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Castor bean poisoning
Toxicology Rounds
lP
The Archives of the American Association of Poison Control Centers, the American Board of Medical Toxicology, and the American Academy of Clinical Toxicology.
Q
Castor Bean Poisoning GREGORY
Although the highly toxic nature of castor bean (Ricinus comis well recognized, reports of human toxicity in the English medical literature are scarce. The potentially lethal doses reported for children and adults are three beans and four to eight beans respectively. Recent experience with two cases provides added insight into the expected course of toxicity. In both cases, repeated vomiting, diarrhea, and transiently elevated serum creatinine occurred. Dehydration was much more pronounced in the second case. Both patients recovered uneventfully. Other reported manifestations of castor bean toxicity, such as hepatic necrosis, renal failure, erythrocyte hemolysis, convulsions, and shock, did not occur. (Am J Emerg Med 1988;4:259-261)
P. WEDIN, PharmD,* JEFFREY S. NEAL, MD,t GARY W. EVERSON, PharmD,* EDWARD P. KRENZELOK, PharmDS CASE REPORTS
munis)
The toxic component of castor beans. ricin, has been extensively studied in attempts to delineate its structure and mechanism of toxicity. Although much has been written about ricin toxicity, reports in the English medical literature of castor bean ingestion and poisoning are scarce. A MEDLINE search from 1966 to present revealed only seven cases of castor bean ingestion and poisoning. Recent experience with two cases in which potentially fatal amounts of castor beans were ingested provides added insight into the expected course of castor bean poisoning. In both cases, toxicity was limited to the gastrointestinal tract.
From the “West Virginia Poison Center and West Virginia University School of Pharmacy, the tcharleston Area Medical Center, Charleston, West Virginia, and the *Pittsburgh Poison Center, Pittsburgh, Pennsylvania. Manuscript 1985.
received
November
7,1985;
accepted
November
20,
Address reprint requests to Dr. Wedin: West Virginia Poison Center, West Virginia University School of Pharmacy, 3110 MacCorkle Ave., SE, Charleston, WV 25304. Key Words: Castor
bean(s),
ricin, poisoning.
Case1 A 21-year-old man ingested approximately 12 castor beans he had mistaken for hazelnuts. The majority of the beans were chewed. He experienced no burning on ingestion and felt well immediately following. Approximately half an hour following ingestion, he was informed that they were extremely poisonous. He then induced vomiting by placing his finger in the back of his throat. No beans were noticed with this vomiting episode. Immediately following this, he began vomiting profusely 1.5 to 25 times, returning a large amount of chewed castor beans. He continued to feel nauseated, and about two hours later he was seen by his family physician. He was given two doses of syrup of ipecac with good results, followed with activated charcoal and magnesium citrate. The patient was then transferred to Charleston Area Medical Center (CAMC). En route, he had three to four episodes of non-charcoal containing diarrhea1 stools. He arrived at CAMC approximately eight hours after ingestion of the castor beans. Physical examination revealed an obviously nauseated white male with a pulse of 100 beats/min, respirations of 201 min, and a blood pressure of 130/70 mm Hg. The HEENT examination was remarkable only for dry oral mucosa without lesions. Abdominal examination revealed a scaphoid abdomen with hypoactive bowel sounds and no tenderness. Rectal examination results, as well as the results of the remainder of the physical examination, were within normal limits. Initial laboratory examination revealed a blood urea nitrogen (BUN) of 16 mg/dl and creatinine value of I. 1 mg/dl. Serum sodium, potassium and chloride levels were within normal limits. Prothrombin time (PT) and partial thromboplastin time (PTT) were normal, glucose was 159 mg/dl, leukocyte count was 14,200/mm3 with 90% neutrophils, hemoglobin was 15.6 gidl, and the hematocrit was 45%. Results of liver function tests were normal, and there was no evidence of hemolysis. The patient was admitted to the intensive care unit for close monitoring. A solution of D, in 1/2normal saline with 20
that
259
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 4, Number 3 n May 1986
