Acute liver failure in two dogs following ingestion of cheese tree (Glochidion ferdinandi) roots.

OBJECTIVE: To describe the management and resolution of acute liver failure (ALF) in two dogs following ingestion of cheese tree (Glochidion ferdinandi) roots. CASE SUMMARIES: A 2-year-old male entire Bullmastiff and a 5-year-old female neutered German Shepherd dog were presented for acute-onset lethargy and vomiting after chewing on tree roots of a cheese tree. Both dogs developed clinical abnormalities consistent with ALF, including hepatic encephalopathy, marked increase in alanine aminotransferase activity and bilirubin concentration, and prolonged coagulation times. Treatment included administration of intravenous fluids, hepatoprotectants, vitamin K1 , antibiotics, lactulose, antacids, antiemetics, and multiple fresh frozen plasma transfusions. Follow-up examinations performed 30 days after initial presentation revealed the dogs to be clinically healthy with serum biochemical and coagulation profiles within reference intervals. NEW OR UNIQUE INFORMATION: This is the first report describing ALF in two dogs following ingestion of cheese tree (G. ferdinandi) roots. In this clinical setting, despite a poor prognosis, survival and recovery of adequate liver function were possible with medical management.

[Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review].

BACKGROUND: Adverse reactions associated with Chinese herbal medicines (CHMs) are usually the result of unpredictable active/toxic ingredients, inaccurate or mistaken beliefs, or poor supervision. The herb that most commonly induces severe adverse effects in Hong Kong and China is aconite root. More than 200 species of Aconitum plants are used for medicinal purposes, with aconite roots producing analgesic, anti-inflammatory, cardiotonic, and anti-tumor effects. The active components are alkaloids; these can be toxic, but CHM processing methods lower their toxicity and increase the pharmacological efficacy. However, aconite poisoning can result from inadequate decoction time or exceeding the recommended dose. CASE REPORT: Here we report the case of a 92-year-old woman who presented with life-threatening bradycardia and hypotension. This started 1 h after she inappropriately consumed a herbal decoction containing Fuzi for mood fluctuation and health maintenance; Fuzi, an aconite root, has known cardiotoxicity. Electrocardiography showed supraventricular abnormalities, including sinus bradycardia and low-amplitude P waves. After an infusion of normal saline and inotropic agents for 25 h, the clinical manifestations subsided, her sinus rhythm returned to normal, and she was discharged. At follow-up 2 weeks later, she was in good health and had ceased taking any CHM. CONCLUSIONS: Standardized processing methods, stringent regulations, and cooperation between health professions can ensure medication safety and establish a fully-fledged operating process for these valuable drugs. We hope this report will help establish correct attitudes toward CHM and will assist Traditional Chinese Medicine practitioners to become more familiar with Aconitum plants.

Aconite poisoning with arrhythmia and shock.

A 55-year-old male presented with history of nausea, vomiting, palpitation paresthesis and profuse sweating in emergency department 2h after ingestion of "Bachnaag" (Aconite) root. Examination revealed shock with irregular pulses. Initial ECG showed frequent multifocal ventricular ectopics (VE), which later turned to short runs of ventricular tachycardia (VT). Immediate gastric lavage was done and activated charcoal given. Patient was treated with fluid resuscitation without any improvement in blood pressure. Patient was started on nor-adrenaline infusion with gradual recovery from hypotension over a period of 6h, but support was continued for 48h. Amiodarone was started to control ventricular excitability, which persisted over 72h with gradual decrease in frequency of VT and VE. Patient was discharged with normal sinus rhythm on oral amiodarone on 5th day of hospitalization. On follow-up after 2 weeks patient was totally asymptomatic and amiodarone was stopped.

Aconitum Alkaloid Poisoning Because of Contamination of Herbs by Aconite Roots.

