742 www.japi.org JAPI VOL.

54 SEPTEMBER 2006
Case Report
Cleistanthus Collinus Poisoning
SPE Benjamin, M Edwin Fernando, J Jerene Jayanth, B Preetha
Abstract
Cleistanthus collinus is an extremely toxic plant poison. Cleistanthin A and B, the toxins of Cleistanthus collinus,
are diphyllin glycosides which produce cardiac arrhythmias, urinary potassium wasting, hypoxia, metabolic
acidosis and hypotension. We report ARDS, distal renal tubular acidosis and distributive shock secondary to
inappropriate vasodilatation in a case following ingestion of its leaves.
L and CK-MB 123 U/L. Ultrasonogram of abdomen and
echocardiogram were normal. ECG showed prominent
U waves. ABG (breathing room air): pH 7.290, pCO
2
34.0
mmHg, pO
2
89.8 mmHg and HCO
3
17.9 mmol/L.
Later, as he became hypoxic despite oxygen
supplementation, ventilator support was given. Peak
airway pressure was 48 cmsH
2
O. PaO
2
/FiO
2
ratio: 142.
Central venous pressure (CVP) was low. A chest X-ray
showed bilateral peripheral alveolar infiltrates (Fig. 1).
ARDS was diagnosed and managed with PEEP and
prone ventilation.
There was increased urinary potassium loss (Table
1). This in combination with hyperchloremic metabolic
acidosis and normal serum anion gap suggested renal
tubular acidosis (RTA). Positive urinary anion gap
Departments of Medicine and Nephrology, CSI Kalyani
Multispeciality Hospital, Mylapore, Chennai.
Received : 31.3.2006; Revised : 10.8.2006; Accepted : 18.8.2006
INTRODUCTION
C
leistanthus collinus poisoning usually occurs
following intentional ingestion of the leaves with
mortality as high as 30%, usually occurs 3-7 days after
ingestion. Thomas K, et al,
1
identified hypokalemia due
to renal potassium wasting and cardiac dysrrhythmias.
Subrahmanyam DKS, et al,
2
identified other clinical
features of severe poisoning (Table 2). S Easwarappa, et
al,
3
have described neuromuscular weakness.
CASE REPORT
A 24 years male was referred from a rural hospital 2
days after ingestion of 40-50 leaves of oduvan with
history of abdominal pain, vomiting and breathlessness.
Gastric lavage had been done. Samples of the plant were
brought with him. It was identified as Cleistanthus collinus
at the Presidency College and Forensic Sciences
Department, Chennai.
On examination, he was conscious, oriented, afebrile
and dyspnoeic. Blood pressure was 110/70 mmHg,
pulse rate 128/min and respiratory rate 33/min. He had
epigastric tenderness. Fine crepitations were heard
bilaterally. Examination of the cardiovascular and
nervous system was unremarkable.
Total WBC count was 9800 cells/cumm with
predominant neutrophils. Serum potassium was 2.5
mEq/L, sodium 144 mEq/L, chloride 112 mEq/L,
bicarbonate 17 mEq/L, total calcium 6.7 mg/dL, urea 37
mg/dL, creatinine 1.4 mg/dL, total bilirubin 0.8 mg/
dL, direct bilirubin 0.4 mg/dL, SGOT 112 U/L, SGPT 90
U/L, SAP 1341 U/L, creatinine kinase (CK) total 883 U/
Fig. 1 : Chest X-ray of the patient showing ARDS. A right internal
jugular catheter and endotracheal tube are seen in position.
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despite low serum bicarbonate confirmed RTA. Acidosis
was corrected using IV sodium bicarbonate followed by
Shohls solution and potassium citrate by Ryles tube.
Normal bicarbonate excretion following this and urinary
pH of 6.5 established distal (Type 1) renal tubular
acidosis (dRTA). Hypokalemia was corrected using IV
KCl and potassium citrate enterally (Table 1) following
which ECG normalised.
About 48 hrs after hospitalisation, he became
hypotensive with tachycardia, low CVP, oliguria and
increased urinary osmolality suggestive of toxin induced
vasodilatation. Blood pressure and urinary output were
corrected promptly when adequate fluids were given.
