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Chloral hydrate intoxication in a newborn infant
104
Chloral hydrate intoxication in a newborn infant
REFERENCES 1. Bergstein JM. Renal failure. In: Behrman RE, Kliegman RM, Jenson HB, eds. Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000:1605–12. 2. Sly M. Asthma. In: Behrman RE, Kliegman RM, Jenson HB, eds. Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000: 664 – 80.
e Chloral Hydrate Intoxication in a Newborn Infant Chloral hydrate (CH) is a sedative-hypnotic (general central nervous system depressant) agent, and it has been widely used for sedation in the pediatric population in numerous centers including our country (1– 4). Herein we report a newborn infant who accidentally ingested an overdose of CH, to draw attention to the importance of intoxication in newborn infants. A 28-day-old boy presented with a convulsion. He was the product of a 40-week term of gestation and labor. After the delivery, he had been hospitalized in another hospital with the diagnosis of perinatal asphyxia and given phenobarbital. During the hospitalization his general condition partially improved and he was discharged from hospital. However, his convulsions resumed at home and he was admitted to our clinic. The patient was hospitalized in order to investigate the etiology of the seizures and for management. The physical examination was normal. A computed tomography (CT) scan of the brain and electroencephalogram (EEG) were scheduled. In our clinic we routinely use oral CH (50 mg/kg/dose maximum 2 g) for sedation, and this was ordered. Thirty minutes after giving the CH, agitation, respiratory distress, and excessive salivation, lasting about 1 hour, were noted. Later, respiratory depression and hypoxia developed. Initially, we could not explain these abnormal clinical findings. Oral feeding was discontinued and he was monitored. Intravenous fluid and nasal oxygen were given. Serum glucose, calcium, electrolytes, renal and liver function tests were measured and all were found to be normal. A chest X-ray study was also normal. Seven hours after ingestion of CH his general condition gradually recovered and respiratory distress and hypoxia completely resolved. The patient was reevaluated and we established that CH was accidentally given in a dose of 250 mg/kg. Later, a CT scan and EEG were studied using another sedative, diazepam. While the CT scan was found to be normal, the EEG showed bilateral multifocal sharp and slow waves. During the hospitalization, phenobarbital dose was rearranged and then he was discharged. At the second month of follow-up he was symptom free. CH has been safely used for sedation in the pediatric population because the dose range of CH in
childhood is large (25–100 mg/kg). After absorption, it is immediately converted to trichloroethanol, which is the active drug. Levels of trichloroethanol at which significant toxicity occurs have been variable (2,5). The chief manifestations of CH toxicity are due to central nervous system depressant action and its dysrhythmogenic potential. Classically, paradoxic excitation, respiratory depression, cyanosis, decreasing cardiac contractility, hypotension, hypothermia, stupor, and coma may be seen with CH toxicity (2,5,6). Aside from these, acute gastric perforation and even death have been reported after an overdose of chloral hydrate (7–9). Our patient ingested 1000 mg (250 mg/kg) of CH and first paradoxic excitation, respiratory distress, and excessive salivation were noted, and then respiratory depression and hypoxia developed. Management includes consideration of gastrointestinal decontamination, supportive care for altered mental status and treatment of dysrhythmias (2). Anyebuno and Rosenfeld have successfully used exchange transfusion in the management of chloral hydrate toxicity in a term infant (10). In our patient, gastrointestinal decontamination was not performed because we were not aware of CH toxicity in the first hours of intoxication. His abnormal findings improved with supportive therapy. We suggest that CH toxicity should be considered in infants who have received CH and then developed unexplained agitation, respiratory distress, and excessive salivation. Ercan Kirimi, MD Hu¨ seyin, C¸ aksen, MD Yasar Cesur, MD Dursun Odabas, MD ˜ zkaya, MD Emin O Nesrin Ceylan, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine PII S0736-4679(02)00425-5
This work has been carried out in the Department of Pediatrics, Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine, Van, Turkey.
REFERENCES 1. Greenberg SB, Faerber EN, Aspinall CL, Adams RC. High-dose chloral hydrate sedation for children undergoing MR imaging: safety and efficacy in relation to age. AJR 1993;161:639 – 41. 2. Pershad J, Palmisano P, Nichols M. Chloral hydrate:.the good and the bad. Pediatr Emerg Care 1999;15:432–5. ¨ ner A, Cesur Y, Abuhandan M, C¸ elebi V, S¸ ar S¸ . 3. C¸ aksen H, U
The Journal of Emergency Medicine
4. 5. 6. 7. 8. 9. 10.
