Clinico-pathological study of Thevetia peruviana (yellow oleander) poisoning

Transcription

1 Journal of Wilderness Medicine 3, (1992) ORIGINAL ARTICLE Clinico-pathological study of Thevetia peruviana (yellow oleander) poisoning K.K. SAMAL, MB, BS', H.K. SAHD, MB, BS 1 and P. GOPALAKRISHNAKONE, MB, BS, PhD 2 * J VSS Medical College, Bur/a, Orissa, India 2 Department ofanatomy, Faculty ofmedicine, National University ofsingapore, Singapore 051 I Clinico-pathological features ofyellow oleander(thevetia peruviana) poisoning in India are described. Clinical features included vomiting, diarrhea, drowsiness and dilated pupil. Pulse was rapid, weak and irregular. Varying degrees of heart block were also present. Jaundice and renal failure have been observed in the present study. Post mortem showed renal tubular necrosis with obliteration of the liver lumen showed focal necrosis around central vein, patchy hemorrhages and dilation of central veins. Key words: yellow oleander, Thevetia peruviana, poisoning, clinical pathogenesis Introduction Yellow oleander, Thevetia peruviana, is a small tree found in India and Sri Lanka and grown in gardens for its beautiful yellow flowers. The active ingredients of the milky juice of yellow oleander plant are thevetin and cerebrin, while those of the kernels of the seeds are thevetin and thevotoxin [1-4]. Thevetin and thevotoxin have digitalis-like action and cerebrin has strychnine-like action. Previously described clinical features in this poisoning have been vomiting, diarrhoea, drowsiness and dilated pupils. The pulse, which is slow initially, later becomes rapid, weak and irregular with varying degrees of heart block. Tetanic convulsions sometimes occur. Death usually occurs from heart failure [1-4]. Postmortem findings include congestion of internal organs, signs of gastrointestinal irritation, engorgement of the veins, and in some cases subendocardial hemorrhage [1 4]. The present study describes additional clinical features and postmortem findings of this poisoning, which have been described briefly in seven earlier cases [5]. The management and clinical course of these cases is also described. Materials and methods Two groups were studied. In Group A, patients were admitted to the hospital with signs and symptoms of poisoning and recovered with treatment. Group B included all the fatal cases. In Group A, ten patients who developed jaundice and renal failure after yellow oleander poisoning were studied. All these patients recovered with treatment. A detailed history, which included the amount of fruits or seeds ingested, the time taken, the symptoms and treatment history (if any) was taken, and a thorough physical examination *To whom correspondence should be addressed Chapman & Hall

2 Clinico-pathological study of Thevetia peruviana (yellow orleander) poisoning 383 Table 1. Case histories Case Age in Sex Number of Symptoms years fruits/seeds ingested 1 24 M 3 fruits Nausea, vomiting, scant urination (red-colored), drowsiness, weakness 2 20 M 2 fruits Abdominal pain, vomiting, fever, weakness, scant urination, confused 3 19 M 3 seeds Abdominal pain, diarrhea, vomiting, weakness 4 40 F 2 fruits Vomiting, diarrhea, weakness 5 30 F 2 seeds Vomiting, diarrhea, weakness 6 19 F 2 fruits Abdominal pain, vomiting, weakness, diarrhea 7 25 F 2 seeds Vomiting, weakness, lethargy 8 22 F 2 seeds Vomiting, drowsy, weakness 9 31 M 4 seeds Vomiting, abdominal pain, weakness F 2 fruits Vomiting, diarrhea, weakness, lethargy carried out, in each case. Urinalysis, total hemogram, and electrocardiogram (ECG) were done in all cases. Benzidine test for demonstration of hemoglobinuria, estimation of serum bilirubin, blood urea, and serum creatinine were performed daily until the values returned to normal. Twenty-four hour urine output was also measured. Urobilinogen, bile salts, and bile pigments were tested (Group A). Post-mortem findings of the fatal cases were described. Results GROUP A The age, sex, amount of fruits or seeds taken, and symptoms are shown in Table 1. All took the poison for suicidal purposes. They were admitted after 48, 6, 72, 12, 8, 10, 5, 14, 7, and 11 h of taking the poison, respectively. Cases 1 and 3 were treated initially at peripheral hospitals, while others were admitted to our hospital directly. The symptoms developed very shortly after taking the poison. The pulse rate, heart rate, and blood pressure (BP) of each case are shown in Table 2. Cases 1, 2, and 8 were drowsy at admission and plantar reflexes were extensor bilaterally. Pupils were constricted bilaterally in cases 2 and 8. All had developed yellow-colored conjunctivae, passed deepcolored urine, and developed fever after 18 and 36 h of ingestion of the poison. The temperature of each case is shown in Table 2. Case 1 had anuria; the others showed 24 hour urine volume of less than 400 ml. Table 3 shows the laboratory parameters which were performed on the day when jaundice developed. Serum bilirubin was mostly of the unconjugated type. Urobilinogen was found in excess in all. Bile salts and bile pigments were absent in all measurements except case 7. Similarly, asparate aminotransferase

