Many plants are poisonous to humans. Surveys of various toxicology centres in Australia,1 Germany,2 3 Morocco,4 New Zealand,5 Sweden,6 Thailand,7 the United Kingdom,8 and the United States9 10 showed that plant exposure was responsible for 1.8% to 8% of all inquiries. Most plant exposures did not result in significant toxicity, but severe and life-threatening poisonings have been reported. As reported by the Moroccan Poison Control Centre from 1980 to 2011, plants were the cause of approximately 5% of all fatal cases of intoxication encountered.4 Consumption of wild plants as “medicinal herbs” or food is not an uncommon practice in Hong Kong, and severe plant poisoning cases have been reported.11 12 13 14 15 16 17 18 19 However, local epidemiology data on plant poisoning are sparse and limited.

Owing to the variable clinical features and rare occurrence of plant poisonings, diagnosing and treating these patients remain a challenge to our frontline clinicians. Although history of plant exposure is important, it is often insufficient to pinpoint the incriminating toxic plant. Misidentification of plant is a common cause of poisoning in the first place. Morphological identification of a poisonous plant and biochemical confirmation are generally not available to guide immediate clinical management. Therefore, clinical features are critical for initiating supportive treatment, which is a common strategy for treating poisonings of an uncertain nature.

Classifications of clinically significant plant toxins have been proposed in order to aid rapid recognition and management of these patients.20 21 Plant toxins can be broadly classified into four groups: (1) cardiotoxic toxins, such as cardiac glycosides; (2) neurotoxic toxins, such as gelsemium alkaloids, grayanotoxins, solanaceous tropane (anticholinergic) alkaloids, strychnine, and brucine; (3) cytotoxic toxins, such as colchicine, mimosine, plumbagin, toxalbumins; vinblastine, and vincristine; and (4) gastrointestinal-hepatotoxic toxins, such as amaryllidaceous alkaloids, calcium oxalate raphide, cycasin, pentacyclic triterpenoids, phorbol esters, phytolaccatoxins, plumericin, pyrrolizidine alkaloids, saponins, steroidal alkaloids, tetrahydropalmatine, and teucvin.

The Hospital Authority Toxicology Reference Laboratory (HATRL), the only tertiary clinical toxicology laboratory in Hong Kong, provides support to all local hospitals in managing patients with complex poisoning problem, including cases of plant poisonings. Besides plant identification, HATRL provides specialised toxicology testing for certain plant toxins, especially for those with significant clinical toxicity and management impact.16 22 The aim of the present study was to identify the plant species most commonly involved in cases of plant poisoning in Hong Kong, in order to promote awareness among local clinicians and to provide a reference for diagnosing and managing plant poisonings.

All cases of suspected plant-related poisoning referred to the HATRL from January 2003 to December 2017 were retrospectively reviewed. Clinical data were collected by reviewing the laboratory database and patient medical records. Demographic characteristics, clinical presentation, drug history, laboratory and toxicological findings, progress, and outcomes of these patients were reviewed. The causal relationships between the clinical presentation and plant use were evaluated based on known adverse effects of the specified plant or toxins, the temporal sequence, exclusion of other underlying or concurrent diseases which could otherwise account for the clinical presentation, and progress after discontinuation of plant use. Severity of the poisoning cases was graded according to an established poisoning severity score as follows23: mild, transient, and spontaneously resolving symptoms (mild); pronounced or prolonged symptoms (moderate); severe or life-threatening symptoms (severe); and fatal poisoning (fatal). Descriptive statistics were used to present the results.

