Approach
The mainstay of treatment for most plant poisoning is symptomatic and supportive care. Very few plant exposures require any specific treatment or antidote.[38] Asymptomatic patients who present for evaluation after consuming a potentially poisonous plant should be observed for several hours after ingestion, and efforts should be made to correctly identify the plant. Activated charcoal is unlikely to be of benefit in most plant poisonings because most plant ingestion already results in vomiting. There are no data available on how well plant or vegetable material binds to activated charcoal; any plant extracts or plants that are brewed into teas are in a liquid vehicle and are rapidly absorbed. In plants that cause coma and seizures or central nervous system (CNS) depression, it should not be given until the airway is secured and there is no risk of aspiration. In some cases of highly toxic plants (e.g., autumn crocus), activated charcoal and/or whole bowel irrigation may be considered.
Gastrointestinal effects
Control of nausea, vomiting, abdominal cramping, and diarrhea caused by plant toxin can be difficult. Treatment modalities including intravenous fluid, antiemetics, gastric acid-reducing agents, and other treatment modalities may be employed, but may be inadequate to control the symptoms of plant-induced gastroenteritis.
Hepatotoxic effects
Very few data exist regarding the use of antidotes in plant poisonings. N-acetylcysteine has been reportedly used to treat hepatic injury from pyrrolizidine alkaloids and pennyroyal oil with varying degrees of success. Considering that there are no major disadvantages to using N-acetylcysteine, it is recommended in cases of proven or potential plant-induced hepatotoxicity.[39]
Patients who demonstrate continued acidosis (pH <7.3) despite maximal resuscitative efforts, or who demonstrate continued deterioration of hepatic synthetic function (e.g., coagulopathy), should be referred to a liver transplant center for optimal management of their hepatotoxicity. Evidence of liver injury and elevation of serum aminotransferases or bilirubin are not in and of themselves reasons for liver transplantation.
Cardiac effects
Standard treatments of tachycardia, including intravenous benzodiazepines to sedate the patient and reduce catecholamine outflow, are indicated in poisonings that cause sympathomimetic or antimuscarinic cardiac effects. Bradycardias should be treated according to the severity of hemodynamic embarrassment and presence of intraventricular conduction delays with the use of atropine, vasopressors/inotropes, and pacemaker as indicated.
Several case reports describe the use of digoxin immune Fab for the treatment of bradycardia and hypotension in patients poisoned after ingesting concentrates of plants that contain cardiac glycosides.[11][40] Digoxin immune Fab will bind with variable success to the cardiac glycoside and prevent further toxicity by inactivating the agent.
Based on limited data, amiodarone and flecainide are first-choice therapies for aconitine-related ventricular arrhythmias, unless the arrhythmia is related to prolonged QTc. Aconitine blocks the inward potassium-rectifying current and may worsen QTc prolongation. High-dose magnesium has been shown in two animal studies to abolish early after-depolarizations and shorten the prolonged action potential related to aconitine toxicity, resulting in termination of polymorphic ventricular tachycardia.[41][42] There are two successful case reports where magnesium was the sole therapy.[43][44] Many aconitine-related ventricular arrhythmias are often refractory to cardioversion. If these treatments fail and cardiogenic shock is present, extracorporeal cardiovascular support with intraaortic balloon pump assist, extracorporeal membrane oxygenation, left ventricular assist device, or cardiopulmonary bypass may be considered.[12][41][42][43][44] Magnesium sulfate may be considered for conduction delays.
Neurologic effects
Neurologic toxicity caused by plant poisoning should be treated with benzodiazepines to reduce catecholamine excess and elevate the seizure threshold. Because much of plant-induced seizure activity is related to gamma-aminobutyric acid (GABA) inhibition, other GABA agents besides benzodiazepines may be helpful. These include barbiturates such as phenobarbital which have a long duration of action and may control repeat seizures. It acts in a synergistic manner with benzodiazepines. Propofol may be an alternative to phenobarbital, due to its GABA agonism and NMDA antagonism.