Comparison of lytic cocktail, chloral hydrate and midazolam for pediatric sedation. J Trop Pediatr 2001;47:316. C¸ aksen H, Odabas¸ D. Skin and mucosal lesions in two children used chloral hydrate. Pediatr Dermatol 2001;18:(in press). Complete Drug Reference. United States Pharmacopeia, 1994th ed. New York: Yonkers; 1994:333– 6. Laptook AR, Rosenfeld CR. Chloral hydrate toxicity in a preterm infant. Pediatr Pharmacol 1984;4:161–5. Lee DC, Vassalluzzo C. Acute gastric perforation in a chloral hydrate overdose. Am J Emerg Med 1998;16:545– 6. Rabl W. Sudden death after consumption of chloral hydrate. Beitr Gerichtl Med 1992;50:131– 4. (Article in German). Cohen MR. Chloral hydrate overdoses implicated in deaths. Nursing 1993;23:25. Anyebuno MA, Rosenfeld CR. Chloral hydrate toxicity in a term infant. Dev Pharmacol Ther 1991;17:116 –20.
e Use of Sulfasalizine in the Treatment of Post Amebic Rectocolitis Amebiasis, endemic in eastern and southeastern regions of Turkey, is still a public health problem in our country. In amebiasis, clinical presentations range from asymptomatic cyst passage to amebic colitis, amebic dysentery, ameboma, and extraintestinal disease (1). Herein we present a child with post amebic rectocolitis who did not respond adequately to amebic treatment but was successfully treated with sulfasalizine. Our purpose is to emphasize the importance of sulfasalizine in the treatment of post amebic rectocolitis in childhood. A 5-year-old boy was admitted to the Emergency Department with a 20-day history of abdominal pain and mucous-bloody diarrhea. The personal and family history were unremarkable. Physical examination revealed a weight of 16 kg (10 –25th percentile) and a height of 106 cm (25th percentile). The vital signs were normal. Abdominal examination revealed nonlocalized diffuse pain and increased bowel sounds. He had no guarding, rebound, or distention. The remainder of physical findings were normal. On laboratory investigation, routine urine and blood analyses including sedimentation rate were normal with the exception of mild high leukocyte count (12,700/mL). Numerous motile trophozoites were observed in fresh stool sample examined with native-lugol method and hematoxylin staining. Stool culture revealed normal intestinal bacterial flora. The patient was hospitalized and metronidazole (50 mg/kg/day) was given for 10 days. However, his mucous-bloody diarrhea and trophozoites on stool examination did not disappear, so chloroquine (10 mg/kg/day) and erythromycin (50 mg/kg/day) were added to the treatment regimen. Eight days after initiation of this triple therapy regimen, stool examination was found to be normal for Entamoeba, but his diarrhea, including blood and mucous, did not improve. On the 24th day of triple therapy, lower gas-
105
trointestinal contrast examination was performed because of persisting mucous-bloody diarrhea. The contrast examination showed extensive loss of haustral markings in the sigmoid colon and rectum. Later, endoscopic examination was performed and biopsy was taken from the colon wall. Rectosigmoidoscopy showed numerous mucosal ulcers, particularly in the sigmoid colon. Histopathological examination of the biopsy specimen was compatible with chronic nonspecific colitis. Based on these findings, the patient was diagnosed with a post amebic rectocolitis and sulfasalizine (50 mg/kg/day) was initiated. On the 5th day of sulfasalizine his complaints dramatically resolved, and the triple therapy was discontinued. Sulfasalizine was given for 6 weeks. The patient was followed for 6 months and no recurrence was noted. It is well known that amebic colitis is improved with amebiasis therapy such as metronidazole or other nitroimidazoles, chloroquine, dehydroemetine, etc. without requiring an additional drug (1,2). However, we did not obtain any improvement in our patient despite triple therapy. In the literature we found that Chong et al used sulfasalazine in four children with non-specific colitis and the symptoms subsided in two of them (3). Sulfasalazine, a complex of sulfonamide, has been used extensively in chronic ulcerative colitis over many years, and its effects are well characterized (4). After reviewing the literature we decided to use sulfasalazine in our patient. It was given in a dose of 50 mg/kg/day over a period of 6 weeks as mentioned in the study of Chong et al, and we obtained a rapid cure with sulfasalazine treatment (3). Ercan Kırımi, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey Hu¨ seyin C¸ aksen, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey Yas¸ar Cesur, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey Abdullah Ceylan, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey
Chloral hydrate intoxication in a newborn infant
REFERENCES 1. Bergstein JM. Renal failure. In: Behrman RE, Kliegman RM, Jenson HB, eds. Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000:1605–12. 2. Sly M. Asthma. In: Behrman RE, Kliegman RM, Jenson HB, eds. Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000: 664 – 80.