mEq KCLil was given at 200 mlihr for the first I2 hours for hydration. He was given calcium carbonate and ascorbic acid as recommended in Poisindexa. His diarrhea abated after approximately 12 hours. On the second hospital day he was transferred to the medical floor. On the third hospital day, his serum creatinine rose to 1.5 mg/dl (normal 0.7-1.5 mg/dl. All other laboratory values remained within normal limits, and he was asymptomatic. When he was discharged on the fourth day, his creatinine level was 1.4 mgidl. He was followed closely as an outpatient with a sequential multiple analyzer with a computer (SMAC 20), urinalysis, and complete blood count performed on the second and fourth days following discharge. These same tests were again performed two times the following week. His peak serum creatinine was 1.5 mgidl, the same as on the third hospital day. Fourteen days following ingestion, his serum creatinine was again 1.1 mg/dl. Results of other laboratory tests, including complete blood count, PT. liver function tests, and electrolytes, remained within normal limits, and he remained asymptomatic. Case 2 An 80-year-old woman presented to the emergency department at 1:30 AM with a two-hour history of vomiting, diarrhea, and abdominl cramps. The patient’s daughter found her at 4 PM chewing several castor beans that had previously been shelled and prepared for planting. Several partially chewed castor beans were removed from the patient’s mouth, although she denied ingestion. An uneventful evening ensued until 11:30 PM, when the patient awoke with several episodes of vomiting. Non-bloody diarrhea and abdominal cramping soon followed. Previous medical history was significant for a diagnosis of rectal adenocarcinoma a year earlier. for which surgery was successful. There was no history of acute or chronic vomiting, diarrhea, or other gastrointestinal disorders. The patient had had some deterioration of mental status in recent years. Physical examination revealed an alert, oriented female whose skin was warm and dry. Blood pressure was 140/90 mm Hg, pulse was 100 beats/min, respiratory rate was 20-24/min, and temperature 37.1”C. The abdomen was diffusely tender, but more so in the epigastrum. Hyperactive bowel sounds were present. The rest of the physical examination results were unremarkable. Admission laboratory values were: leukocyte count. 7,800/mm3; erythrocyte count, 4.39 x lo6 cells/mm3: hemoglobin, 13.9 gidl; hematocrit. 41%: glucose, 103 mgidl; and BUN, 25 mg/dl. Electrolytes were within normal limits. Liver enzymes were not analyzed. The patient continued to have multiple vomiting episodes resulting in 300 ml of emesis. Non-bloody diarrhea continued. One liter of DS solution in % normal saline solution with IO mEq of KCI was started at 75 mlihr. and the patient was admitted to the intensive care unit. Initially, 60g of activated charcoal in 70% sorbitol solution was administered. followed by 50 g every three to four hours. The patient experienced periodic vomiting of charcoal solution and had large amounts of non-bloody diarrhea1 stool throughout the day. Intravenous (IV) fluids were continued, and the patient ingested nothing orally except for the 260
charcoal sorbitol solution. Vital signs remained stable, and the patient’s skin was warm. dry, and pale throughout the first day. Fluid input and output were 1,860 ml and 4,300 ml, respectively. Abdominal pain and large amounts of non-bloody charcoal diarrhea continued throughout the second day of admission. Occasional vomiting of charcoal solution occurred during the day. The patient remained alert and oriented. and vital signs remained stable. Laboratory data were significant for a rise in the BUN to 37 mg/dl and a creatinine of 2.0 mgidl. Urinary output on the second day was only 325 ml. Urinalysis was I + for protein and blood. Fluid input and output were 2,900 ml and 2,400 ml, respectively. Results of liver function tests as well. as all other laboratory data, were within normal limits. The rate of IV fluids was increased to 150 mlihr. and activated charcoal in sorbitol solution was discontinued. On the third day of admission. the patient’s gastrointestinal symptoms resolved. However, her mental status had decresed substantially from the prior two days. She became increasingly pale and lethargic, and her extremities appeared somewhat cyanotic. Blood pressure was 100/80 mm Hg. pulse was I12 beatsimin. respiratory rate was 36imin. and temperature was 37.9”C. Serum electrolytes were: sodium, 165 mEq/l: potassium. 5.3 mEq/l: chloride. 147 mEq/l: and bicarbonate. 