3 384 Samal, Sahu and Gopalakrishnakone Table 2. Physical findings (on admission) Case Pulse Heart rate BPinmmHg Temperature 1 84 min- I regular 84 min- I 110/86 lol"p (38.3 C) 2 63 min- I regular 63 min- I 106/ P (38.TC) 3 92 min- I regular 92 min- I 120/ P (39.1 C) 4 50 min- I irregular 58 min- I lol"p (38.3 C) min- I regular 118 min- I P (37.4 C) 6 44 min- I regular 44 min P (38.3 C) 7 48 min- 1 regular 48 min- I 108/50 99 P (37.2 C) min- 1 irregular 108 min / P (37.4T) 9 78 min- 1 regular 78 min / P (37.7 C) min- 1 regular 68 min P (38.8 C) (AST) and alanine aminotransferase (ALT) were within normal range except in case 7, where their values were elevated. Benzidine test for demonstration of hemoglobinuria was positive in all. ECG showed digitalis-like effects in all cases, except for cases 5, 6, 9 and 10. Sinus bradycardia was seen in cases 4, 6, and 7. Multiple artial ectopic beats were observed in Case B and occasional atrial ectopic beats in Case 4. Management Stomach wash was done with tap water in all patients. Atropine was given parenterally with a view to keep the pulse rate above 80 beats per minute in cases 2, 4, 6, 7, 8, and 10. The duration of atropinization was less than four days in cases 2 and 7, but in others it ranged from 10 to 18 days. Glucose solution was given parenterally to all patients. Antacids and antiemetics were given to Case 8. Case 1 was put on hemodialysis. Course Yellow-colored conjunctive persisted for two to three days. Serum bilirubin came down to normal after the second day of development of jaundice. Temperature was normalized in all patients after h. Urine output became normal and blood urea and serum creatinine approached normal levels after h in all cases except Case 1. Hemo- Table 3. Laboratory parameters Case Hb Bilirubin BUN Creatinine Proteinuria Urine microscopic gmdi 1 mgdi 1 mgdi 1 mgdi l findings RBC 12-14/hpfWBC 2-3/hpf RBC 2-3/hpf WBC 2-3/hpf RBC 2-3/hpfWBC 8-1O/hpf RBC 2-3/hpf WBC 2-3/hpf RBC 1-2/hpf WEe 3-4/hpf RBC 2-3/hpf WBC 2-3/hpf RBC 1-2/hpfWBC 2-3/hpf RBC 2-3/hpf WBC 3-4/hpf RBC 8-1O/hpf WBC 5-6/hpf RBC 8-1O/hpfWBC 4-5/hpf

