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Oil of chenopodium poisoning
0 I L OF CHENOPODIU]V[ POISONING CtfARI,ES H. BRANT, M'.D.,* SYBm 1). I[AIRE, M.D., AZ~DALFRED R. CHARLOTTE, N. C. EP OR TS of death due to oil of
chenopodium are infrequent in R American literature. The majority of deaths recorded are due to an overdose of the drug, or of the therapeutic dose being repeated at short intervals. We recently had the opportunity to observe a case of oil of chenopodium poisoning at this hospital. CASE REPORT
A 3-year-old white girl was admitted to Charlotte Memorial Hospital on Jan. 22, 1951, with the chief complaint of a fainting spell which occurred approximately two hours p r i o r to admission. H er family history was noncontributory. She had been treated on two previous occasions with gentian violet for pinworms. The patient received the oil of chenopodium from her doctor because of pinworms. She was given onefourth teaspoonful of oil of chenopodium daily for the four days prior to her admission. She received no laxative or other medication. After lunch of the fourth day of treatment she vomited and then fainted. She was immediately b r o u g h t to the emergency room of this hospital. Physical examination revealed a poorly nourished white girl, who could be aroused only with difficulty. Her weight was 29 pounds, temperature 98.6 ~ F., pulse 90, and respirations 22. Her skin showed some evidence of dehydration. The remainder of the physical examination was noncontributory. The laboratory examination on admission showed a red blood cell count of 4.1 million, hemoglobin 10 Gin., white blood cell count of 18,450 with 78 per cent polymorphonuclear leuco*Present address: Richmo nd 27, Va.
4810
Old
Brook
Rd.,
STUMPE,'
]~i.]).
cytes, 20 per cent lymphocytes, and 2 per cent eosinophiles. A voided urine specimen was within normal limits. On admission to the ward she was given 15 c.c. of milk of magnesia and 5 c.c. of aromatic cascara orally, 0.25 Gm. of caffeine and sodium benzoate intramuscularly, and offered liquids. Because of refusal to take liquids she was given 250 c.c. of 5 per cent glucose in distilled water by subcutaneous infusion over a two-hour period. One hour after the infusion was started the patient became more alert and asked for her mother. She slept throughout the night. On the second hospital day she took liquids with encouragement. She received 250 c.c. of t t a r t m a n n ' s solution by subcutaneous infusion over a onehour period. Because of her refusal to take liquids or solids a gastric gavage was done. The patient was given eggnog but vomited the entire amount after one and one-half hours' retention. That evening twitching movements of her left arm and leg were noted. She was given 30 rag. sodium phenobarbital intramuscularly for the twitchings. The twitchings stopped but her respirations slowed to about eight per minute. The patient then received 0.25 Gm. caffeine sodium benzoate intramuscularly and her respirations returned to within the normal range. She received another 250 c.c. of Hartmann's solution by subcutaneous infusion over a one and one-half-hour period. A f t e r these fluids she appeared much more alert and seemed to be improved. E arl y in the morning of the third hospital day she began to have twitchings of her right arm and leg. Oral suction was necessary because of excessive salivation. She became very cyanotic and 0.25 Gin. caffeine sodium benzoate was given intramuscularly. 742
BRANT ET AL. :
OIL O F CHENOPODIU~r
Oxygen was started. H er twitchings became more violent but after about forty-five minutes these ceased. Her temperature went to 103 ~ F., the first time it had been elevated. "Approximately two hours later, twitchings of both the right and left sides of her body were noted and she again became very c y a n o t i c . H e r respirations ceased and she was given 0.25 Gin. caffeine sodium benzoate intramuscularly. Her respirations restarted shortly thereafter. She vomited a large amount of dark brown material. Her temperature rose to 104.8 ~ F., and she was given 0.3 Gin. of aspirin bv rectum. The aspirin was expelled in a large brown stool. A lumbar puncture was done with the finding of clear colorless fluid under normal pressure. The carbon-dioxide combining power was 20 volumes per cent, nonprotein nitrogen 34 rag. per cent, plasma chlorides 640 rag. per cent, and thymol turbidity 2 units. Four hundred cubic centimeters of molar sodium lactate with 5 per cent glucose were given intravenously over a five-hour