|Year : 2022 | Volume
| Issue : 3 | Page : 184-186
Activated charcoal hemadsorption in Cerbera odollam poisoning
Dyna Jones, Meenakshi Kalyan, Chaitra Kolli, Hemant Kumar
Department of Medicine, Vydehi Institute of Medical Science and Research Centre, Bengaluru, Karnataka, India
|Date of Submission||06-Jan-2022|
|Date of Decision||27-Feb-2022|
|Date of Acceptance||04-May-2022|
|Date of Web Publication||30-May-2022|
Department of Medicine, Vydehi Institute of Medical Science and Research Centre, Whitefield, Bengaluru - 560 066, Karnataka
Source of Support: None, Conflict of Interest: None
Cerbera odollam belongs to the poisonous Apocynaceae family, which grows in coastal salt swamps, creeks and along river banks found in South India. The poisonous part of the plant is the kernel containing the toxin cerberin which is a cardiac glycoside that produces symptoms and signs similar to acute digoxin poisoning. The treatment is mainly symptomatic as well as administration of digoxin immune fab antibodies. Digoxin immune fab antibodies bind with cardiac glycosides to reduce their active concentration. However, there could be various barriers in developing countries in regard to the administration of DigiFab antibodies such as availability and affordability. Activated charcoal, a cheaper alternative, reduces gastrointestinal absorption and enterohepatic recirculation. Although its role in C. odollam poisoning remains unclear, there have been various trials where multidose activated charcoal has been beneficial in glycoside poisoning. We present a case report of a young female with an alleged history of consumption of an unknown plant compound, identified as C. odollam presenting with acute-onset vomiting, altered mental status and laboratory parameters showed hyperkalemia and thrombocytopenia. Electrocardiogram (ECG) showed sinus bradycardia followed by inverted tick mark sign. Serum digoxin levels were raised (4.2 ng/ml). The patient was stabilized with supportive measures and hemadsorption with 300 g of cellulose-coated activated charcoal, which led to the reversal of the ECG and laboratory parameters to normal, leading to the complete recovery of the patient.
Keywords: Activated charcoal, cardiac glycoside, hemadsorption
|How to cite this article:|
Jones D, Kalyan M, Kolli C, Kumar H. Activated charcoal hemadsorption in Cerbera odollam poisoning. Apollo Med 2022;19:184-6
| Introduction|| |
Cerbera odollam belongs to the poisonous Apocynaceae family, found in southern India, particularly Kerala; southern and central Vietnam; Cambodia; Sri Lanka; and Myanmar. The poisonous part of the plant is the kernel, containing the bioactive toxin cerberin which is a cardiac glycoside of the cardenolide class producing symptoms and signs similar to acute digoxin poisoning. Although the role of activated charcoal in this poisoning is unclear, there have been various trials where multidose activated charcoal (MDAC) has been beneficial in glycoside poisoning. We present a survivor of C. odollam poisoning with hemadsorption with activated charcoal.
| Case Report|| |
A 35-year-old female presented to our hospital 12 h after an alleged history of consumption of an unknown plant compound boiled in water, following which she had recurrent vomiting and fatigue and subsequently developed reduced responsiveness. The plant was identified as C. odollam as per the picture shown by the relatives. On presentation, her vitals showed a heart rate of 64 beats/min, blood pressure: 90/50 mmHg, temp: 99.4 F, and respiratory rate of 16 cycles/min. Nervous system examination revealed bilateral pupils 3 mm reactive to light, Glasgow Coma Scale (GCS) of E1 V1M1 and bilateral plantars were flexors. There were no signs of meningeal irritation. Respiratory and cardiovascular system examinations were normal. In view of low GCS, the patient was intubated and put on mechanical ventilation on synchronized intermittent mandatory ventilation/volume control mode. The patient was further stabilized with intravenous fluids and inotropes. Activated charcoal was administered through nasogastric tube. On arrival in the hospital, electrocardiogram (ECG) showed sinus bradycardia and T-wave inversion in V5 and V6 [Figure 1]. Seven hours later, the patient's ECG showed a reverse tick mark sign in V4-V6 and an early reverse tick mark sign in leads I, II, and arteriovenous fistula [Figure 2]. Hemadsorption with 300 g of cellulose-coated activated charcoal was done for 4 h, following which there was a reversal of the ECG changes [Figure 3] and the serum potassium levels normalized to 3.35 mEq/L. Laboratory investigations showed serum digoxin: 4.20 ng/ml (normal: 0.8–2 ng/ml) done by the chemiluminescence immunoassay method, serum sodium: 132 mEq/L, serum potassium: 5.43 mEq/L (normal: 3.5–5.1 mEq/L), serum chloride: 106.5 mEq/L, serum calcium: 8.5 mg/dl, bicarbonate: 15.3 mmol/L, urea: 20.33 mg/dl, serum creatinine: 1.45 mg/dl, total bilirubin: 0.42 mg/dl, direct bilirubin: 0.10 mg/dl, aspartate transaminase: 31 U/L, alanine transaminase: 21 U/L, albumin: 4.03 g/dl, prothrombin time: 14.2 s, international normalized ratio: 1.24, and troponin I: 0.125 ng/ml. On day 1, Hb was 10.7 g/dl, white blood cell: 4600 cells/mm3, platelet count: 434,000 cells/mm3, mean corpuscular volume: 81.7 fL, mean corpuscular hemoglobin: 25.2 pg, hematocrit: 34.7%, and urine for toxicology: negative. Two-dimensional echo showed normal left ventricular and right ventricular function, no regional wall motion abnormality, and ejection fraction of 60%. There was a persistent drop in the platelet count during the hospital stay noted as follows: on day 2, platelet count: 1 lakh cells/mm3; on day 3, platelets: 69,000 cells/mm3; on day 4, platelets: 50,000 cells/mm3; and on day 5, platelets: 20,000 cells/mm3, following which six random donor platelets were transfused. Following the platelet transfusion, there was a steady increase in platelets that subsequently were normal. The patient was weaned off mechanical ventilation after 48 h. The patient's vitals improved in 48 h, and laboratory reports normalized during the remaining stay in the hospital. The patient was discharged after 9 days of hospital stay.
