Cleistanthus collinus (Oduvanthalai poisoning): A case report
Siranjeevi. P1, Rubeshwaran. B2
1,2Clinical Pharmacist-Internship, Kauvery Hospital, Trichy
Introduction
Cleistanthus collinus, also known as Oduvanthalai in Tamil, is the most commonly encountered plant poison in southern India. The leaves are used for poisoning humans (suicide or homicide) and animals (cattle and fish) and as an abortifacient, especially in rural south India.
All parts of the plant are potentially toxic. The method of ingestion of the plant for deliberate self-harm includes swallowing the crushed plant parts; chewing the leaves; consuming a paste/juice of the leaves or a decoction prepared by boiling the leaves in water.
It results in chest pain, breathlessness, central nervous system symptoms, and vision disturbances. There is no specific antidote for the C. collinus poisoning.
Clinical Manifestation
They include epigastric pain, breathlessness, fever, tachycardia, hypotension, giddiness, and visual disturbances like clouding/ blurring/colored vision. Cardiac abnormalities such as premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation may occur.
Mechanism of Toxicity
C. collinus causes the depletion of thiol-containing enzymes that are responsible for the manifestation of toxicity. It was suggested that thiol compounds might be the possible antidotes for C. collinus poisoning. The neuromuscular weakness caused by the poisoning resembles myasthenia gravis, which is owing to the postsynaptic acetylcholine receptor blockade. The mechanism proposed for the toxicity is deoxyribonucleic acid (DNA) synthesis inhibition, increased DNA damage apoptosis, and reduced thiol-containing enzymes.
Case Presentation
A 50-year-old male patient consumed 20 oduvanthalai seeds and crushed leaves at his residence with a suicidal intention. After receiving the initial treatment of gastric lavage at a local hospital, he was referred to our centre for further treatment.
At admission, he had vomiting, two-episodes, blurred vision, and giddiness. There was no history of loss of consciousness, ENT bleeding, seizure, altered sensorium and chest pain. He had a known history of Hypertension, Diabetes mellitus and CKD and was on medications: Metformin 500mg 1-0-1, Glimepiride 1mg 1-0-1 and Amlong 5mg 1-0-1.
On examination, the patient was conscious, well oriented and afebrile to time, place, and person. On the day of admission, pulse rate was 100/min, BP—160/90 mmHg in the supine position, and saturation level was 96% in room air. The abdomen was soft and bowel sounds were normal. Examination of the cardiovascular (s1 s2+) and Respiratory system was normal.
Laboratory Investigations
| CBC | 21/09 | 22/09 |
|---|---|---|
| HB | 12.0 g/dl | 11.0 g/dl |
| WBC | 17900 million cell/ml | 14200 |
| RBC | 4.22 10*3u/l | 3.78 |
| Platelets | 190000 million cell/ml | 190000 |
| PCV | 35.8 % | 32.2 |
| Neutrophils | 91.4 % | 92.4 |
| Lymphocytes | 3.3 % | 2.7 |
| Basophils | 0.0 % | 0.1 |
| Monocytes | 5.3 % | 4.4 |
| Esnophils | 0.0 % | 0.4 |
| MCV | 84.8 fl | 85.2 |
| MCH | 28.5 pg | 29.1 |
| MCHC | 33.6 mg/dl | 34.1 |
| HbA1C | 8.4% |
| Electrolytes | 21/09 | 22/09 | 23/09 |
|---|---|---|---|
| Sodium | 130 mEq/L | 136 | 133 |
| Potassium | 3.9 mEq/L | 3.9 | 3.3 |
| Chloride | 102 mEq/L | 110 | 186 |
| Bicarbonate | 23 mEq/L | 18 | 17 |
| ABG | 21/09/24 | 23/09/24 |
|---|---|---|
| PH blood | 7.31 | 7.31 |
| PCO2 | 34 mm hg | 36 mm hg |
| PO2 | 96 mm hg | 74 mm hg |
| NA+ | 139 mmol/L | 132 mmol/L |
| K+ | 3.4 mmol/L | 3.1 mmol/L |
| HCO3 | 18.4 mmol/L | 19.1 mmol/L |
| HCO3(C) | 17.1 mmol/L | 18.1 mmol/L |
| LFT | 21/09 | 22/09 |
|---|---|---|
| T. Bilirubin | 0.31 mg/dl | 0.26 |
| D. Bilirubin | 0.3 mg/dl | 0.12 |
| Indirect Bilirubin | 0.18 mg/dl | 0.14 |
| SGOT | 69.9 u/l | 60.5 |
| SGPT | 45.6 u/l | 73.2 |
| ALP | 162.8 | 258.5 |
| T. Protein | 6.94 mg/dl | 6.46 |
| Albumin | 4.07 g/dl | 3.61 |
| Globulin | 2.87 g/dl | 2.85 |
| RFT | 21/09 | 22/09 | 23/09 |
|---|---|---|---|
| S. Urea | 62.08 mg/dl | 79.18 | 94.16 |
| S. Uric acid | 2.93 mg/dl | 3.28 | 3.51 |
Management
Day 1 revealed Haemoglobin level to be 12.0 gm% with normal RBC indices. Total WBC count was 17,900 cells/mm3 with predominant neutrophils. The platelet count was 190,000 cells/mm3. Serum electrolytes and renal parameters revealed sodium-130 mEq/L; potassium-3.9 mEq/L; and chloride – 102 mEq/L; urea-62.8 mg/dl.