18.5 mEq/l. Blood glucose was 188 mgidl. BUN was 43 mgidl. hemoglobin was 17.6 g/d]. and the hematocrit was 54.1%. A diagnois of dehydration secondary to hypovolemia was made. Intravenous fluid therapy was evaluated and fluids were increased to correct 7. l-l fluid deficit. By the end of the day, fluid input and output were 4,632 ml and 900 ml, respectively. with urinary output recorded at 375 ml. The urinalysis results returned to normal. The patient’s condition had significantly improved by the fourth hospital day. Color in the extremities had improved, and the skin was warm and dry. No diarrhea or gastrointestinal distress had been observed for over 24 hours. Vita1 signs had returned to normal, and electrolyte values reflected an improvement in the patient’s fluid status. The BUN was still elevated at 48 mgidl. but the creatinine fell to I .7 mgidl. Fluid input and output were 4,620 ml and 550 ml, respectively, and urinary output was 550 ml. Intravenous fluids were continued, and supportive therapy was maintained. The following day the patient continued to improve. Vital signs had stabilized. and urinary output had increased to 2100 ml. The BUN fell to 24 mgidl. Intravenous fluid therapy was tapered, and a liquid diet was initiated. An uneventful recovery followed. DISCUSSION
Ricin, the toxic protein found within the castor bean, is one of the most potent toxins known. The estimated lethal dose in man is 1.0 mg/kg.’ Ricin is a glycoprotein composed of two peptide chains of differing molecular weights attached by a disulfide bond. The larger chain binds to galactose-containing receptors on the cell surface. Following this, the peptides uncouple, and the smaller chain is taken up into the cell by endocytosis. It then interferes with the
WEDIN ET AL n CASTOR BEAN POISONING
chain elongation step of protein synthesis, This leads to death of the cell.’ Castor beans also have an agglutinating protein composed of four polypeptide chains.3 It is non-toxic orally. Toxic effects that have been attributed to castor bean poisoning include nausea, headache, general malaise, somnolence, loss of consciousness, convulsions, bloody diarrhea with tenesmus, dehydration, thirst, cyanosis. tachycardia, hypotension, electrocardiographic (ECG) changes, exanthema, liver necrosis, nephritis, proteinuria. optic nerve lesion, and mydriasis.4 The potentially fatal dose of castor beans is reported to be three beans in children and four to eight beans in adults.5 The effects of growing conditions, maturity of the beans, or other variables that could influence the ricin content are not as well described. The degree of toxicity produced upon ingestion of castor beans is largely dependent upon whether the beans are swallowed intact or chewed. Chewing castor beans releases the ricin from within. In Case 1, approximately 12 chewed beans were ingested, and in Case 2, the exact number of beans ingested was unknown, although several partially chewed beans were found in her mouth. Severe gastrointestinal manifestations, such as persistent vomiting and diarrhea, appear to be the most consistent finding following the ingestion of castor beans, as demonstrated in these cases and elsehwere.‘.6 As seen in Case 2, these effects may be delayed for several hours. Early spontaneous vomiting, as in Case 1, may play an important role in eliminating the castor beans from the GI tract, thereby limiting toxicity. Because of the persistence and severity of the gastrointestinal symptoms, dehydration is an important complication of castor bean poisoning. Many of the systemic signs and symptoms following castor bean ingestion may be the result of dehydration rather than a direct effect of ricin itself. A patient with moderate to severe dehydration may experience tachycardia, oliguria, hypotension, and even shock. Dehydration may also produce effects upon the central nervous system, such as lethargy, weakness, confusion, or obtundation.7 Acute renal failure is reported to be a manifestation of castor bean poisoning. However, the elevated creatinine in both cases, as well as the elevated BUN and poor urinary output in Case 2, improved following adequate fluid administration. These findings suggest that dehydration is the primary cause of these manifestations in these two cases. Likewise, in neither case was there clinical or laboratory evidence of liver necrosis or dysfunction. Slight alterations in laboratory values that suggest erythro-
