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Management of a child with acute thyroxine ingestion
CASE REPORT drug, ingestion, thyroxine; thyroxine, ingestion, pediatric
Management of a Child with Acute Thyroxine Ingestion We report a case of thyroxine overdose in a child. Despite extremely high thyroxine (T4RIA) levels on admission, the patient's only symptoms were mild hypertension and tachycardia. Both symptoms responded to propranoloi, with a drop in pulse rate and a decrease in blood pressure to normal levels. After four days of cardiac monitoring, the patient was released and received propranolol for five additional days as an outpatient. [Roesch C, Becker PG, Sklar S: Management of a child with acute thyroxine ingestion. Ann Emerg Med November 1985;14:1114-1115.] INTRODUCTION Acute ingestion of excess levothyroxine is gaining notice in the medical literature. TM Despite c o m m o n use of this drug, overdoses in children have not been reported frequently. We report a case of excess ingestion in a 22-month-old child resulting in u n c o m m o n l y high T4RIA levels and a benign clinical course. The roles of propranolol and other counteracting drugs are discussed.
Charles Roesch, MD, PhD Patricia G Becker, MD Stephen Sklar, PharmD Indianapolis, Indiana From the St Vincent Hospital and Health Care Center, Indianapolis, Indiana. Received for publication December 17, 1984. Revision received April 16, 1985. Accepted for publication July 8, 1985. Address for reprints: Patricia G Becker, MD, St Vincent Hospital and Health Care Center, Department of Pediatrics, 2001 West 86th Street, Indianapolis, Indiana 46260.
CASE REPORT
A 22-month-old boy weighing 12.7 kg was admitted after ingesting 38 Synthroid ® (sodium levothyroxine) tablets (0.15 mg each). In the ED 15 mL syrup of ipecac was given 30 and 60 minutes after ingestion, resulting in emesis. One tablet was recovered. An IV line of D s V2 normal saline at 25 mL per hour was begun. Treatment continued with activated charcoal and magnesium citrate, yielding some bowel evacuation. The child's vital signs were as follows: blood pressure, 110/50 m m Hg; pulse, 136; temperature, 36.7 C; and respirations, 20. There was a grade 2/6 systolic ejection m u r m u r at the midleft sternal border that had not been heard at previous examinations in the private physician's office. The level of T4RIA drawn in the ED was 90 ~g/dL (normal values, 5.1 to 12.8 ~g/dL). The report initially was available ten hours after admission. Because the value was so high, the result was reconfirmed with repeated testings. The patient was placed on a cardiac monitor in the intensive care unit, with the IV line continuing to infuse. Six hours after ingestion, monitoring revealed several six-second runs of junctional bradycardia at a rate of 60 and one premature junctional beat. A 12-lead ECG showed only a tachycardia at a rate of 150. Twenty-four hours after ingestion, the serum T4RIA level had dropped to 73 ~g/dL. The blood pressure was 110/60 m m Hg and the heart rate was 147. Because there was little clinical change in the patient during the previous 24 hours, propranolol 10 mg orally every eight hours was initiated. After two doses the patient's blood pressure was 90/50 m m Hg and the heart rate was 120. The m u r m u r disappeared after two days on propranolol. T4RIA levels on days 2, 3, and 4 postingestion were 53, 42, and 40 ~g/dL, respectively. The patient was discharged on day 5. Propranolol 10 mg every eight hours, was continued orally for another week. The patient was seen the following week with normal blood pressure and pulse. Because he remained clinically stable, no further T4RIA levels were done. DISCUSSION
During the past 25 years there have been few reports concerning the man-
14:11 November 1985
Annals of Emergency Medicine
1114/117
ACUTE THYROXINE INGESTION Roesch, Becker & Sklar