Aconitum alkaloid poisoning can occur after drinking decoction and soup made from non-toxic herbs contaminated by aconite roots. In the present review, the main objective is to describe the clinical features, investigations and possible sources of contamination. A combination of neurological, gastrointestinal and cardiovascular signs and symptoms was seen. Ventricular tachyarrhythmias could occur in 18% of subjects. Yunaconitine and crassicauline A, mainly found in certain aconite roots from Southwest China, are most commonly involved. Herbal residues and unused herbs should first be inspected for gross contamination. On-site inspection at the retailer should exclude accidental mix-up or cross-contamination when handling aconite roots. Samples of prescribed herbs are examined for gross contamination and analysed for the presence of Aconitum alkaloids. Samples of the implicated herb are also collected from the wholesaler for investigation. If post-import contamination is unlikely, the regulatory authorities of the exporting countries should be notified for follow-up actions. It is a challenging task to work out how non-toxic herbs become contaminated by aconite roots. The source control with good agricultural and collection practices and quality assurance must be enhanced.

Incidence and Causes of Aconitum Alkaloid Poisoning in Hong Kong from 1989 to 2010.

Aconite roots contain Aconitum alkaloids, which are highly toxic cardiotoxins and neurotoxins. In this review, the main objective was to determine the incidence and causes of Aconitum alkaloid poisoning in Hong Kong between 1989 and 2010, based on six published reports from the territory-wide poison control units. In the New Territories East of Hong Kong, the incidence of aconite poisoning showed a sudden and sustained decrease from 0.60 (1989-1991) to 0.16 (1992-1993) and 0.17 (1996-1998) per 100 000 population, after publicity measures in late 1991 to promote awareness of the toxicity of aconite roots. In the whole of Hong Kong, the incidence of aconite poisoning was even lower in January 2000-June 2004 (0.03 per 100 000 population). However, aconite poisoning became more common again in April 2004-July 2009 and 2008-2010 (0.15 and 0.28 per 100 000 population). Overdoses and use of inadequately processed aconite roots were important causes. As from 2004 to 2009, 'hidden' aconite poisoning (toxicity caused by contaminants in other dispensed herbs) emerged as an important cause. It is important to continue the safety monitoring of potent herbs and the networking of poison control units. Further systematic studies would be required to identify the likely sources of contamination of herbs.

Aconitum alkaloid poisoning related to the culinary uses of aconite roots.

Aconite roots (roots or root tubers of the Aconitum species) are eaten as root vegetables and used to prepare herbal soups and meals, mainly for their purported health benefits. Aconite roots contain aconitine and other Aconitum alkaloids, which are well known cardiotoxins and neurotoxins. To better understand why Aconitum alkaloid poisoning related to the culinary uses of aconite roots can occur and characterize the risks posed by these "food supplements", relevant published reports were reviewed. From 1995 to 2013, there were eight reports of aconite poisoning after consumption of these herbal soups and meals, including two reports of large clusters of cases (n = 19-45) and two reports of cases (n = 15-156) managed by two hospitals over a period of 4.5 to 5 years. The herbal formulae used did not adhere to the suggested guidelines, with regarding to the doses (50-500 g instead of 3-30 g per person) and types (raw instead of processed) of aconite roots used. The quantities of Aconitum alkaloids involved were huge, taking into consideration the doses of aconite roots used to prepare herbal soups/meals and the amounts of aconite roots and herbal soups/meals consumed. In a large cluster of cases, despite simmering raw "caowu" (the root tuber of A. kusnezoffii) in pork broth for 24 h, all 19 family members who consumed this soup and boiled "caowu" developed poisoning. Severe or even fatal aconite poisoning can occur after consumption of herbal soups and foods prepared from aconite roots. Even prolonged boiling may not be protective if raw preparations and large quantities of aconite roots are used. The public should be warned of the risk of severe poisoning related to the culinary and traditional medicinal uses of aconite roots.

Acute interstitial nephritis following kudzu root juice ingestion.