cyte hemolysis in Case 2 may also have been the result of dehydration. The findings of these two cases are similar to a case recently reported by Kopferschmitt et al. ’ They describe the case of a 21-year-old man who ingested 31 castor beans, some of which were chewed. Soon after ingestion, he developed vomiting and profuse diarrhea, which resulted in marked dehydration. Circulatory collapse with cyanosis of the extremities, an elevated BUN, and laboratory evidence of hemoconcentration were present. This patient recovered rapdily with fluid administration and was discharged on the fifth hospital day without sequelae. CONCLUSION The two cases presented herein clearly demonstrate the severe toxicity that may occur with the ingestion of only small quantities of castor beans. Toxicity was limited to severe gastrointestinal symptoms and resulting dehydration. Other previously reported manifestations of castor bean poisoning, such as hepatic necrosis, renal failure, erythrocyte hemolysis, convulsions, and shock, did not occur. Until further information on the toxicity of ingested castor beans is obtained, any ingestion of castor beans should be considered as potentially life-threatening and requiring hospitalization for close observation and monitoring. Therapy should include early gastrointestinal decontamination with syrup of ipecac and/or activated charcoal. The use of cathartics may not be necessary because of excessive diarrhea. Close monitoring of the patient’s hematologic, hepatic, and renal systems should be performed. Careful monitoring of the patient’s fluid and electrolyte status is absolutely essential to prevent dehydration and its complications. With significant loss of intestinal function. parenteral alimentation will be needed. REFERENCES 1. Kopferschmitt J, Flesch F, Lugnier A, et al. Acute voluntary intoxication by ricin. Hum Toxicol 1983;2:239-242. 2. Olsnes S, Refsnes K, Pihl A. Mechanism of action of the toxic lectins abrin and ricin. Nature 1974;249:627-631. 3. Olsnes S, Saltvedt E, Pihl A. Isolation and comparison of galactose-binding lectins from abrus prectorius and Ricinus communis. J Biol Chem 1974;249:803-810. Balint GA. Ricin: The toxic protein of castor oil seeds. Toxicology 1974;2:77-102. Poisindexm. Denver: Micromedex, 1985. Malizia E, Sarcinelli L, Andreucci G. Ricinus poisoning: A familiar epidemy. Acta Pharmacol Toxicol (suppl) 1977;41:351-361. Isselbacher, Adams RD, Braunwald E, et al. (eds): Harrison’s Principles of Internal Medicine, 9th ed. New York: McGraw-Hill Book Company, 1980:436-437.
261
lP
The Archives of the American Association of Poison Control Centers, the American Board of Medical Toxicology, and the American Academy of Clinical Toxicology.
Q
Castor Bean Poisoning GREGORY
Although the highly toxic nature of castor bean (Ricinus comis well recognized, reports of human toxicity in the English medical literature are scarce. The potentially lethal doses reported for children and adults are three beans and four to eight beans respectively. Recent experience with two cases provides added insight into the expected course of toxicity. In both cases, repeated vomiting, diarrhea, and transiently elevated serum creatinine occurred. Dehydration was much more pronounced in the second case. Both patients recovered uneventfully. Other reported manifestations of castor bean toxicity, such as hepatic necrosis, renal failure, erythrocyte hemolysis, convulsions, and shock, did not occur. (Am J Emerg Med 1988;4:259-261)
P. WEDIN, PharmD,* JEFFREY S. NEAL, MD,t GARY W. EVERSON, PharmD,* EDWARD P. KRENZELOK, PharmDS CASE REPORTS
munis)
The toxic component of castor beans. ricin, has been extensively studied in attempts to delineate its structure and mechanism of toxicity. Although much has been written about ricin toxicity, reports in the English medical literature of castor bean ingestion and poisoning are scarce. A MEDLINE search from 1966 to present revealed only seven cases of castor bean ingestion and poisoning. Recent experience with two cases in which potentially fatal amounts of castor beans were ingested provides added insight into the expected course of castor bean poisoning. In both cases, toxicity was limited to the gastrointestinal tract.
From the “West Virginia Poison Center and West Virginia University School of Pharmacy, the tcharleston Area Medical Center, Charleston, West Virginia, and the *Pittsburgh Poison Center, Pittsburgh, Pennsylvania. Manuscript 1985.
received
November
7,1985;
accepted
November
20,
Address reprint requests to Dr. Wedin: West Virginia Poison Center, West Virginia University School of Pharmacy, 3110 MacCorkle Ave., SE, Charleston, WV 25304. Key Words: Castor
bean(s),
ricin, poisoning.