Cyanide poisoning
Although not described in the literature, symptomatic patients poisoned with cyanogenic glycosides (e.g., from cassava or prunus plants) should logically be treated with a cyanide antidote. Nithiodote® contains sodium nitrite and sodium thiosulfate. Alternatively, CyanoKit® contains hydroxocobalamin, and has demonstrated efficacy in treating cyanide-poisoned patients. Both of these drugs are considered safe to use. Some institutions believe hydroxocobalamin is the safer of the two; however, there are no data demonstrating increased efficacy or safety of hydroxocobalamin over sodium nitrite/sodium thiosulfate in plant poisonings.
If cyanide antidotes are not available, good supportive measures (including oxygenation and intubation) are often associated with good outcomes.
Hematologic toxicity and myelotoxicity
Treatment of hematologic toxicity and bone marrow suppression (myelotoxicity) is supportive. The most important intervention is to stop the exposure to the toxin. If the patient exhibits anemia, thrombocytopenia, or neutropenia they may require a transfusion of the appropriate cell line. Pancytopenia and a general decrease in all blood cell lines including leukocytes (neutropenia) will result in the patient becoming immunocompromised, requiring exquisite vigilance to monitor for infections. The use of erythropoietin or a granulocyte-stimulating factor may be a useful adjunct. There are no specific treatments or antidotes for plant-induced myelotoxicity.
Bleeding
If bleeding is caused by ingestion of plant-derived coumarin compounds, vitamin K may reverse the coagulopathy. Recommendations regarding the management of patients on vitamin K antagonist therapy with elevated INR can be amended to apply to individuals who have developed coagulopathy as a result of ingestion of plant-derived coumarin derivatives, according to local specialist protocol.[45]
Dermatologic toxicity
After decontamination with soap and water, most dermatologic manifestations of plant toxicity can be treated with topical emollients and corticosteroids.
Multiorgan toxicity: nicotinic toxicities
Nicotinic poisonings can be very challenging as autonomic instability can be severe. Supportive care is paramount, with careful cardiac and pulmonary monitoring and intravenous fluid supplementation and replacement to correct acidemia. Benzodiazepines are provided to treat seizures, agitation, and hypertension; vasopressors are provided to treat hypotension.
Multiorgan toxicity: antimuscarinic toxicities
Antimuscarinic toxicity is treated primarily with supportive care, cardiopulmonary and temperature monitoring, and intravenous fluid hydration. Seizures and tachycardia are usually treated with benzodiazepines. Physostigmine may be indicated in patients with a clear antimuscarinic toxidrome and serious central toxicity characterized by an altered mental status, particularly delirium, requiring chemical and/or physical restraint. The use of physostigmine for antimuscarinic toxicity is increasing, and there is growing evidence that it is safe and has minimal cholinergic side effects.[46][47] Physostigmine is not commercially available in the US, but it may be available via a temporary importation service via the Food and Drug Administration.[36][37] An ECG is recommended prior to using physostigmine as it can cause arrhythmias. It is not recommended in patients with suspected or known tricyclic antidepressant intoxication. Consultation with a poison center or medical/clinical toxicologist is recommended prior to using physostigmine, and it should be given in a monitored environment.
If physostigmine is not available, some experts recommend using rivastigmine; however, this is an off-label use.[48]
Multiorgan toxicity: muscarinic toxicities
Muscarinic poisonings are treated primarily with supportive care, cardiopulmonary and temperature monitoring, and intravenous fluid hydration. Bradycardia and hypotension are treated with atropine and vasopressors/inotropes or pacemaker as indicated. Atropine can also be used to treat pulmonary edema along with supplemental oxygen, adjunctive respiratory assistance, endotracheal intubation, and mechanical ventilation if necessary. Ipratropium may be useful in relieving bronchospasm. Seizures are treated with benzodiazepines.
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