e Chloral Hydrate Intoxication in a Newborn Infant Chloral hydrate (CH) is a sedative-hypnotic (general central nervous system depressant) agent, and it has been widely used for sedation in the pediatric population in numerous centers including our country (1– 4). Herein we report a newborn infant who accidentally ingested an overdose of CH, to draw attention to the importance of intoxication in newborn infants. A 28-day-old boy presented with a convulsion. He was the product of a 40-week term of gestation and labor. After the delivery, he had been hospitalized in another hospital with the diagnosis of perinatal asphyxia and given phenobarbital. During the hospitalization his general condition partially improved and he was discharged from hospital. However, his convulsions resumed at home and he was admitted to our clinic. The patient was hospitalized in order to investigate the etiology of the seizures and for management. The physical examination was normal. A computed tomography (CT) scan of the brain and electroencephalogram (EEG) were scheduled. In our clinic we routinely use oral CH (50 mg/kg/dose maximum 2 g) for sedation, and this was ordered. Thirty minutes after giving the CH, agitation, respiratory distress, and excessive salivation, lasting about 1 hour, were noted. Later, respiratory depression and hypoxia developed. Initially, we could not explain these abnormal clinical findings. Oral feeding was discontinued and he was monitored. Intravenous fluid and nasal oxygen were given. Serum glucose, calcium, electrolytes, renal and liver function tests were measured and all were found to be normal. A chest X-ray study was also normal. Seven hours after ingestion of CH his general condition gradually recovered and respiratory distress and hypoxia completely resolved. The patient was reevaluated and we established that CH was accidentally given in a dose of 250 mg/kg. Later, a CT scan and EEG were studied using another sedative, diazepam. While the CT scan was found to be normal, the EEG showed bilateral multifocal sharp and slow waves. During the hospitalization, phenobarbital dose was rearranged and then he was discharged. At the second month of follow-up he was symptom free. CH has been safely used for sedation in the pediatric population because the dose range of CH in
childhood is large (25–100 mg/kg). After absorption, it is immediately converted to trichloroethanol, which is the active drug. Levels of trichloroethanol at which significant toxicity occurs have been variable (2,5). The chief manifestations of CH toxicity are due to central nervous system depressant action and its dysrhythmogenic potential. Classically, paradoxic excitation, respiratory depression, cyanosis, decreasing cardiac contractility, hypotension, hypothermia, stupor, and coma may be seen with CH toxicity (2,5,6). Aside from these, acute gastric perforation and even death have been reported after an overdose of chloral hydrate (7–9). Our patient ingested 1000 mg (250 mg/kg) of CH and first paradoxic excitation, respiratory distress, and excessive salivation were noted, and then respiratory depression and hypoxia developed. Management includes consideration of gastrointestinal decontamination, supportive care for altered mental status and treatment of dysrhythmias (2). Anyebuno and Rosenfeld have successfully used exchange transfusion in the management of chloral hydrate toxicity in a term infant (10). In our patient, gastrointestinal decontamination was not performed because we were not aware of CH toxicity in the first hours of intoxication. His abnormal findings improved with supportive therapy. We suggest that CH toxicity should be considered in infants who have received CH and then developed unexplained agitation, respiratory distress, and excessive salivation. Ercan Kirimi, MD Hu¨ seyin, C¸ aksen, MD Yasar Cesur, MD Dursun Odabas, MD ˜ zkaya, MD Emin O Nesrin Ceylan, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine PII S0736-4679(02)00425-5
This work has been carried out in the Department of Pediatrics, Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine, Van, Turkey.
REFERENCES 1. Greenberg SB, Faerber EN, Aspinall CL, Adams RC. High-dose chloral hydrate sedation for children undergoing MR imaging: safety and efficacy in relation to age. AJR 1993;161:639 – 41. 2. Pershad J, Palmisano P, Nichols M. Chloral hydrate:.the good and the bad. Pediatr Emerg Care 1999;15:432–5. ¨ ner A, Cesur Y, Abuhandan M, C¸ elebi V, S¸ ar S¸ . 3. C¸ aksen H, U
The Journal of Emergency Medicine
4. 5. 6. 7. 8. 9. 10.