period. Her temperature after the fluids rose to 106.4 ~ F. and respirations became very rapid. Shortly after the above fluids had run into the patient another intravenous infusion of 5 per cent glucose in distilled water was started but was discontinued because of inability to keep the needle in the child's vein. Her respirations ceased and she was given 0.25 Gm. caffeine sodium benzoate intramuscularly. Resuscitation was used intermittently for the next forty-five minutes. During this period she did not breathe but her heart sounds were good. H er heart sounds gradually became weaker and she was given 2 c.c. of Coramine intravenously without effect. The patient expired in the evening of the third hospital day. The autopsy was performed ten hours after death. Pertinent findings include : Heart : Grossly the heart was wittiin normal limits. Histological examination revealed solitary, minute interstitial collection of round cells, chiefly ]ymphocytes. Lungs :
POISONING
743
Grossly within the parenchyma were several areas of hemorrhage, measuring 0.5 cm. in greatest diameter. Histological examination disclosed rather large a r e a s of bronchopneumonia, characterized by the p r e s e n c e of numerous polymorphonuclear leucocytes within the alveoli and bronchi. In one section there was seen a small amount of recent intra-alveo]ar hemorrhage. Intestines: Grossly the small and large bowel were normal except in the region of the cecum where the mucosa was found to be s l i g h t l y roughened and hyperemic. Histological examination was essentially norma]. Brain: Grossly i t was noted that the brain appeared somewhat enlarged and softer than usually seen. Histological examination revealed a focus of proliferating glial cells within the basal ganglia in addition to occasional iron pigmented macrophages, surrounding several of the blood vessels. Some vessels are seen ~vith small perivascular accumulations of round cells, chiefly lymphocytes. In addition there are focal areas of subarachnoid hemorrhage, the hemorrhage being without reaction or organization. The anatomical impression was (1) toxicity due to oil of chenopodium and (2) ~ocal hemorrhage in lungs. COMMENT
Oil of chenopodium, or oil of wormseed, i s a n effective anthelmintic against hookworm, roundworm, intestinal amoebae, pinworm, and whipworm. The activity is due chiefly to ascaridol, which is present in 45 to 70 per cent concentrations. 1 In therapeutic doses the drug produces, in approximately one-third of the patients, such symptoms as dizziness, nausea, vomiting, tingling in the hands, temporary deafness, albuminuria, and hematuria. Care should be used when administering it to debilitated patients. The drug is absorbed from the stomach and the small intestine. It is eliminated by the lungs and possibly by the kidneys over a long period of time. Its mode Of action is to paralyze
744
THE JOURNAL OF PEDIATRICS
the worm so that purgation is necessary a f t e r the t r e a t m e n t 3 Roth a reported three eases in 1918 with insignificant autopsy findings. W o l P in 1935 reported one case with findings at autopsy of f a t t y degeneration of the liver and kidneys, brain edema, bronehopneumonia, and sicklecell anemia. Guyton ~ reports one case with autopsy findings of degeneration of the liver, acute nephritis, acute enteritis, and acute bronchitis. In Guyton's case the odor of oil of ehenopodium was noted at the autopsy table. In the case presented the doctor who prescribed the medication told the mother to give the child a single dose, but the mother misunderstood and gave a dose each day. SUMMARY
A case of poisoning due to oil of chenopodium has been presented and the literature briefly reviewed. Mild
toxicity to the use of oil of chenopodium is common in therapeutic doses, death usually resulting from an overdose of the drug. An i m p o r t a n t point brought ()at by this case is the necessity of giving accurate directions which are understood by the patient or parents. REFERENCES 1. Sollmann, T. : A Manual of Pharmacology, ed. 7, Philadelphia, 1948, W. B. Saunders Co., pp. 188-189. 2. Davison, F. R.: Synopsis of Materia Medica, Toxicology, and Pharmacology, ed. 2, St. Louis, 1942, The C. u Mosby Co., pp. 183-184. 3. l~oth, D. A.: Some Dangers of Chenopodium Treatment, South. M. J. 11: 733, 1918. 4. Wolf, I. J. : F a t a l Poisoning With Oil of Chenopodium in a Negro Child With Sickle Cell Anemia, Arch. Pedlar. 52: 126, 1935. 5. Guyton, W . L . : Poisoning Due to Oil of Chenopodium, J. A. M. A. 132: 330, 1946.