Recently, the use of herbal remedies and complementary and alternative medicine has increased globally. Kudzu root (Pueraria lobata) is a plant commonly used in traditional medicine to promote health. A middle-aged woman consumed kudzu root juice to promote health and well-being for 10 days. Subsequently, she developed anorexia, epigastric discomfort and azotemia. These symptoms improved rapidly within several days after discontinuation of the suspected offending agent and conservative treatment. Acute interstitial nephritis was diagnosed by renal biopsy. To our knowledge, this is the first case report describing acute interstitial nephritis following the ingestion of kudzu root juice.

Distribution of Aconitum alkaloids in autopsy cases of aconite poisoning.

Aconite is a well-known toxic-plant containing Aconitum alkaloids such as aconitines, benzoylaconines, and aconins. We describe here the distribution of Aconitum alkaloids detected by liquid chromatography-tandem mass spectrometry (LC/MS/MS) in three autopsy cases of suicide by aconite poisoning. Case 1: a male in his fifties had eaten aconite leaves. The concentrations of jesaconitine in cardiac blood, urine, and kidney were 12.1 ng/ml, 993.0 ng/ml, and 114.2 ng/g, respectively. Case 2: a female in her fifties had eaten aconite root. The aconite root in the stomach included a high level of mesaconitine. The concentrations of mesaconitine in cardiac blood, liver, and kidney were 69.1 ng/ml, 960.9 ng/g, and 776.9 ng/g, respectively. Case 3: a male in his sixties had drunk liquor in which aconite root had been soaked. The concentrations of mesaconitine and aconitine in cardiac blood were 259.5 and 228.5 ng/ml, respectively. The Aconitum alkaloid levels were very high in the liver. The absorption of ethanol and Aconitum alkaloids might have been increased because of his having undergone total gastrectomy. In all three cases, the Aconitum alkaloid levels were high in the liver and kidney and low in the heart and cerebrum. The level in the cerebrum was lower than that in blood. Data on the distribution of the Aconitum alkaloids in the body in cases of aconite poisoning is useful to elucidate various actions of aconite alkaloids.

Contributory factors in herb-induced fatal aconite poisoning.

Detailed investigations of all reported cases of herb-induced aconite poisoning are necessary to identify the major contributory causes so that preventive measures can be formulated. In the present review of 12 fatal cases that were published in the medical journals during 1992 and 2011, the available clinical data and forensic toxicological analyses indicated that poor post-harvest processing of aconite roots, use of greater than the recommended doses and inadequate boiling of processed aconite roots during decoction preparation were important contributory factors in herb-induced aconite poisoning. Under such circumstances, the actual amount of Aconitum alkaloids ingested was much larger than intended. Good manufacturing practice to ensure adequate processing of aconite roots, use of the recommended doses, clear instructions for the patients and their compliance during decoction preparation are important preventive measures.

Aconite poisoning following the percutaneous absorption of Aconitum alkaloids.

In vitro experiment using the modified Franz-type diffusion cell has demonstrated that the human skin is permeable to aconitine and mesaconitine. To characterise the risk of systemic toxicity following the topical applications of aconite tincture and raw aconite roots, relevant reports of percutaneous absorption of Aconitum alkaloids and aconite poisoning are reviewed. Published reports indicate that aconite tincture and raw aconite roots can be absorbed through the skin into systemic circulation to cause fatal and non-fatal aconite poisoning. Both aconite tincture and raw aconite roots contain very high concentrations of Aconitum alkaloids, which allow penetration of the stratum corneum along the diffusion gradient. The risk of systemic toxicity is even higher if Aconitum alkaloids are held in occlusive contact with the skin and the epidermis (stratum corneum) is already damaged. The public should be warned of the danger in using these topical aconite preparations and the risk of systemic toxicity following percutaneous absorption of Aconitum alkaloids.

Aconitum alkaloid content and the high toxicity of aconite tincture.