Comparison of lytic cocktail, chloral hydrate and midazolam for pediatric sedation. J Trop Pediatr 2001;47:316. C¸ aksen H, Odabas¸ D. Skin and mucosal lesions in two children used chloral hydrate. Pediatr Dermatol 2001;18:(in press). Complete Drug Reference. United States Pharmacopeia, 1994th ed. New York: Yonkers; 1994:333– 6. Laptook AR, Rosenfeld CR. Chloral hydrate toxicity in a preterm infant. Pediatr Pharmacol 1984;4:161–5. Lee DC, Vassalluzzo C. Acute gastric perforation in a chloral hydrate overdose. Am J Emerg Med 1998;16:545– 6. Rabl W. Sudden death after consumption of chloral hydrate. Beitr Gerichtl Med 1992;50:131– 4. (Article in German). Cohen MR. Chloral hydrate overdoses implicated in deaths. Nursing 1993;23:25. Anyebuno MA, Rosenfeld CR. Chloral hydrate toxicity in a term infant. Dev Pharmacol Ther 1991;17:116 –20.
e Use of Sulfasalizine in the Treatment of Post Amebic Rectocolitis Amebiasis, endemic in eastern and southeastern regions of Turkey, is still a public health problem in our country. In amebiasis, clinical presentations range from asymptomatic cyst passage to amebic colitis, amebic dysentery, ameboma, and extraintestinal disease (1). Herein we present a child with post amebic rectocolitis who did not respond adequately to amebic treatment but was successfully treated with sulfasalizine. Our purpose is to emphasize the importance of sulfasalizine in the treatment of post amebic rectocolitis in childhood. A 5-year-old boy was admitted to the Emergency Department with a 20-day history of abdominal pain and mucous-bloody diarrhea. The personal and family history were unremarkable. Physical examination revealed a weight of 16 kg (10 –25th percentile) and a height of 106 cm (25th percentile). The vital signs were normal. Abdominal examination revealed nonlocalized diffuse pain and increased bowel sounds. He had no guarding, rebound, or distention. The remainder of physical findings were normal. On laboratory investigation, routine urine and blood analyses including sedimentation rate were normal with the exception of mild high leukocyte count (12,700/mL). Numerous motile trophozoites were observed in fresh stool sample examined with native-lugol method and hematoxylin staining. Stool culture revealed normal intestinal bacterial flora. The patient was hospitalized and metronidazole (50 mg/kg/day) was given for 10 days. However, his mucous-bloody diarrhea and trophozoites on stool examination did not disappear, so chloroquine (10 mg/kg/day) and erythromycin (50 mg/kg/day) were added to the treatment regimen. Eight days after initiation of this triple therapy regimen, stool examination was found to be normal for Entamoeba, but his diarrhea, including blood and mucous, did not improve. On the 24th day of triple therapy, lower gas-
105
trointestinal contrast examination was performed because of persisting mucous-bloody diarrhea. The contrast examination showed extensive loss of haustral markings in the sigmoid colon and rectum. Later, endoscopic examination was performed and biopsy was taken from the colon wall. Rectosigmoidoscopy showed numerous mucosal ulcers, particularly in the sigmoid colon. Histopathological examination of the biopsy specimen was compatible with chronic nonspecific colitis. Based on these findings, the patient was diagnosed with a post amebic rectocolitis and sulfasalizine (50 mg/kg/day) was initiated. On the 5th day of sulfasalizine his complaints dramatically resolved, and the triple therapy was discontinued. Sulfasalizine was given for 6 weeks. The patient was followed for 6 months and no recurrence was noted. It is well known that amebic colitis is improved with amebiasis therapy such as metronidazole or other nitroimidazoles, chloroquine, dehydroemetine, etc. without requiring an additional drug (1,2). However, we did not obtain any improvement in our patient despite triple therapy. In the literature we found that Chong et al used sulfasalazine in four children with non-specific colitis and the symptoms subsided in two of them (3). Sulfasalazine, a complex of sulfonamide, has been used extensively in chronic ulcerative colitis over many years, and its effects are well characterized (4). After reviewing the literature we decided to use sulfasalazine in our patient. It was given in a dose of 50 mg/kg/day over a period of 6 weeks as mentioned in the study of Chong et al, and we obtained a rapid cure with sulfasalazine treatment (3). Ercan Kırımi, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey Hu¨ seyin C¸ aksen, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey Yas¸ar Cesur, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey Abdullah Ceylan, MD Department of Pediatrics Yu¨ zu¨ ncu¨ Yıl University Faculty of Medicine Van, Turkey