Hong Kong poison information centre: Annual report 2020

Case 1 ‒ endogenous lead exposure in a patient with end-stage renal failure

A woman in her 70s with a history of end-stage renal failure (ESRF) on haemodialysis was investigated for bilateral hand numbness for 2 years. Electromyography showed moderate-to-severe carpal tunnel syndrome and underlying generalised axonal neuropathy. Upon routine investigation for alternative causes of peripheral neuropathy, she was found to have elevated blood lead level (BLL) 13.9 µg/dL (reference < 10 µg/dL). The elevated BLL was confirmed upon repeating the blood tests 2 weeks later. There was no other clinical feature of lead poisoning. There was no exogenous source of lead exposure identified in detailed history taking. The patient was noted to have an elevated parathyroid hormone (PTH) concentration of 53 pmol/L (reference 1.3–6.8 pmol/L) and a corrected serum calcium concentration of 2.54 mmol/L (reference 2.24–2.63 mmol/L), which is at the high end of the normal range. Blood alkaline phosphatase concentration was elevated to 203 U/L (reference 47–124 U/L). Hyperparathyroidism related to ESRF and renal osteodystrophy was suspected in this patient. Based on the literature review, bone demineralization and mobilisation of lead from the bone store was reported to be a cause of endogenous lead exposure in ESRF patients.^{7 –10} In patients with renal osteodystrophy, the kidneys fail their function in maintaining normal calcium and phosphate homeostasis. The associated hyperphosphataemia and hypocalcaemia lead to hyperparathyroidism and increased bone turnover. ¹¹ As 95% of environmental absorbed lead is stored in bones in adults, hyperparathyroidism and increased bone turnover cause increased lead mobilisation from the bone in ESRF patients. ⁷ This will result in a slight elevation of BLL in ESRF patients when compared with the normal population. An exogenous source of lead exposure is typically absent in these cases. ¹² This type of endogenous lead exposure was also reported in other physiological states with calcium stress (e.g. pregnancy, lactation and osteoporosis) or calcium deficiency.

The slight elevation of BLL in this case was not compatible with lead neurotoxicity and it is unlikely the cause of peripheral neuropathy. Lead-induced peripheral neuropathy is one of the clinical manifestations of moderate to severe lead poisoning when BLL > 70–100 µg/dL in adults. Typical clinical presentation is primarily a motor weakness, initially in wrist and finger extensors, then other muscular involvements manifest as wrist drop and foot drop. Sensory involvement is generally minimal. ¹³ Other clinical features of lead poisoning such as anaemia, abdominal colic and encephalopathy are always present in patients with lead-induced peripheral neuropathy.

Case 2 ‒ risk of cyanide poisoning related to excessive bitter almonds consumption

A woman in her 50s attended the emergency department because of dizziness, headache, palpitation and shortness of breath. She had consumed a decoction 2 h ago, which was made by boiling 120 g of bitter almonds (北杏) in water. Cyanide poisoning related to excessive bitter almonds consumption was suspected. She was fully conscious and had stable vital signs upon presentation. Venous blood gas showed normal acid–base status. Serum lactate was not elevated. Based on the stable condition and the absence of lactic acidosis, the patient was unlikely to suffer from clinically significant cyanide poisoning. The use of cyanide antidote was not recommended. Her symptoms gradually resolved within several hours after in-patient observation. Qualitative analysis of cyanide in urine was negative and the patient was diagnosed to have mild bitter almond poisoning.

Cyanide poisoning is a rare cause of potentially fatal poisoning in Hong Kong. Cyanide compounds exposure is typically associated with smoke inhalation in fire victims, accidental exposure to laboratory or industrial chemicals and suicidal attempts. Many plant species contain cyanogenic glycosides and are considered as a potential cause of cyanide poisoning upon excessive consumption or improper preparation. The Prunus species consisting of apricots, bitter almonds, cherry and peaches have fruits containing the glycoside amygdalin. ¹⁴ When ingested, amygdalin is hydrolysed by intestinal enzymes to give hydrogen cyanide. Bitter almonds or bitter apricot seeds refer to 北杏 or 苦杏仁 in Chinese medicine. They are known to contain a higher amygdalin content when compared with sweet almonds or other Prunus species kernel. Accidental poisonings were well-reported in the literature and ingestion of 5–10 raw bitter almonds can result in severe toxicity in young children.^{15 –18} Early clinical features of cyanide poisoning are non-specific and may include gastrointestinal disturbances, dizziness, headache and weakness. Severe poisoning will progress to coma, seizures, cardiovascular collapse and severe lactic acidosis. Laboratory confirmation of cyanide poisoning is available in all acute public hospitals in Hong Kong, which includes qualitative cyanide screening and quantitative analysis of urine or blood samples. The turnaround time can be several hours for cyanide qualitative screening tests and two to 4 days for cyanide quantitative analysis. Due to the long turnaround time of cyanide tests, cyanide poisoning is diagnosed and treated clinically before the availability of laboratory confirmation in most circumstances.