agement of acute thyroxine ingestion. Recently Lehrner and Weir 4 reported their success with two cases. Despite the frequent use of Synthroid ®, only 11 such cases have been described, making medical management guidelines scarce. Lehmer based his treatment on review of the literature. In one instance he used the customary gastric lavage, activated charcoal, and m a g n e s i u m citrate. This was followed by administration of propranolol. The patient's peak T4RIA level was 37.8 txg/dL. The second patient, who was treated m u c h more aggressively, received customary treatment followed by administration of propranolol, propylthiouracil, and cholestyramine. Nineteen hours later the thyroxine level remained elevated at 28.6 ixg/dL. Because of a few reports of delayed toxicity,I, 5 Lehrner chose to treat the patient further with charcoal hemoperfusion. A t 22 hours post ingestion, just before initiating the hemoperfusion, the thyroxine level peaked at 35.1 ~g/dL. Both of Lehrner's patients remained a s y m p t o m a t i c during t r e a t m e n t except for mild tachycardias. This is similar to our patient. These high levels of thyroxine in the absence of serious toxicity add to an earlier report of a 3-year-old child who swallowed 13.2 mg levothyroxine and developed a protein-bound iodine level of 89 ~xg/100 mL (approximately equal to 115 ~g/100 mL thyroxine). 1 T h a t child also e x p e r i e n c e d m i l d tachycardia but no other acute symp-
118/1115
tomatology. This contrasts with the case of a 51-year-old w o m a n who ingested an overdose of thyroid tablets and developed hyperpyrexia, atrial fibrillation, and coma despite a m u c h lower protein-bound iodine level of 24.8 Ixg/100 mL. 2 Lehrner recommends the following for thyroxine ingestions: 1) gastric lavage, emesis, and the use of activated charcoal to decrease absorption; 2) cholestyramine to bind thyroid horm o n e s ; 3) p r e d n i s o n e a n d / o r propylthiouracil to decrease peripheral conversion of T 4 to T3; and 4) propranolol to block metabolic effects of thyroid hormones. He speculated that charcoal h e m o p e r f u s i o n was inadequate because exogenous thyroid hormones were bound tightly to plasma proteins. Consequently the charcoal appeared to absorb little T 3 or T 4. For deterioration unresponsive to these measures, Lehrner recommended exchange transfusion. 6 He believed that the majority of thyroid hormone removed from the circulation occurred with the partial exchange transfusion performed with each change of charcoal units. We also advocate the use of propran0101. Lehmer used 20 mg propranolol e v e r y six h o u r s . O u r p a t i e n t responded to propranolol 10 mg every eight hours with a drop in pulse rate and blood pressure. It also is advisable to observe patients w i t h levothyroxine ingestion for several days. The potential exists for the T 4 to be monodeiodinated to T 3 or to reverse T&. T 3 has three to
Annals of Emergency Medicine
four times the metabolic potency of T4; rT 3 is largely inactive metabolically.7
SUMMARY Although an asymptomatic state in a child following thyroxine ingestion m i g h t encourage i m m e d i a t e release from the ED, serum T4RIA levels can be quite revealing and do not always correlate with the degree of toxicity.
The authors express their appreciation to Bertram Roth, MD, for his help.
REFERENCES 1. Funderburk SJ, Spaulding JS: Sodium levothyroxine (Synthroid R) intoxication in a child. Pediatrics 1970;45:298-301. 2. Schottstaedt ES, Smoller M: "Thyroid Storm i' produced by acute thyroid hormone poisoning. Ann Intern Med 1966; 64:847-849. 3. Levy RP, Gilger WG: Acute thyroid poisoning, report of a case. N e w Engl [ Med 1957;256:459-466. 4. Lehrner LM, Weir MR: Acute ingestions of thyroid hormones. Pediatrics 1984;73:313-317. 5. Von Hole SE, Young RL: Thyrotoxicosis after a single ingestion of levothyroxine. JAMA 1977;237:1361. 6. Gerard P, Malvaux P, deVisscher M: Accidental poisoning with thyroid extract treated by exchange transfusion. Arch Dis Child 1972;47:981-982. 7. Rudolph A (ed): Pediatrics. New York, Appleton-Century-Crofts, 1977, p 1667.