In collaboration with the Hong Kong Herbarium, Agriculture, Fisheries and Conservation Department, available plant specimens were sent for morphological identification. Mass spectrometry–based and microscopy-based tests for specific plant toxin(s) were developed, and performed on selected cases, guided by clinical presentation of the patients and types of the toxic plant(s) exposed. Mass spectrometry–based analytical platforms can identify the majority of the clinically significant plant toxins affecting the cardiovascular, neurological, gastrointestinal, hepatological, and renal systems in plant and biological specimens. The poisonous plants commonly encountered in Hong Kong and the corresponding plant toxins are summarised in Table 1.24

The ethics committee exempted the study group from obtaining patient consent because the presented data were anonymised, and the risk of identification was low. The STROBE guidelines were used to ensure the reporting of this study.25

A total of 62 cases of confirmed plant poisoning, involving 26 plant species, were identified within the study period. The patients were referred from 14 local hospitals administered by the Hospital Authority. Almost all patients (n=60, 97%) were Chinese, 29 (47%) were male, and 33 (53%) were female. The median age was 50 years (range, 1 month to 83 years), including three children (range, 1-23 months) and four adolescents (range, 15-18 years). The route of exposure was oral in 60 (97%) patients and topical in two (3%) patients. The majority of the patients (n=55, 89%) developed acute toxic symptoms after a single use of the plants, while the remaining patients (n=7, 11%) reported a history of prolonged exposure. Details of the plant poisoning cases, including the involved plant species and toxins, clinical presentation and outcome of these patients are summarised in Table 2.

Gastrointestinal toxicity was the most common clinical presentation (n=30, 48%). Of these 30 patients, 17 developed oromucosal irritation after ingestion of calcium oxalate raphide–containing plants. The other 13 patients presented with gastroenteritis-like symptoms, such as nausea, vomiting, abdominal pain and diarrhoea, after ingestion of plant containing gastrointestinal irritants (n=11) or cytotoxic toxins (n=2). Neurological toxicity was the second most common presenting symptoms (n=22, 35%), mainly caused by gelsemium alkaloids (n=12), Solanaceous tropane alkaloids (n=4), and grayanotoxins (n=3). Hepatotoxicity was encountered in six (10%) patients. Five patients had abnormal liver function test results owing to the use of teucvin (n=1), pyrrolizidine alkaloids (n=1), and other unknown hepatotoxin(s) (n=3); one patient developed cholestasis after exposure to pentacyclic triterpenoids. Cases of nephrotoxicity (n=2, 3%), cardiotoxicity (n=1, 2%), and dermatological toxicity (n=1, 2%) were also recorded.

Most of the patients experienced mild (n=49, 79%) or moderate toxicity (n=8, 13%). Of them, 55 patients recovered within days with supportive treatment. The other two patients with nephrotoxicity had residual renal impairment after discontinuation of plant use; in one of them a renal biopsy study showed tubulonephritic changes. The remaining five patients (8%) experienced severe toxicity after the use of Abrus precatorius (n=1), Gelsemium elegans (n=2), Rhododendron species (n=1), and Emilia sonchifolia (n=1), and all five required intensive care support.

The morphological identification and biochemical analysis process followed to identify the plants involved in the 62 cases of intoxication is shown in Figure 2. Most patients provided fresh plant specimens (n=53, 85%) or photograph of the plant (n=3, 5%) they had consumed. Among these specimens received by our laboratory, 43 could be identified morphologically with the aid of the Hong Kong Herbarium, Agriculture, Fisheries and Conservation Department. Biochemical analysis for specific plant toxin(s) were attempted in the plant or the biological specimens in 45 (73%) cases, with 41 yielding diagnostic information, including six cases with no plant specimens for identification and 13 cases with unsuccessful identification. There were 22 (35%) cases with both informative morphological identification and biochemical results. Among these 22 cases, the morphological identification and biochemical results were coherent in 20. For the remaining two cases with clinical gelsemium poisoning, gelsemium alkaloids were detected in both the urine and plant specimens. However, the plant specimen was morphologically identified as Cassytha filiformis. Cassytha filiformis is a non-toxic plant that has been shown to parasitise Gelsemium elegans and absorb gelsemium alkaloids, leading to poisoning.18 Patient accuracy in identification of plants was low. Although 56 (90%) patients had given common names of the plants they consumed, only 19 of them were correct.