Case1 A 21-year-old man ingested approximately 12 castor beans he had mistaken for hazelnuts. The majority of the beans were chewed. He experienced no burning on ingestion and felt well immediately following. Approximately half an hour following ingestion, he was informed that they were extremely poisonous. He then induced vomiting by placing his finger in the back of his throat. No beans were noticed with this vomiting episode. Immediately following this, he began vomiting profusely 1.5 to 25 times, returning a large amount of chewed castor beans. He continued to feel nauseated, and about two hours later he was seen by his family physician. He was given two doses of syrup of ipecac with good results, followed with activated charcoal and magnesium citrate. The patient was then transferred to Charleston Area Medical Center (CAMC). En route, he had three to four episodes of non-charcoal containing diarrhea1 stools. He arrived at CAMC approximately eight hours after ingestion of the castor beans. Physical examination revealed an obviously nauseated white male with a pulse of 100 beats/min, respirations of 201 min, and a blood pressure of 130/70 mm Hg. The HEENT examination was remarkable only for dry oral mucosa without lesions. Abdominal examination revealed a scaphoid abdomen with hypoactive bowel sounds and no tenderness. Rectal examination results, as well as the results of the remainder of the physical examination, were within normal limits. Initial laboratory examination revealed a blood urea nitrogen (BUN) of 16 mg/dl and creatinine value of I. 1 mg/dl. Serum sodium, potassium and chloride levels were within normal limits. Prothrombin time (PT) and partial thromboplastin time (PTT) were normal, glucose was 159 mg/dl, leukocyte count was 14,200/mm3 with 90% neutrophils, hemoglobin was 15.6 gidl, and the hematocrit was 45%. Results of liver function tests were normal, and there was no evidence of hemolysis. The patient was admitted to the intensive care unit for close monitoring. A solution of D, in 1/2normal saline with 20
that
259
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
n Volume 4, Number 3 n May 1986
mEq KCLil was given at 200 mlihr for the first I2 hours for hydration. He was given calcium carbonate and ascorbic acid as recommended in Poisindexa. His diarrhea abated after approximately 12 hours. On the second hospital day he was transferred to the medical floor. On the third hospital day, his serum creatinine rose to 1.5 mg/dl (normal 0.7-1.5 mg/dl. All other laboratory values remained within normal limits, and he was asymptomatic. When he was discharged on the fourth day, his creatinine level was 1.4 mgidl. He was followed closely as an outpatient with a sequential multiple analyzer with a computer (SMAC 20), urinalysis, and complete blood count performed on the second and fourth days following discharge. These same tests were again performed two times the following week. His peak serum creatinine was 1.5 mgidl, the same as on the third hospital day. Fourteen days following ingestion, his serum creatinine was again 1.1 mg/dl. Results of other laboratory tests, including complete blood count, PT. liver function tests, and electrolytes, remained within normal limits, and he remained asymptomatic. Case 2 An 80-year-old woman presented to the emergency department at 1:30 AM with a two-hour history of vomiting, diarrhea, and abdominl cramps. The patient’s daughter found her at 4 PM chewing several castor beans that had previously been shelled and prepared for planting. Several partially chewed castor beans were removed from the patient’s mouth, although she denied ingestion. An uneventful evening ensued until 11:30 PM, when the patient awoke with several episodes of vomiting. Non-bloody diarrhea and abdominal cramping soon followed. Previous medical history was significant for a diagnosis of rectal adenocarcinoma a year earlier. for which surgery was successful. There was no history of acute or chronic vomiting, diarrhea, or other gastrointestinal disorders. The patient had had some deterioration of mental status in recent years. Physical examination revealed an alert, oriented female whose skin was warm and dry. Blood pressure was 140/90 mm Hg, pulse was 100 beats/min, respiratory rate was 20-24/min, and temperature 37.1”C. The abdomen was diffusely tender, but more so in the epigastrum. Hyperactive bowel sounds were present. The rest of the physical examination results were unremarkable. Admission laboratory values were: leukocyte count. 7,800/mm3; erythrocyte count, 4.39 x lo6 cells/mm3: hemoglobin, 13.9 gidl; hematocrit. 