages to survive 4 to 6 hours with treatment it may recover, however the animal may suffer permanent or temporary damage to the heart and skeletal muscle. Unfortunately, even with treatment death from respiratory paralysis and terminal convulsions is a likely outcome.
Species Affected:
Toxic To Dogs
Toxic To Cats
Toxic To Horses