|Figure 1: Electrocardiogram showing sinus bradycardia and T-wave inversion in V5 and V6|
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|Figure 2: Electrocardiogram showing reverse tick mark sign in V4–V6 and early reverse tick mark sign in leads I, II, and aVF|
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| Discussion|| |
C. odollam is a cardiac glycoside with cardiotoxic effects, and the toxins are concentrated in the seeds and oil of the plant. The glycosides responsible for the toxicity include cerberin, cerebroside, and odollin. Cerberin binds to and reversibly inhibits the sodium–potassium adenosine triphosphatase (Na-K-ATPase) exchanger in cardiac cells, which results in extracellular accumulation of potassium and intracellular accumulation of sodium leading to a decrease in the heart rate and increased inotropy. The resultant hyperkalemia itself can cause arrhythmias. There have been reports of C. odollum toxicity which included symptoms of headache, muscle weakness, dizziness, altered status, nausea, vomiting, abdominal pain, chest pain, palpitations, bradycardia, hyperkalemia and thrombocytopenia. A wide range of ECG abnormalities have been reported, namely sinus bradycardia, sinus pauses, junctional rhythm, prominent U-waves, wandering pacemaker, atrial fibrillation, ventricular tachycardia, digoxin-like ST changes, nodal rhythm, and first-, second-, and third-degree heart block. Our patient presented with vomiting, altered mental status, bradycardia, hyperkalemia, thrombocytopenia, and digoxin toxicity-like ST changes. In a study done by Menon et al., the most common clinical features noted were vomiting (54%), thrombocytopenia (50%), and sinus bradycardia (32%). The need for cardiac pacing had a significant association with dosage in kernels ingested and with thrombocytopenia. Thrombocytopenia was attributed to bone marrow suppression due to the anticancer properties of the plant. The underlying psychiatric disorders of depression or anxiety could be the cause for suicidal attempts. The possibility of dysfunction of hypothalamic–pituitary–adrenal axis (HPA), autonomic nervous system activity, and inflammation could be the predisposing factor for poor GCS in this patient. In a study conducted by Selladurai et al., neurological manifestations such as drowsiness (8%) and restlessness (16.6%) were noted. Management includes supportive treatment of bradycardia with atropine or temporary pacemaker insertion, treatment of hyperkalemia as well as administration of digoxin immune fab. Digoxin immune fab antibodies bind with cardiac glycosides to reduce their active concentration. There are mixed results with digoxin immune fab antibodies, perhaps due to a lower affinity of the digoxin-specific antibody fragments for C. odollam toxins. The recent advances in the treatment of severe cardiotoxicity are the use of lipid emulsion and extracorporeal membrane oxygenation. There could be various barriers in developing countries in regard to the administration of DigiFab antibodies. Activated charcoal reduces gastrointestinal absorption and enterohepatic recirculation. Although its role remains unclear, there have been various trials where MDAC has been beneficial in glycoside poisoning. Studies have shown a reduction in the postingestion plasma glycoside concentrations following activated charcoal administration. However, survival benefit has not yet been demonstrated. There are only very few studies reported. Our patient responded to one cycle of hemadsorption with cellulose-coated activated charcoal. There could be a possible role of activated charcoal in the management of C. odollam poisoning. However, further studies are needed for the same.
| Conclusion|| |
This case report raises awareness among the clinicians about the clinical manifestations and management options of C. odollam toxicity. It also provides a treatment alternative of dialysis using activated charcoal in developing countries where there could be treatment barriers in the usage of DigiFab antibodies.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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