chenopodium are infrequent in R American literature. The majority of deaths recorded are due to an overdose of the drug, or of the therapeutic dose being repeated at short intervals. We recently had the opportunity to observe a case of oil of chenopodium poisoning at this hospital. CASE REPORT
A 3-year-old white girl was admitted to Charlotte Memorial Hospital on Jan. 22, 1951, with the chief complaint of a fainting spell which occurred approximately two hours p r i o r to admission. H er family history was noncontributory. She had been treated on two previous occasions with gentian violet for pinworms. The patient received the oil of chenopodium from her doctor because of pinworms. She was given onefourth teaspoonful of oil of chenopodium daily for the four days prior to her admission. She received no laxative or other medication. After lunch of the fourth day of treatment she vomited and then fainted. She was immediately b r o u g h t to the emergency room of this hospital. Physical examination revealed a poorly nourished white girl, who could be aroused only with difficulty. Her weight was 29 pounds, temperature 98.6 ~ F., pulse 90, and respirations 22. Her skin showed some evidence of dehydration. The remainder of the physical examination was noncontributory. The laboratory examination on admission showed a red blood cell count of 4.1 million, hemoglobin 10 Gin., white blood cell count of 18,450 with 78 per cent polymorphonuclear leuco*Present address: Richmo nd 27, Va.
4810
Old
Brook
Rd.,
STUMPE,'
]~i.]).
cytes, 20 per cent lymphocytes, and 2 per cent eosinophiles. A voided urine specimen was within normal limits. On admission to the ward she was given 15 c.c. of milk of magnesia and 5 c.c. of aromatic cascara orally, 0.25 Gm. of caffeine and sodium benzoate intramuscularly, and offered liquids. Because of refusal to take liquids she was given 250 c.c. of 5 per cent glucose in distilled water by subcutaneous infusion over a two-hour period. One hour after the infusion was started the patient became more alert and asked for her mother. She slept throughout the night. On the second hospital day she took liquids with encouragement. She received 250 c.c. of t t a r t m a n n ' s solution by subcutaneous infusion over a onehour period. Because of her refusal to take liquids or solids a gastric gavage was done. The patient was given eggnog but vomited the entire amount after one and one-half hours' retention. That evening twitching movements of her left arm and leg were noted. She was given 30 rag. sodium phenobarbital intramuscularly for the twitchings. The twitchings stopped but her respirations slowed to about eight per minute. The patient then received 0.25 Gm. caffeine sodium benzoate intramuscularly and her respirations returned to within the normal range. She received another 250 c.c. of Hartmann's solution by subcutaneous infusion over a one and one-half-hour period. A f t e r these fluids she appeared much more alert and seemed to be improved. E arl y in the morning of the third hospital day she began to have twitchings of her right arm and leg. Oral suction was necessary because of excessive salivation. She became very cyanotic and 0.25 Gin. caffeine sodium benzoate was given intramuscularly. 742
BRANT ET AL. :
OIL O F CHENOPODIU~r
Oxygen was started. H er twitchings became more violent but after about forty-five minutes these ceased. Her temperature went to 103 ~ F., the first time it had been elevated. "Approximately two hours later, twitchings of both the right and left sides of her body were noted and she again became very c y a n o t i c . H e r respirations ceased and she was given 0.25 Gin. caffeine sodium benzoate intramuscularly. Her respirations restarted shortly thereafter. She vomited a large amount of dark brown material. Her temperature rose to 104.8 ~ F., and she was given 0.3 Gin. of aspirin bv rectum. The aspirin was expelled in a large brown stool. A lumbar puncture was done with the finding of clear colorless fluid under normal pressure. The carbon-dioxide combining power was 20 volumes per cent, nonprotein nitrogen 34 rag. per cent, plasma chlorides 640 rag. per cent, and thymol turbidity 2 units. Four hundred cubic centimeters of molar sodium lactate with 5 per cent glucose were given intravenously over a five-hour period. Her temperature after the fluids rose to 106.4 ~ F. and respirations became very rapid. Shortly after the