We used N-acetyl cysteine 150 mg/Kg over 1 hr
followed by 50 mg/Kg over 4 hrs and 100mg/Kg over
the next 16 hrs as glutathione depletion
4
and benefit
from SH containing compounds
5
has been reported in
animal studies. Cardiac and liver enzymes normalised
in a week. Distal RTA improved over 2 weeks. He was
off the ventilator on the 10th day and lung shadows
Table 1 : Estimated urinary potassium loss and serum potassium
Day 1 Day 1 Day 2 Day 2 Day 3 Day 5 Day 8
(Noon) (9 p. m.) (7 a. m.) (6 p. m.)
Urinary K
+
Loss (mEq/day) 210 170 335 611 120
Serum K
+
(mEq/L) 2. 6 2. 4 2. 5 3. 6 3. 6 4. 4 3. 9
Table 2 : Summary of previous observations and our investigations that lead to the diagnosis in this case and formulation
of the pathogenesis
Clinical and laboratory Published in the study by Further investigations done in Indicated a diagnosis of
features pertaining to Subrahmanyam DK, et al, as this patient
statistically significant risk
factors for death in Cleistanthus
collinus poisoning
Electrolyte and acid-base 1. ST depression, 1. Urinary potassium excretion, Distal renal tubular
disturbances 2. Potassium <3.1 mEq/L, 2. Normal Sr. Anion gap, acidosis.
3. Mean pH 7.28, 3. Urine anion gap,
4. Mean HCO
3
-
13.64, 4. Urine pH 6.5,
5. pH <7.3. 5. Normal urine HCO
3
-
excretion (after correction
of acidosis).
Shock 1. Clouding/blurring of vision, 1. Low central venous Distributive shock due to
2. Giddiness, pressure (CVP), inappropriate vasodilatation.
3. Pulse >120/min, 2. Normal LV function in
4. Hypotension. Echocardiography,
3. Oliguria and response to fluids.
Respiratory failure 1. Dyspnoea after 24 Hrs, 1. Infiltrates in chest X-ray, Non-cardiogenic pulmonary
2. Respiratory rate >30/min. 2. Low central venous pressure, oedema (ARDS).
3. Normal LV function in
Echocardiography,
4. PaO
2
/FiO
2
Ratio: 142.
disappeared after 3 weeks.
DISCUSSION
Hypokalemic metabolic acidosis, hypotension and
hypoxia have been described in this poisoning. We
evaluated further and identified dRTA, distributive
shock and ARDS respectively in this patient (Table 2).
Specific interventions against these entities were
initiated.
Hypokalemia was corrected by estimating urinary
losses and compensating for it. ARDS, dRTA and
distributive shock were also meticulously corrected.
Arrhythmias were either offset by these measures or
probably occur at higher blood levels of the toxin with a
permissive role for hypokalemia similar to digitoxicity.
Though we cannot categorically attribute this patients
survival to any of these measures or to N-acetyl cysteine,
these deserve evaluation in further trials.
Though the pathogenesis of Cleistanthus collinus
poisoning is well established, progress in our
744 www.japi.org JAPI VOL. 54 SEPTEMBER 2006
understanding of the pathophysiology could have
therapeutic and prognostic implications.
Acknowledgement
Our sincere thanks to Dr. S. Amerjothy. Ph. D., Reader
in Botany, Presidency College, Chennai, for her help in
identifying the plant.
REFERENCES
1. Thomas K, Dayal AK, Narasimhan, Alka G, Seshadri MS,
Cherian AM, Kanakasabapathi, Molly B. Metabolic and
Cardiac effects of Cleistanthus Collinus poisoning. J Assoc
Physicians India 1991;39:3124.
2. Subrahmanyam DK, Mooney T, Raveendran R, Zachariah B.
A clinical and laboratory profile of Cleistanthus collinus
poisoning. J Assoc Physicians India 2003;51:1052-4.
3. Eswarappa S, Chakraborty AR, Palatty BU, Vasnik M.
Cleistanthus Collinus Poisoning: Case Reports and Review of
the Literature. Clinical Toxicology 2000;41:369-72.
4. Sarathchandra G, Balakrishnamoorthy P. Acute toxicity of
Cleistanthus collinus, an indigenous poisonous plant in Cavia
procellus. Journal of Environmental Biology 1998:145-8.
5. Annapoorani KS, Damodaran C, Chandrasekharan P. A
promising antidote to Cleistanthus collinus poisoning. J Sci Soc
Ind 1986;2:3-6.
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