Patients consumed the plants as medicinal herbs (n=31, 50%), as food (n=29, 47%), in an attempted suicide (n=1, 2%), or accidentally, in one paediatric patient (n=1, 2%). Causes of poisoning in patients using the plants as medicinal herbs or food included plant misidentification (n=34), unawareness/underestimation of the potential toxicity (n=20), or contamination of non-toxic plants with poisonous ones (n=6). The sources of the poisonous plants used included self-collecting from parks or the countryside (n=37, 60%), obtaining from friends or relatives (n=20, 32%), growing at home (n=3, 5%), and buying from wet markets (n=2, 3%). The plants were obtained in Hong Kong (n=49, 79%) or mainland China (n=12, 19%), with one (2%) case collected from the Philippines.

The 62 cases reported herein represent the largest series of plant poisoning cases in Hong Kong confirmed by either morphological identification or biochemical confirmation. Comparing our results with those of studies from other regions, the pattern of plant poisoning is considerably different. Plant poisonings reported in Western countries are predominantly accidental exposure in children,3 7 10 whereas in the present study, most patients were adults poisoned after intentional use of wild plants. The highly urbanised and industrialised nature of Hong Kong explains the low incidence of paediatric accidental poisoning. The relatively high rate of adult poisoning may be related to the long-standing tradition and Chinese culture of using wild plant as “medicinal herbs” and “vegetables”. Recreational abuse of toxic plants, such as Datura species,26 27 which are responsible for a significant number of poisoning cases reported in other regions, was not observed locally.

The most common type of poisoning in the current study was the use of raphide-containing plants, such as Alocasia macrorrhizos, accounting for more than 25% of cases. The roots of these plants are frequently mistaken as edible taro.28 Although all cases in this study were mild, severe outcomes including oropharyngeal oedema, upper airway obstruction, or systemic toxicity are possible.29 30

Similar to previous reports of plant poisoning,3 5 7 most patients in the present study developed mild transient symptoms and recovered with supportive management and discontinuation of exposure. However, there were five cases of severe poisoning requiring intensive care support, involving the use of Gelsemium elegans, Rhododendron species, Abrus precatorius, and Emilia sonchifolia (Fig 1).

Gelsemium elegans is one of the most notorious poisonous plants in Hong Kong and South-East Asian countries and has been used for homicidal and suicidal purposes.31 32 Severe gelsemium toxicity can result in respiratory depression and even death. In our case series, two clusters of “hidden” gelsemium poisoning were identified where the patients consumed non-toxic parasitic Cassytha filiformis which absorbed gelsemium alkaloids from Gelsemium elegans on which it grew.18 Similar cases of hidden gelsemium poisoning from contaminated dried herbs Ficus hirta have been reported in Hong Kong.16

Rhododendron species and other plants in the Ericaceae family contain grayanotoxins.33 Severe grayanotoxin poisoning may result in respiratory depression and arrhythmias.34 “Mad honey” containing nectar of Ericaceae plants is known to be a source of exposure in Hong Kong,35 but poisonings due to direct consumption of Rhododendron flowers are not uncommon.12

The seed of Abrus precatorius contains the protein abrin, an extremely poisonous toxin similar to ricin that can result in multi-organ failure.36 37 These seeds are sometimes used in beaded jewellery, in addition to being collected, providing another potential source of exposure.37 Cases of abrin poisoning due to suicidal attempt or accidental ingestion have been reported worldwide,38 39 40 but such poisoning is rare in Hong Kong.

The toxic constituents in Emilia sonchifolia are pyrrolizidine alkaloids.41 Massive acute ingestion can lead to hepatotoxicity and coagulopathy, while chronic low-dose exposure can result in liver cirrhosis and hepatic veno-occlusive disease.42 43 44 Certain types of traditional Chinese medicine, such as Flos farfarae and Herba senecionis scandentis, are potential sources of pyrrolizidine alkaloids exposure in Hong Kong,45 46 but toxicity due to wild plant consumption is relatively rare.14

Timely diagnosis of plant poisonings is very difficult. Local epidemiology data are scarce, and reports published in other parts of the world are of limited use because plant species are geographically specific. Patients might volunteer a history of plant exposure, but the information they provide may be uninformative, misleading, or incorrect. In our case series, among those who provided a common name of the plant, only 34% were correct.

