Rodenticide poisoning in a family of three in Singapore

Dear Sir, We report an unusual case of rodenticide poisoning in a young woman and the subsequent discovery of rodenticide poisoning in her brother and paternal aunt, and discuss the challenges encountered during diagnosis and treatment. Written informed consents for the underaged patients were obtained from their mother. Case 1 is a healthy 19-year-old woman with a 4-day history of worsening generalised abdominal pain and 1-day history of bloody urine. Vital signs showed a heart rate of 135 beats per minute and blood pressure of 81/56 mmHg. The patient was alert with conjunctival pallor and a distended abdomen that was tender with guarding. Blood investigations revealed anaemia with normal platelet count and extensive coagulopathy [Table 1], but the levels were normalised with addition of control plasma, suggesting underlying coagulation factor deficiencies. Subsequent factor assays revealed a warfarin-like deficiency picture with markedly reduced serum levels of factors II (prothombin), VII, IX and X. Serum liver function panel was normal. Concurrently, contrast-enhanced computed tomography showed extensive haemoperitoneum with a left ovarian ruptured corpus luteal cyst identified as the bleeding source [Figure 1].Table 1: Results of blood investigations on arrival at the hospital for Cases 1 and 2.Figure 1: Axial contrast-enhanced CT images of the abdomen and pelvis show (a) massive haemoperitoneum extending into the pouch of Douglas, (b) with the left adnexa showing a 3.8 cm × 3.4 cm × 4.0 cm heterogeneous mass (arrow) representing a ruptured corpus luteal cyst.The patient lived with her 9-year-old brother and 50-year-old paternal aunt. Her aunt had recently been admitted to another hospital with a similar clinical picture of abdominal pain and haemorrhagic shock with extensive warfarin-like coagulopathy. The patient reported that the family of three had eaten at a restaurant 4 days prior to her presentation, and denied personal and family history of coagulation disorders. On admission to the intensive care unit, the patient received six units of packed red cells, five units of fresh frozen plasma (FFP), one unit of pooled platelets, 10 units of cryoprecipitate and 2.5 L of balanced crystalloids. Intravenous tranexamic acid 1 g slow bolus with subsequent dosing every 8 h and intravenous vitamin K 10 mg slow bolus and subsequent dosing every 8 h were initiated. The patient then underwent an emergency laparoscopic cystectomy, and her coagulopathy resolved postoperation with continued daily intravenous vitamin K supplementation. She was subsequently transitioned to oral vitamin K and discharged well after 13 days. Serum toxicology panel later revealed that the patient and her aunt were positive for bromadiolone poisoning. Case 2 is the brother of the patient, a healthy 9-year-old boy weighing 24 kg, who was admitted for a 4-day history of frequent epistaxis. Vital signs on arrival showed a heart rate of 99 beats per minute and blood pressure of 95/58 mmHg. The patient was lethargic but alert, with distinct pallor and dry mucous membranes. A bedside nasoendoscopy showed blood clots over the right Little’s area region with no active bleeding. Blood investigations demonstrated a similar clinical picture as that of Case 1 [Table 1] and were also positive for bromadiolone poisoning. The patient received 10 mL/kg of crystalloid bolus, 20 mL/kg of FFP transfusions, 500 mg of oral tranexamic acid taken thrice daily and 7.2 mg of intravenous vitamin K daily. The patient’s coagulopathy subsequently normalised and he was discharged after 8 days on oral vitamin K supplementation. While there are reported cases of rodenticide poisoning globally,[1] there has not been any local case report published at the time of writing. Bromadiolone belongs to the second-generation long-acting dicoumarin class, also known as superwarfarins. Instead of the terminal methyl group in warfarin, these superwarfarins contain phenyl groups that render them fat soluble and long-acting, giving them a 100-fold increase in potency compared to warfarin.[2] The effects of rodenticide poisoning may not be immediate and can be delayed for up to 24–48 h.[3] The mainstay of treatment is phytomenadione (vitamin K) to counteract the antagonistic effects of superwarfarins on vitamin K epoxide reductase enzyme complex, of which both intravenous and oral routes have similar efficacies at 24 h.[4] The intravenous route is used to reverse coagulopathy in active bleeding, but this should be balanced against the potential dangers of an anaphylactoid reaction to intravenous formulation.[5] In addition, when considering starting vitamin K treatment, it is important to weigh the potential benefits against the risks of thrombosis, especially in high-risk situations, such as in patients with mechanical heart valves or existing pulmonary emboli. In the event of catastrophic or life-threatening bleeding and when urgent correction of coagulopathy is required, FFP or prothrombin complex concentrate can be considered.[5] Once the coagulation function is stabilised, continuing oral vitamin K daily with weekly coagulation panel checks is recommended.[6] For both our cases, initial septic workup was negative and inflammatory markers were not raised. Normal platelet and leucocyte levels excluded causes of coagulopathy due to thrombocytopenia, such as viral infections (commonly dengue), bone marrow disorders, autoimmune disorders and consumptive causes (disseminated intravascular coagulopathy, sepsis). In the absence of a clear history of exposure to bromadiolone, suspicion was raised only after laboratory tests showed a markedly abnormal coagulation panel accompanied with a normal liver function panel that was disproportionate to the amount of bleeding. Differentials for an out-of-proportion deranged coagulation profile that were considered included vitamin K or factor deficiencies, or inhibitors, including warfarin poisoning. The main differentiating factor between warfarin and superwarfarin poisoning is the rapid correction of coagulopathy due to the short half-life of warfarin. A diagnosis of rodenticide poisoning is paramount, as prolonged, high doses of vitamin K therapy would be required with prolonged admission and outpatient monitoring due to the longer half-life of superwarfarins, where coagulopathy can resurface after initial correction following vitamin K therapy. In conclusion, we present this case report to increase awareness of rodenticide poisoning in the local community. All three patients had similar clinical presentations of acute onset warfarin-like coagulopathy with no history of coagulation disorders and normal liver functions and platelet counts. It is important to maintain clinical perceptiveness to recognise possible rodenticide poisoning and initiate treatment early, without waiting for confirmatory diagnosis from toxicology that may be delayed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.