According to a local study performed by the Centre for Food Safety, the uncooked bitter almonds contained an average content of 330 mg/kg free cyanide. A 98% reduction of free cyanide content was observed after cooking bitter almonds in boiling water for 15 min. ¹⁹ Cyanide poisoning after bitter almonds consumption is considered rare in Hong Kong as bitter almonds are always cooked or boiled before consumption in usual cooking recipes or Chinese herbal medicine practice. Adequate cooking or boiling can release the cyanide from bitter almonds and significantly reduce their toxicity. This observation may also explain the relatively mild symptoms and negative urine cyanide screening in our patient, who reported consumption of a large amount of boiled bitter almonds.

Case 3 ‒ LSD (Lysergic acid diethylamide)

An 18-year-old man was found to be wandering in the street with aggressive behaviour. He was put on physical restraint and brought to the emergency department. On examination, he was confused with irrelevant speech. There was diaphoresis and hyperthermia with a temperature of 37.6℃. His pulse rate was 173 beats per minute (bpm), pupils were 6 mm. Blood pressure could not be recorded initially as the patient was struggling. It was noted to be 115/56 mm Hg 15 min later. He reported to have ingested LSD (lysergic acid diethylamide) given by his friend but the details were not available. A total of 10 mg of midazolam and 50 mg diazepam was given intravenously in the first hour, together with a further 20 mg of diazepam 15 min later to control his sympathomimetic toxidrome. The serum creatine kinase level was peaked at 3982 U/L the next day (reference 39–308 U/L) and his other blood results were unremarkable. The patient’s confusion resolved the next day. In the urine specimen, LSD, diazepam, midazolam and temazepam were detected. Specific screening of novel psychoactive substances was negative.

LSD is a semi-synthetic hallucinogen structurally similar to serotonin (5-hydroxytryptamine; 5HT). ²⁰ It has agonistic effect on the 5HT_2A, 5HT₁ and dopamine receptors. ²¹ It is a very potent abusive agent and is most commonly used in the form of small squares of liquid-impregnated ‘blotter’ paper, resembling the appearance of a stamp. It was widely used as a psychotropic drug in the 1960s. Abuse of LSD has resurged in Hong Kong in recent years. ²¹ A single case of LSD abuse was recorded in our system each year from 2014 to 2016, but the number of cases rose to three, eight and 14 in 2018, 2019 and 2020, respectively.

Although LSD is traditionally classified as a psychedelic and severe toxicity is thought to be rare, significant sympathomimetic features may also result from its abuse. Agitation, violent behaviour, hypertension, tachycardia and rhabdomyolysis after LSD use have been reported in a recent case series in Hong Kong. ²² Another concern in patients presenting with significant toxicities is the possibility of adulteration with other potent hallucinogens such as NBOMes (N-benzyl-oxy-methyl), DOC (dimethoxy-4-chloroamphetamine) and DOI (dimethoxy-4-iodoamphetamine), which may not be detected routinely by urine toxicology. ²³ The prompt recovery of our case illustrated the importance of treating the sympathomimetic toxicity early in the emergency department.

Case 4 ‒ tramadol overdose (obtained from give-away of unused medications)

A woman in her 20s with repeated attempts of self-harm by drug overdose was brought to the emergency department for taking 70 capsules of tramadol (50 mg per capsule). She was noted to be semi-conscious, with a Glasgow Coma Score of E3V1M6 and sweaty. Her blood pressure was 122/94 mm Hg, pulse 90 bpm, temperature 37.2℃ and pupil size 3 mm. Her limb tones were increased but there was no ankle clonus. Haemoglucostix was 3.4 mmol/L and 20 g of dextrose was given intravenously followed by a dextrose infusion. The blood glucose level was 3.7 mmol/L and her other biochemistry results were normal. Her condition improved afterward. It was later noted that the tramadol was given to her freely by a member of a ‘self-help recycle group’ on social media who had some unused tramadol. The patient and her family refused psychiatric admission and she was discharged with acknowledgement of medical advice 3 days later.