Our results demonstrate the importance of adopting a complementary approach, incorporating clinical toxidrome, morphological identification of plant specimens, and biochemical analysis of plant toxins, in order to achieve maximal diagnostic efficacy. Clinical history may not be particularly informative. The presenting toxidrome is more objective and useful for identifying the plant responsible for the poisoning, and this diagnostic approach is well supported in the literature.20 21

Table 1 summarises and categorises commonly encountered local poisonous plants by toxidromes. This may serve as quick reference for clinicians to allow rapid identification of the plant and prompt management of the poisoning. However, clinicians should also be aware that the toxicity of some plants may not be well characterised, and that some plants may give rise to non-specific toxidrome, rendering this approach less useful in certain cases.

Specialised toxicological investigation may provide additional evidence to confirm or refute the provisional diagnosis. In most situations, morphological identification of the plant is sufficient to achieve a diagnosis, if a well-preserved plant specimen is provided. However, a plant specimen is not always available; even if available, it may not be representative of the plants consumed by the patient, or may have been deformed due to prior processing. An equally important tool is target testing for specific plant toxin(s) in the plant or biological specimens based on clinical suspicion. This is a powerful tool for confirming the diagnosis, especially when plant specimen is not available; and for identifying cases of contamination with an unclear or hidden source.18 However, these investigations cannot aid immediate management in the emergency room.

Diagnosis of plant poisoning requires a proactive rather than a reactive approach. A knowledge database comprising the clinical toxicity, morphology, and biochemical analysis of local toxic plants is an important tool to prepare clinicians and healthcare professionals, such as that provided by the Hospital Authority.24 This public resource can also be used to educate the general public on the dangers of wild plants.

As a retrospective study, this study has several limitations. This study is subjected to selection bias as the data collection is a passive procedure depending on test or consultation requests by clinicians, and there might be incomplete or missing data. Moreover, for those with history of exposure or mild clinical symptoms, toxicology testing or consultation may not be requested, our data might therefore include only cases with more severe outcome in the overall continuum of plant poisoning. Inevitably, some plant exposures were not reported to our laboratory, and thus our findings may underestimate the actual number of cases.

Diagnosing plant poisoning is challenging and the epidemiology of plant poisonings is geographically specific. Clinicians should consider a complementary approach with consideration of the clinical toxidromes, local epidemiological data, botanical and toxicological findings to help recognition of the plants involved in cases of intoxication. Plant specimens and biological specimens should be saved whenever possible for toxicological analysis. Clinicians should be aware of local poisonous plants and their toxicities. Although most plant exposure resulted in a self-limiting disease, severe poisonings were encountered. The public should be educated about the potential hazards of consuming plants obtained from the wild and discouraged from engaging in this practice.

All authors had full access to the data, contributed to the study (including concept or design, acquisition of data, analysis or interpretation of data, drafting of the manuscript, and critical revision for important intellectual content), approved the final version for publication, and take responsibility for its accuracy and integrity.

All authors have disclosed no conflicts of interest.

Some of the cases have been published by the authors in electronic form24 and in book form (Mak WL, Lam YH, Ching CK, Chan SS, Chong YK, Ng WY, editors. Atlas of Poisonous Plants in Hong Kong—A Clinical Toxicology Perspective. Hong Kong: Hospital Authority Toxicology Reference Laboratory; 2016), and presented at the Hospital Authority Toxicology Services Scientific Conference 2016 (“Poisonous plants in Hong Kong—a clinical perspective”). Some of the cases have been previously published as case reports by the authors and other units.12 13 14 15 16 17 18 19

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

The study was approved by the Hong Kong Hospital Authority Kowloon West Cluster Research Ethics Committee (Ref. KW/EX-16-036[96-18(TCM)]).

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