14:11 November1985
Management of a Child with Acute Thyroxine Ingestion We report a case of thyroxine overdose in a child. Despite extremely high thyroxine (T4RIA) levels on admission, the patient's only symptoms were mild hypertension and tachycardia. Both symptoms responded to propranoloi, with a drop in pulse rate and a decrease in blood pressure to normal levels. After four days of cardiac monitoring, the patient was released and received propranolol for five additional days as an outpatient. [Roesch C, Becker PG, Sklar S: Management of a child with acute thyroxine ingestion. Ann Emerg Med November 1985;14:1114-1115.] INTRODUCTION Acute ingestion of excess levothyroxine is gaining notice in the medical literature. TM Despite c o m m o n use of this drug, overdoses in children have not been reported frequently. We report a case of excess ingestion in a 22-month-old child resulting in u n c o m m o n l y high T4RIA levels and a benign clinical course. The roles of propranolol and other counteracting drugs are discussed.
Charles Roesch, MD, PhD Patricia G Becker, MD Stephen Sklar, PharmD Indianapolis, Indiana From the St Vincent Hospital and Health Care Center, Indianapolis, Indiana. Received for publication December 17, 1984. Revision received April 16, 1985. Accepted for publication July 8, 1985. Address for reprints: Patricia G Becker, MD, St Vincent Hospital and Health Care Center, Department of Pediatrics, 2001 West 86th Street, Indianapolis, Indiana 46260.
CASE REPORT
A 22-month-old boy weighing 12.7 kg was admitted after ingesting 38 Synthroid ® (sodium levothyroxine) tablets (0.15 mg each). In the ED 15 mL syrup of ipecac was given 30 and 60 minutes after ingestion, resulting in emesis. One tablet was recovered. An IV line of D s V2 normal saline at 25 mL per hour was begun. Treatment continued with activated charcoal and magnesium citrate, yielding some bowel evacuation. The child's vital signs were as follows: blood pressure, 110/50 m m Hg; pulse, 136; temperature, 36.7 C; and respirations, 20. There was a grade 2/6 systolic ejection m u r m u r at the midleft sternal border that had not been heard at previous examinations in the private physician's office. The level of T4RIA drawn in the ED was 90 ~g/dL (normal values, 5.1 to 12.8 ~g/dL). The report initially was available ten hours after admission. Because the value was so high, the result was reconfirmed with repeated testings. The patient was placed on a cardiac monitor in the intensive care unit, with the IV line continuing to infuse. Six hours after ingestion, monitoring revealed several six-second runs of junctional bradycardia at a rate of 60 and one premature junctional beat. A 12-lead ECG showed only a tachycardia at a rate of 150. Twenty-four hours after ingestion, the serum T4RIA level had dropped to 73 ~g/dL. The blood pressure was 110/60 m m Hg and the heart rate was 147. Because there was little clinical change in the patient during the previous 24 hours, propranolol 10 mg orally every eight hours was initiated. After two doses the patient's blood pressure was 90/50 m m Hg and the heart rate was 120. The m u r m u r disappeared after two days on propranolol. T4RIA levels on days 2, 3, and 4 postingestion were 53, 42, and 40 ~g/dL, respectively. The patient was discharged on day 5. Propranolol 10 mg every eight hours, was continued orally for another week. The patient was seen the following week with normal blood pressure and pulse. Because he remained clinically stable, no further T4RIA levels were done. DISCUSSION
During the past 25 years there have been few reports concerning the man-
14:11 November 1985
Annals of Emergency Medicine
1114/117
ACUTE THYROXINE INGESTION Roesch, Becker & Sklar