above fluids had run into the patient another intravenous infusion of 5 per cent glucose in distilled water was started but was discontinued because of inability to keep the needle in the child's vein. Her respirations ceased and she was given 0.25 Gm. caffeine sodium benzoate intramuscularly. Resuscitation was used intermittently for the next forty-five minutes. During this period she did not breathe but her heart sounds were good. H er heart sounds gradually became weaker and she was given 2 c.c. of Coramine intravenously without effect. The patient expired in the evening of the third hospital day. The autopsy was performed ten hours after death. Pertinent findings include : Heart : Grossly the heart was wittiin normal limits. Histological examination revealed solitary, minute interstitial collection of round cells, chiefly ]ymphocytes. Lungs :
POISONING
743
Grossly within the parenchyma were several areas of hemorrhage, measuring 0.5 cm. in greatest diameter. Histological examination disclosed rather large a r e a s of bronchopneumonia, characterized by the p r e s e n c e of numerous polymorphonuclear leucocytes within the alveoli and bronchi. In one section there was seen a small amount of recent intra-alveo]ar hemorrhage. Intestines: Grossly the small and large bowel were normal except in the region of the cecum where the mucosa was found to be s l i g h t l y roughened and hyperemic. Histological examination was essentially norma]. Brain: Grossly i t was noted that the brain appeared somewhat enlarged and softer than usually seen. Histological examination revealed a focus of proliferating glial cells within the basal ganglia in addition to occasional iron pigmented macrophages, surrounding several of the blood vessels. Some vessels are seen ~vith small perivascular accumulations of round cells, chiefly lymphocytes. In addition there are focal areas of subarachnoid hemorrhage, the hemorrhage being without reaction or organization. The anatomical impression was (1) toxicity due to oil of chenopodium and (2) ~ocal hemorrhage in lungs. COMMENT
Oil of chenopodium, or oil of wormseed, i s a n effective anthelmintic against hookworm, roundworm, intestinal amoebae, pinworm, and whipworm. The activity is due chiefly to ascaridol, which is present in 45 to 70 per cent concentrations. 1 In therapeutic doses the drug produces, in approximately one-third of the patients, such symptoms as dizziness, nausea, vomiting, tingling in the hands, temporary deafness, albuminuria, and hematuria. Care should be used when administering it to debilitated patients. The drug is absorbed from the stomach and the small intestine. It is eliminated by the lungs and possibly by the kidneys over a long period of time. Its mode Of action is to paralyze
744
THE JOURNAL OF PEDIATRICS
the worm so that purgation is necessary a f t e r the t r e a t m e n t 3 Roth a reported three eases in 1918 with insignificant autopsy findings. W o l P in 1935 reported one case with findings at autopsy of f a t t y degeneration of the liver and kidneys, brain edema, bronehopneumonia, and sicklecell anemia. Guyton ~ reports one case with autopsy findings of degeneration of the liver, acute nephritis, acute enteritis, and acute bronchitis. In Guyton's case the odor of oil of ehenopodium was noted at the autopsy table. In the case presented the doctor who prescribed the medication told the mother to give the child a single dose, but the mother misunderstood and gave a dose each day. SUMMARY
A case of poisoning due to oil of chenopodium has been presented and the literature briefly reviewed. Mild
toxicity to the use of oil of chenopodium is common in therapeutic doses, death usually resulting from an overdose of the drug. An i m p o r t a n t point brought ()at by this case is the necessity of giving accurate directions which are understood by the patient or parents. REFERENCES 1. Sollmann, T. : A Manual of Pharmacology, ed. 7, Philadelphia, 1948, W. B. Saunders Co., pp. 188-189. 2. Davison, F. R.: Synopsis of Materia Medica, Toxicology, and Pharmacology, ed. 2, St. Louis, 1942, The C. u Mosby Co., pp. 183-184. 3. l~oth, D. A.: Some Dangers of Chenopodium Treatment, South. M. J. 11: 733, 1918. 4. Wolf, I. J. : F a t a l Poisoning With Oil of Chenopodium in a Negro Child With Sickle Cell Anemia, Arch. Pedlar. 52: 126, 1935. 5. Guyton, W . L . : Poisoning Due to Oil of Chenopodium, J. A. M. A. 132: 330, 1946.