Tramadol is a centrally acting analgesic that inhibits the reuptake of serotonin and noradrenaline, with a weak µ-opioid receptor agonistic effect. Tramadol overdose may produce nausea, vomiting, agitation, tachycardia, central nervous system and respiratory depression, seizure and serotonin syndrome. ²⁴ Hypoglycaemia of about 2 mmol/L following tramadol overdose has also been reported.^25,26 An increase in peripheral glucose utilisation and insulin levels have been proposed as the mechanisms for hypoglycaemia. ²⁷

Giving away unused medicines to a stranger without medical consultation is a dangerous practice. Although most people share medications with good intentions, the danger of misuse of the medications, for example, the risk of improper indications, incorrect dosage, missing proper follow-up and so on would outweigh the benefits. While many thought that analgesics are harmless medications, an overdose of paracetamol and opioid analgesics may produce significant toxicity. Some opioid analgesics also have abuse potential and access to these medications in an unsupervised manner may increase the risk of abuse in some patients.

Case 5 ‒ multiple wasp stings

A man in his 50s enjoying good past health was attacked by wasps while cutting down a tree. He was stung more than 30 times on his scalp, limbs and trunk. He presented immediately to the hospital with itchy and painful swelling over the sting wounds. His vital signs were stable with no sign of anaphylaxis despite having multiple wasp stings. After more than 10-h of observation, he developed a low-grade fever and was found to have coagulopathy with prolonged activated partial thromboplastin time (APTT) > 200 s and prolonged prothrombin time (PT) of 16.3 s with an international normalised ratio (INR) of 1.4. His platelet count and haemoglobin were normal but the white cell count was raised at 13.4 × 10⁹/L. His urea and creatinine concentrations were mildly raised at 9.8 mmol/L (reference 2.8–7.2 mmol/L) and 106 µmol/L (reference 59–104 µmol/L), respectively. His creatinine kinase was normal initially but raised slightly and peaked at 902 U/L (reference 61–399 U/L). He was admitted to the general medical ward with intravenous fluid and antibiotic treatment for the apparently infected pustular sting wounds. His renal function recovered in 24 h but the coagulopathy improved much slowly over the next four days without developing any bleeding complication. Both fibrinogen level and D-dimer concentration were raised on day 1 at 6.31 g/L (reference 1.85–3.83 g/L) and 1566.7 ng/mL (reference < 500 ng/ml), respectively. The platelet count of the patients had been normal during hospitalisation.

Coagulopathy after multiple wasps or bee stings has been well reported before. Many mechanisms have been proposed. One is heparin and tryptase released by mast cell activation as a part of venom-induced anaphylaxis. ²⁸ Heparin exerts its anticoagulant effect by activation of antithrombin III while tryptase increases lysis of fibrinogen that could result in hypofibrinogenaemia. Heavy wasp and bee envenomation can result in disseminated intravascular coagulopathy. ²⁹ Reduction of titres of multiple clotting factors independent of intravascular coagulation has also been reported. ³⁰ Our patient presented with coagulopathy and mild renal function abnormality without clinical evidence of anaphylaxis which was typical for heavy wasp stings. A large review of 1091 wasp-stung patients in Hubei of China documented a 5.1% mortality, about 90% of deaths were due to multi-organ dysfunction instead of anaphylaxis. The envenomation syndrome comprised of coagulopathy, acute kidney injury, haemolysis, liver injury and rhabdomyolysis were observed in the severe cases. Wasp sting more than 10 times was associated with in-hospital mortality. ³¹ Massive wasp or bee sting can cause multi-organ dysfunction and even death. Clinicians should be aware of the danger of multiple-wasp/bee stings.

Case 6 ‒ cicada flower poisoning

A family of three adults developed dizziness two to four hours after consuming homemade meatball soup prepared with a total of 18 pieces of golden Chanhua (金蟬花), a type of cicada flower. They presented with vertigo, nausea, vomiting, hyperventilation and generalised weakness. Their vital signs were stable but the father and mother had a mildly elevated systolic blood pressure. All three recovered uneventfully after symptomatic treatment overnight. The clustering was highly indicative of a food poisoning event so biological and herb samples were collected for investigation. Similar to the herb Ophiocordyceps sinesis (冬蟲夏草) which was a fungus-infected moth caterpillar, the much less expensive herb golden Chanhua (Isaria cicadae) referred to cicada nymph infected by a specific fungus of the Isaria genus. It might be collectively grouped under the herb name of cicada flower (蟬花) that also included Ophiocordyceps sobolifera (小蟬花) and Ophiocordyceps cicadae (大蟬花). They were the same cicada nymphs but infected by different fungal species. Morphological examination by an expert mycologist on the unused herb revealed the presence of Ophiocordyceps sobolifera and an unexpected species Ophiocordyceps heteropoda that was potentially toxic.