agement of acute thyroxine ingestion. Recently Lehrner and Weir 4 reported their success with two cases. Despite the frequent use of Synthroid ®, only 11 such cases have been described, making medical management guidelines scarce. Lehmer based his treatment on review of the literature. In one instance he used the customary gastric lavage, activated charcoal, and m a g n e s i u m citrate. This was followed by administration of propranolol. The patient's peak T4RIA level was 37.8 txg/dL. The second patient, who was treated m u c h more aggressively, received customary treatment followed by administration of propranolol, propylthiouracil, and cholestyramine. Nineteen hours later the thyroxine level remained elevated at 28.6 ixg/dL. Because of a few reports of delayed toxicity,I, 5 Lehrner chose to treat the patient further with charcoal hemoperfusion. A t 22 hours post ingestion, just before initiating the hemoperfusion, the thyroxine level peaked at 35.1 ~g/dL. Both of Lehrner's patients remained a s y m p t o m a t i c during t r e a t m e n t except for mild tachycardias. This is similar to our patient. These high levels of thyroxine in the absence of serious toxicity add to an earlier report of a 3-year-old child who swallowed 13.2 mg levothyroxine and developed a protein-bound iodine level of 89 ~xg/100 mL (approximately equal to 115 ~g/100 mL thyroxine). 1 T h a t child also e x p e r i e n c e d m i l d tachycardia but no other acute symp-
118/1115
tomatology. This contrasts with the case of a 51-year-old w o m a n who ingested an overdose of thyroid tablets and developed hyperpyrexia, atrial fibrillation, and coma despite a m u c h lower protein-bound iodine level of 24.8 Ixg/100 mL. 2 Lehrner recommends the following for thyroxine ingestions: 1) gastric lavage, emesis, and the use of activated charcoal to decrease absorption; 2) cholestyramine to bind thyroid horm o n e s ; 3) p r e d n i s o n e a n d / o r propylthiouracil to decrease peripheral conversion of T 4 to T3; and 4) propranolol to block metabolic effects of thyroid hormones. He speculated that charcoal h e m o p e r f u s i o n was inadequate because exogenous thyroid hormones were bound tightly to plasma proteins. Consequently the charcoal appeared to absorb little T 3 or T 4. For deterioration unresponsive to these measures, Lehrner recommended exchange transfusion. 6 He believed that the majority of thyroid hormone removed from the circulation occurred with the partial exchange transfusion performed with each change of charcoal units. We also advocate the use of propran0101. Lehmer used 20 mg propranolol e v e r y six h o u r s . O u r p a t i e n t responded to propranolol 10 mg every eight hours with a drop in pulse rate and blood pressure. It also is advisable to observe patients w i t h levothyroxine ingestion for several days. The potential exists for the T 4 to be monodeiodinated to T 3 or to reverse T&. T 3 has three to
Annals of Emergency Medicine
four times the metabolic potency of T4; rT 3 is largely inactive metabolically.7
SUMMARY Although an asymptomatic state in a child following thyroxine ingestion m i g h t encourage i m m e d i a t e release from the ED, serum T4RIA levels can be quite revealing and do not always correlate with the degree of toxicity.
The authors express their appreciation to Bertram Roth, MD, for his help.
REFERENCES 1. Funderburk SJ, Spaulding JS: Sodium levothyroxine (Synthroid R) intoxication in a child. Pediatrics 1970;45:298-301. 2. Schottstaedt ES, Smoller M: "Thyroid Storm i' produced by acute thyroid hormone poisoning. Ann Intern Med 1966; 64:847-849. 3. Levy RP, Gilger WG: Acute thyroid poisoning, report of a case. N e w Engl [ Med 1957;256:459-466. 4. Lehrner LM, Weir MR: Acute ingestions of thyroid hormones. Pediatrics 1984;73:313-317. 5. Von Hole SE, Young RL: Thyrotoxicosis after a single ingestion of levothyroxine. JAMA 1977;237:1361. 6. Gerard P, Malvaux P, deVisscher M: Accidental poisoning with thyroid extract treated by exchange transfusion. Arch Dis Child 1972;47:981-982. 7. Rudolph A (ed): Pediatrics. New York, Appleton-Century-Crofts, 1977, p 1667.
14:11 November1985