On ABG, pH (7.31) indicated hypoventilation accompanied by metabolic acidosis which was treated with sodium bicarbonate.
Abdominal ultrasonography showed B/L Mild renal parenchymal changes and mild prostatomegaly. The cardiologist opined normal LV function based on Echo. The nephrologist advised conservative management. He was treated with N- Acetyl cystine, inj. Pan, inj. Emeset which helped overcome vomiting, inj. potassium chloride, inj. Human actrapid.
On day, 3 evening patients became tachypnoeic, febrile, and desaturated started on Non-invasive ventilation (NIV) support. ABG showed type 1 respiratory failure. CT chest was taken and it showed multiple patchy perivascular ground glass opacities in bilateral lungs. Treated with inj. Meropenem, neb. Duolin and Budecort. NIV was continued.
By 6:20 pm patient went into bradycardia and cardiac arrest. Resuscitated and intubated, and started on ventricular support. The patient again went into cardiac arrest 3 times. CPR done as per ACLS protocol. ROSC (Return of spontaneous circulation) obtained. ABG showed severe metabolic and respiratory acidosis with hypoxia. Spo2 was 55–62% with Fio2- 100%. Again patient went into cardiac arrest at 8 pm CPR continued for 30 min, but ROSC was not achieved. Despite all effective measures no signs of life were seen, hence declared dead at 8.30 pm on 23.09.2024.
Discussion
The toxins in C. collinus leaf extracts have thus far been thought to be cleistanthin A and cleistanthin B which are aryl naphthalide lignans.
The following are the mechanism of actions of the active principle of oduvanthalai. Inhibition of ATPase enzyme in liver, kidney, heart, brain and skeletal muscles. Inhibition of LDH isoenzymes and cholinesterase. Cleistanthin A also induces DNA damage and apoptosis by inhibiting DNA synthesis. Cleistanthin A accumulates in the brain, liver and skeletal muscles while cleistanthin B accumulates in the cardiac muscle and skeletal muscles.
Consumption of decoctions of C. collinus leaves causes hypokalemia, renal failure, severe metabolic acidosis, ARDS and cardiac arrhythmias occur in severe poisonings and predict mortality (Anugrah Chrispal et al.), In this patient cause of death is due to Immediate severe ARDS, type 1 respiratory failure, severe Metabolic acidosis, Acute severe Hypoxia.
Metabolic Acidosis
Distal renal tubular acidosis with hyperchloremic normal anion gap metabolic acidosis, alkaline urine, and hypokalemia with kaliuresis appear to be a consistent feature in patients with C. collinus poisoning. Metabolic acidosis is another persistent feature reported by many authors. It was probably due to a type of toxin-induced RTA as supported by a recent study.
ARDS
In the study of Anugrah Chrispal et al.., said mechanisms other than oxidative stress may play a role in cardiac damage like a direct action of the toxin on enzymes/proteins that mainly affected the lungs.
Antidotes
There is no specific antidote for C. collinus poisoning. Supportive measurement N-acetylcysteine, L-cysteine, melatonin and thiol-containing compounds have all been suggested as possible antidotes for the management of C. collinus toxicity.
In the study of Anugrah Chrispal et al.., said N-acetylcysteine has been reported to be used, but the benefit of this intervention is unclear.
Conclusion
Cleistanthus collinus is a plant poison consumed with a suicidal intention. Based on laboratory investigation showed. These findings would explain the end organ effects of the toxins and cause of death in Oduvan poisoning. Human toxicity results in renal tubular dysfunction, commonly dRTA, with resultant hypokalemia and abnormal anion gap metabolic acidosis. Acute respiratory distress syndrome (ARDS) in this study. Based on the amount of consumption of the oduvanthalai seed determines the patient mortality and clinical outcomes.
Reference
- M. Senthilvelan, Dr. Resveen- Oduvan Thalai Poisoning -A Case Report Volume 3, Issue 3, March 2015.
- Raman P. Priyadharsini1, Subramani Parasuraman- A Review on the Poisonous Plant Cleistanthus Collinus 09 May 2024.
- Shreya Sharma, Ramachandran Rameshkumar- N-acetylcysteine in Cleistanthus collinus Poisoning: A Report of Two Cases in Children 29 May 2016.
- Anugrah Chrispal- Cleistanthus collinus poisoning Jun 2012.
- S Arthanareeswaran1, Shabana S2- A Case report: Oduvan leaf poisoning. Volume 3; Issue 4; October 2018.
- Nandakishore Bompelli,1 rakesh reddy C- Cleistanthus collinus poisoning: a case report of intentional poisoning 18 January 2019.
- Siddhartha Das,1 M.B.B.S., M.D.; Abdoul Hamide- Fatal Cleistanthus collinus Toxicity: A Case Report and Review of Literature. J Forensic Sci, 2014.
Mr. Siranjeevi. P
Clinical Pharmacist – Internship
Mr. Rubeshwaran. B
Clinical Pharmacist – Internship