Ophiocordyceps heteropoda had been identified to be the cause of 60 cases of poisoning after cicada nymph ingestion in Vietnam. ³² All patients in the case series reported dizziness, vomiting and salivation within one hour. About one-third of them developed more severe neurological symptoms that included agitated delirium, hallucination and seizure. Jaw stiffness was an interesting symptom among three patients. About 20% of the cases developed coma and one of them died with respiratory failure, hypotension and cardiac arrhythmias despite intensive care. The psychoactive compound ibotenic acid was detected from Ophiocordyceps heteropoda samples collected in the area. Ibotenic acid is well known to be present in the hallucinogenic mushroom species Amanita muscaria. It is psychoactive and neurotoxic in being a potent glutamate receptor agonist which can explain the spectrum of symptoms in the Vietnamese case series. In our cases, consumption of Ophiocordyceps heteropoda was the likely cause of the poisoning. However, we were not certain if Ibotenic acid was the culprit as subsequent chemical analysis of the unused herb sample did not find Ibotenic acid. Possible explanations included missing the toxic species on laboratory sampling or the presence of other unidentified toxic compounds in Ophiocordyceps heteropoda.

Case 7 ‒ slow K overdose with endoscopic removal of pharmacobezoar

A teenage girl with borderline personality disorder intentionally overdosed 30 tablets of slow K (potassium chloride extended released 600 mg). She remained asymptomatic and presented to the emergency department 1.5 h after ingestion. Her vital signs and physical examinations were normal. Initial blood tests showed hyperkalaemia 5.7 mmol/L, which increased to 6.0 mmol/L on repeated testing. ECG showed normal sinus rhythm with no hyperkalaemic changes. Calcium gluconate 10% 10 mL, sodium bicarbonate 8.4% 50 mL and regular human insulin 10 units with 25 g dextrose infused over 30 min were given intravenously. A dose of activated charcoal was given despite potassium is not adsorbed by charcoal. An abdominal X-ray (Figure 6(a)) showed multiple (more than 20) radio-opaque drug tablets in her stomach. Given the presence of multiple drug tablets in the stomach, gastric lavage was performed after intubation by rapid sequence induction (RSI) using etomidate and suxamethonium for airway protection and yielded one tablet only. Repeat X-ray (Figure 6(b)) showed similar pattern of radio-opaque tablets in the stomach and formation of pharmacobezoar was suspected. She was then transferred to paediatric intensive care unit (ICU) for close monitoring, with a dose of polystyrene sulphonate sodium 15 g given via nasogastric tube. Upper endoscopy was performed by paediatric surgeon after urgent consultation at post-ingestion 8 h during which activated charcoal was seen over her stomach. A total of 23 tablets were retrieved by a basket in multiple attempts. Post-endoscopy X-ray (Figure 6(c)) showed few remaining tablets passed beyond the stomach. The potassium level was peaked at 6.0 mmol/L in the ED and remained normal after admission. Her condition was stable and she was discharged to a psychiatric unit on day 2 after admission.

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Figure 6.

Case 7 abdominal X-ray (AXR): (a) on admission, (b) post-gastric lavage and (c) post-upper endoscopy.

Intentional potassium overdose is not common in Hong Kong. There have been only nine recorded cases related to potassium overdose in PICMS since 2007. The toxic dose of potassium is not well defined. Each tablet of slow K 600 mg contains 8mmol potassium. Dose as low as 2–2.5 mmol/kg (i.e. 2.5–3 tablets of slow K in a 10-kg child) can cause hyperkalaemia in patients with normal renal function. Management mainly includes medical therapy for hyperkalaemia, together with timely and appropriate gastrointestinal (GI) decontamination. Activated charcoal is ineffective in binding potassium. Its use may also obscure the view of endoscopy in case removal of drug clumps by upper endoscopy is required, as in our patient. Gastric lavage is often not useful as the slow K tablets are often too big to pass through the holes of the gastric lavage tube. The formation of pharmacobezoar also limits the usefulness of gastric lavage. Whole bowel irrigation is another GI decontamination option. Since our patient had hyperkalaemia and X-ray showed evidence of drug tablets with suspected pharmacobezoar formation inside the stomach and failed gastric lavage, urgent upper endoscopy was arranged. The successful removal of the slow K tablets by endoscopic technique renders our patient’s subsequent clinical wellness with a short duration of hospital stay. Finally, therapeutic use of suxamethonium during RSI can cause an increase in potassium level of 0.5–1 mmol/L in healthy individuals ³³ and therefore should be avoided in case of potassium overdose with risk of hyperkalaemia.