Although proprietary medicines and decoction of processed aconite roots are the most widely used, tincture accounts for the great majority of aconite poisoning cases in China, indicating that it is much more toxic than other formulations. Aconite tincture is often self-prepared at home and raw aconite plants or roots are often used. Even if processed aconite roots were used to make the tincture, the amount of Aconitum alkaloids is highly variable, depending on the adequacy of processing and quality control. Aconitum alkaloids dissolve efficiently in alcohol. For these reasons, tincture contains very high concentrations of Aconitum alkaloids. Despite its high intrinsic toxicity, overdose of aconite tincture by the users has been common. Severe aconite poisoning can be complicated by fatal ventricular tachyarrhythmias and asystole. The public should be repeatedly warned of the danger of taking aconite tincture by mouth.

Appearance of konzo in South-Kivu, a wartorn area in the Democratic Republic of Congo.

Konzo is an upper motor neuron disease characterized by sudden-onset and irreversible spastic paraparesis occurring in nutritionally compromised people. It is associated with consumption of insufficiently processed cyanogenic-toxic cassava. Cassava, the main caloric source in the Democratic Republic of Congo, has been safely consumed for decades in the Eastern Province of South-Kivu. However, in the context of long-lasting war and violent conflicts, cases of spastic paraparesis resembling konzo appeared in a populous area (Burhinyi). Two field surveys (2003 and 2005) identified 41 subjects meeting clinical criteria of konzo and suffering from (chronic) malnutrition. Their urinary thiocyanate concentrations (median 129, range 20-688, SD 146 µg/L), and cyanogen levels (median 20 ppm, range 5-300 ppm, SD 73 ppm) in cassava roots from their household stocks were high. The source of cyanogenic-toxicity was unprocessed fresh cassava roots during harvest period, but probably also insufficiently processed roots. This first report of konzo in South-Kivu concludes that occurrence of konzo was triggered by food shortages because of the longstanding state of insecurity. Contributory factors included the introduction of new varieties of (bitter) cassava, but konzo may actually be caused by a combination of factors that are yet to be understood.

Chemical safety of cassava products in regions adopting cassava production and processing--experience from Southern Africa.

The cassava belt area in Southern Africa is experiencing an unforeseen surge in cassava production, processing and consumption. Little documentation exists on the effects of this surge on processing procedures, the prevailing levels of cyanogenic glucosides of products consumed and the levels of products commercially available on the market. Risk assessments disclose that effects harmful to the developing central nervous system (CNS) may be observed at a lower exposure than previously anticipated. We interviewed farmers in Zambia and Malawi about their cultivars, processing procedures and perceptions concerning cassava and chemical food safety. Chips, mixed biscuits and flour, procured from households and markets in three regions of Zambia (Luapula-North, Western and Southern) as well as products from the Northern, Central and Southern regions of Malawi, were analyzed for total cyanogenic potential (CNp). Processed products from Luapula showed a low CNp, <10 mg HCN equiv./kg air dried weight, while samples from Mongu, Western Province, exhibited high levels of CNp, varying from 50 to 290 mg HCN equiv./kg. Even the lowest level is five times higher than the recommended safety level of 10mg/kg decided on for cassava flour. Our results call for concerted efforts in promoting gender oriented processing technologies.

Plant poisoning.

Each year over 100,000 exposures to toxic plants are reported to poison centers throughout the United States. Most of these exposures are of minimal toxicity largely because of the fact that they involve pediatric ingestions, which are of low quantity. The more serious poisonings usually involve adults who have either mistaken a plant as edible or have deliberately ingested the plant to derive perceived medicinal or toxic properties. The plants within this manuscript have been chosen because they have been documented to cause fatalities or account for emergency medicine visits. In this discussion, plants are grouped by their toxins rather than on the basis of their taxonomy.

[Poisoning with Aconitum napellus (monkshood)]. / Forgiftning med Aconitum napellus (stormhat).

A lethal case of aconite poisoning due to ingestion of pieces of monkshood (Aconitum napellus) is described.