41%: glucose, 103 mgidl; and BUN, 25 mg/dl. Electrolytes were within normal limits. Liver enzymes were not analyzed. The patient continued to have multiple vomiting episodes resulting in 300 ml of emesis. Non-bloody diarrhea continued. One liter of DS solution in % normal saline solution with IO mEq of KCI was started at 75 mlihr. and the patient was admitted to the intensive care unit. Initially, 60g of activated charcoal in 70% sorbitol solution was administered. followed by 50 g every three to four hours. The patient experienced periodic vomiting of charcoal solution and had large amounts of non-bloody diarrhea1 stool throughout the day. Intravenous (IV) fluids were continued, and the patient ingested nothing orally except for the 260
charcoal sorbitol solution. Vital signs remained stable, and the patient’s skin was warm. dry, and pale throughout the first day. Fluid input and output were 1,860 ml and 4,300 ml, respectively. Abdominal pain and large amounts of non-bloody charcoal diarrhea continued throughout the second day of admission. Occasional vomiting of charcoal solution occurred during the day. The patient remained alert and oriented. and vital signs remained stable. Laboratory data were significant for a rise in the BUN to 37 mg/dl and a creatinine of 2.0 mgidl. Urinary output on the second day was only 325 ml. Urinalysis was I + for protein and blood. Fluid input and output were 2,900 ml and 2,400 ml, respectively. Results of liver function tests as well. as all other laboratory data, were within normal limits. The rate of IV fluids was increased to 150 mlihr. and activated charcoal in sorbitol solution was discontinued. On the third day of admission. the patient’s gastrointestinal symptoms resolved. However, her mental status had decresed substantially from the prior two days. She became increasingly pale and lethargic, and her extremities appeared somewhat cyanotic. Blood pressure was 100/80 mm Hg. pulse was I12 beatsimin. respiratory rate was 36imin. and temperature was 37.9”C. Serum electrolytes were: sodium, 165 mEq/l: potassium. 5.3 mEq/l: chloride. 147 mEq/l: and bicarbonate. 18.5 mEq/l. Blood glucose was 188 mgidl. BUN was 43 mgidl. hemoglobin was 17.6 g/d]. and the hematocrit was 54.1%. A diagnois of dehydration secondary to hypovolemia was made. Intravenous fluid therapy was evaluated and fluids were increased to correct 7. l-l fluid deficit. By the end of the day, fluid input and output were 4,632 ml and 900 ml, respectively. with urinary output recorded at 375 ml. The urinalysis results returned to normal. The patient’s condition had significantly improved by the fourth hospital day. Color in the extremities had improved, and the skin was warm and dry. No diarrhea or gastrointestinal distress had been observed for over 24 hours. Vita1 signs had returned to normal, and electrolyte values reflected an improvement in the patient’s fluid status. The BUN was still elevated at 48 mgidl. but the creatinine fell to I .7 mgidl. Fluid input and output were 4,620 ml and 550 ml, respectively, and urinary output was 550 ml. Intravenous fluids were continued, and supportive therapy was maintained. The following day the patient continued to improve. Vital signs had stabilized. and urinary output had increased to 2100 ml. The BUN fell to 24 mgidl. Intravenous fluid therapy was tapered, and a liquid diet was initiated. An uneventful recovery followed. DISCUSSION
Ricin, the toxic protein found within the castor bean, is one of the most potent toxins known. The estimated lethal dose in man is 1.0 mg/kg.’ Ricin is a glycoprotein composed of two peptide chains of differing molecular weights attached by a disulfide bond. The larger chain binds to galactose-containing receptors on the cell surface. Following this, the peptides uncouple, and the smaller chain is taken up into the cell by endocytosis. It then interferes with the
WEDIN ET AL n CASTOR BEAN POISONING