4 Clinico-pathological study of Thevetia peruviana (yellow orleander) poisoning 385 dialysis was carried out three times in Case 1. This patient was discharged on request after one month because adequate urine output and normal BUN were achieved. Vomiting persisted for five days in Case 8, who also had diarrhoea on the third day of poisoning. POSTMORTEM FINDINGS (GROUP B) Postmortem was performed in six cases (four females and two males). Their ages were 16, 25, 28, 19, 34, and 22 years. Three cases came directly from rural areas; the clinical features and case data were not available. Three cases died in V.S.S. hospital. The number of seeds taken by these fatalities were 12, 10, and 9. All were admitted within 12 h of taking the poison. The pulse rates were 30, 40, and 36 beats per minute at admission. Blood pressure was 60, 50 and 54 mmhg on palpatory method. They died after 15 min, 20 min and 30 min of admission. All had severe pain in the abdomen, vomiting, and anuria. They were treated with dopamine, atropine, and glucose solution. No jaundice was seen. On postmortem examination, there was renal tubular necrosis with obliteration of the lumen in all six cases and vaculated areas in the glomerular spaces in two cases. Two livers showed focal necrosis around the central veins, patchy hemorrh~gic areas, and dilatation of the central veins. Hearts showed subendocardial hemorrhage in three cases. Gastrointestinal systems showed congestion, signs of irritation, and generalized venous engorgement in all cases. Discussion Jaundice and fever developed on the second day of ingestion of the yellow oleander. We have not observed these features in persons who died before this period. Usually, there is dilatation of the pupils in this poisoning. However, we found constricted pupils in two cases. Extensor plantar response has not been described in this poisoning previously. These neurologic findings might be due to direct action ofthe poison on the brain or due to hemorrhage into the brain tissues. Postmortem showed subendocardial hemorrhage and patchy hemorrhagic areas in the liver. However, the brain showed focal necrosis and loss of neurons in only two cases, without any hemorrhage. In one patient, there was liver cell damage as evidenced by presence of bile salts and bile pigments, with elevation of AST and ALT. Postmortem also showed liver cell necrosis in two cases. Hence, some components of yellow oleander might be directly affecting the liver. Parenthetically, our investigations did not reveal any co-ingestants. The jaundice was of the hemolytic type, as there was excess urobilinogen in the urine with absence of bile salts and bile pigments, unconjugated hyperbilirubinemia, and a drop in hemoglobin levels. Dark-colored urine indicated hemoglobinuria. Positive benzidine test confirmed intravascular hemolysis. Fever may in fact be due to hemolysis. The renal failure may be due to direct action of the poison on the renal tubules, as postmortem showed renal tubular necrosis. There was also hematuria and proteinuria indicating an affect upon the glomeruli. Postmortem showed signs of congestion and diffuse dilatation of veins. These might be factors for subendocardial hemorrhage, patchy hemorrhage in the liver, and also hematuria. These clinical features were observed equally in persons who took the seeds or fruits. The clinical features which were not fatal were reversible. All persons did not show

5 386 Samal, Sahu and Gopalakrishnakone digitalis-like effects. The number of persons who declared vomiting as a predominant symptom ranged regurgitated from three to four times, except Case 7. Diarrhoea occurred occasionally. All the patients in Group A did not develop hypotension. However, Group B patients showed gross hypotension. Symptoms like abdominal pain, vomiting, diarrhoea, and weakness seen in Group A patients are consistent with earlier observations [1-4]. The postmortem findings of gastrointestinal and heart damage are consistent with previous reports [1-4, 6]. However, in the present series, we observed liver cell necrosis, focal necrosis of the brain, and renal tubular necrosis, which have not been reported previously. The mechanisms which caused these changes are not clearly understood, but it could be concluded that some active ingredient from the plant Thevetia peruviana is the causative agent for these toxic effects. References 1. Yellow oleander. In: Reddy, K.S.N., ed. The Essentials of Forensic Medicine and Toxicology. 8th ed. Hyderabad: SV printing works, 1984; Yellow oleander. In: Modi, N.J. ed. Modi's Textbook of Medical Jurisprudence and Toxicology. 20th ed. Bombay: Indian Printing works, 1977: Yellow oleander. In: Parikh, C.K., ed. A Simplified Textbook of Medical Jurisprudence and Toxicology. 1st ed. Colaba Causeway: Bombay Medical publications, 1970: Yellow oleander. In: Sengupta, B.K., ed. Medical Jurisprudence and Toxicology, 1st ed. India: Academic publishers, 1978: Samal, K.K., Sahu, H.K., Kar, M.K., Palit, S.K., Kar, B.C. and Sahu, C.S. Yellow oleander (Cerbera thevetia) poisoning with jaundice and renal failure. J Assoc Physician India 1989; 37, Saravanapavananthan, N. and Ganeshamoorthy, J. Yellow oleander poisoning - a study of 170 cases. Forensic Sci Internat, 1985; 26,