chain elongation step of protein synthesis, This leads to death of the cell.’ Castor beans also have an agglutinating protein composed of four polypeptide chains.3 It is non-toxic orally. Toxic effects that have been attributed to castor bean poisoning include nausea, headache, general malaise, somnolence, loss of consciousness, convulsions, bloody diarrhea with tenesmus, dehydration, thirst, cyanosis. tachycardia, hypotension, electrocardiographic (ECG) changes, exanthema, liver necrosis, nephritis, proteinuria. optic nerve lesion, and mydriasis.4 The potentially fatal dose of castor beans is reported to be three beans in children and four to eight beans in adults.5 The effects of growing conditions, maturity of the beans, or other variables that could influence the ricin content are not as well described. The degree of toxicity produced upon ingestion of castor beans is largely dependent upon whether the beans are swallowed intact or chewed. Chewing castor beans releases the ricin from within. In Case 1, approximately 12 chewed beans were ingested, and in Case 2, the exact number of beans ingested was unknown, although several partially chewed beans were found in her mouth. Severe gastrointestinal manifestations, such as persistent vomiting and diarrhea, appear to be the most consistent finding following the ingestion of castor beans, as demonstrated in these cases and elsehwere.‘.6 As seen in Case 2, these effects may be delayed for several hours. Early spontaneous vomiting, as in Case 1, may play an important role in eliminating the castor beans from the GI tract, thereby limiting toxicity. Because of the persistence and severity of the gastrointestinal symptoms, dehydration is an important complication of castor bean poisoning. Many of the systemic signs and symptoms following castor bean ingestion may be the result of dehydration rather than a direct effect of ricin itself. A patient with moderate to severe dehydration may experience tachycardia, oliguria, hypotension, and even shock. Dehydration may also produce effects upon the central nervous system, such as lethargy, weakness, confusion, or obtundation.7 Acute renal failure is reported to be a manifestation of castor bean poisoning. However, the elevated creatinine in both cases, as well as the elevated BUN and poor urinary output in Case 2, improved following adequate fluid administration. These findings suggest that dehydration is the primary cause of these manifestations in these two cases. Likewise, in neither case was there clinical or laboratory evidence of liver necrosis or dysfunction. Slight alterations in laboratory values that suggest erythro-
cyte hemolysis in Case 2 may also have been the result of dehydration. The findings of these two cases are similar to a case recently reported by Kopferschmitt et al. ’ They describe the case of a 21-year-old man who ingested 31 castor beans, some of which were chewed. Soon after ingestion, he developed vomiting and profuse diarrhea, which resulted in marked dehydration. Circulatory collapse with cyanosis of the extremities, an elevated BUN, and laboratory evidence of hemoconcentration were present. This patient recovered rapdily with fluid administration and was discharged on the fifth hospital day without sequelae. CONCLUSION The two cases presented herein clearly demonstrate the severe toxicity that may occur with the ingestion of only small quantities of castor beans. Toxicity was limited to severe gastrointestinal symptoms and resulting dehydration. Other previously reported manifestations of castor bean poisoning, such as hepatic necrosis, renal failure, erythrocyte hemolysis, convulsions, and shock, did not occur. Until further information on the toxicity of ingested castor beans is obtained, any ingestion of castor beans should be considered as potentially life-threatening and requiring hospitalization for close observation and monitoring. Therapy should include early gastrointestinal decontamination with syrup of ipecac and/or activated charcoal. The use of cathartics may not be necessary because of excessive diarrhea. Close monitoring of the patient’s hematologic, hepatic, and renal systems should be performed. Careful monitoring of the patient’s fluid and electrolyte status is absolutely essential to prevent dehydration and its complications. With significant loss of intestinal function. parenteral alimentation will be needed. REFERENCES 1. Kopferschmitt J, Flesch F, Lugnier A, et al. Acute voluntary intoxication by ricin. Hum Toxicol 1983;2:239-242. 2. Olsnes S, Refsnes K, Pihl A. Mechanism of action of the toxic lectins abrin and ricin. Nature 1974;249:627-631. 3. Olsnes S, Saltvedt E, Pihl A. Isolation and comparison of galactose-binding lectins from abrus prectorius and Ricinus communis. J Biol Chem 1974;249:803-810. Balint GA. Ricin: The toxic protein of castor oil seeds. Toxicology 1974;2:77-102. Poisindexm. Denver: Micromedex, 1985. Malizia E, Sarcinelli L, Andreucci G. Ricinus poisoning: A familiar epidemy. Acta Pharmacol Toxicol (suppl) 1977;41:351-361. Isselbacher, Adams RD, Braunwald E, et al. (eds): Harrison’s Principles of Internal Medicine, 9th ed. New York: McGraw-Hill Book Company, 1980:436-437.
261