chelation therapy in iron poisoning

1
Abstracts 149 ingestion of 150 mg/kg or more of acetamino- phen or (2) plasma acetaminophen level in the potentially toxic range on the nomogram by Rumack and Matthew. Patients were given ap- propriate emergency care, including gastric as- piration and lavage without administration of charcoal or cathartics. Acetylcysteine was ad- ministered in a loading dose of 140 mg/kg fol- lowed by up to 17 additional doses of 70 mg/kg every four hours. Serum electrolytes, liver func- tion tests, and clotting studies were serially measured. Fifty-five patients had documented toxic acetaminophen levels. Only three of these patients developed SGOT levels consistent with hepatotoxic effects. All of these patients received their loading dose of acetylcysteine more than 16 hours after ingestion. Patients with toxic acet- aminophen levels who had also ingested alcohol had significantly lower SCOT levels than those who had not, suggesting a hepato-protective role of alcohol in these cases. Concomitant ingestion of other substances (anticholinergics, antihista- mines, codeine, and propoxyphene) with aceta- minophen was associated with an increased in- cidence of lethargy and higher transient SGOT elevation. The author concludes that acetamino- phen ingestion rarely causes serious consequences in the age group studied. Acetaminophen re- mains the safest antipyretic for children. [M. Jeff Slepin, MD] Editor’s Note: All emergency physicians should be thoroughly familiar with the management of known or suspected acetaminophen ingestion because of both the increasing number of prep- arations that contain it and the documented long-term hepatocellular damage it may pro- duce. Although this study provides reassurance for physicians and parents that the likelihood of deleterious consequences from acetaminophen ingestion in young children is low, this should not alter the ED physician’s rapid and aggressive management of these patients. U CHELATION THERAPY IN IRON Pot- SONING. Lovejoy FH Jr. J Tosicol: C/in Toxi- c-o/ 1983; 19:871-874. This article reviews iron poisoning with par- ticular attention to treatment with high-dose intravenous deferoxamine. Toxicity of iron poi- soning occurs once plasma transferrin is satu- rated and serum iron exceeds the iron-binding capacity. Free iron damages blood vessels and is particularly toxic to the liver, kidney, lungs, and heart. Electron microscopic studies localize iron to the mitochondrial membrane where, in toxic amounts, the Krebs cycle is substantially affected. Deferoxamine is a highly specific che- lator of iron and is the treatment of choice for iron overdose. It binds to free ferric iron circu- lating in the plasma; it has little effect on trans- ferrin or hemoglobin-bound iron. Recent studies indicate that deferoxamine also works intracel- lularly, binding ferritin iron in the hepatocyte. Toxicity of deferoxamine includes hypotension and gastrointestinal discomfort. Continuous in- travenous dosing of deferoxamine appears most efficacious with an initial dose of approximate11 15 mg/kg/h; total daily dose should not exceed 8 g. Subsequent reduction in dose should follow as the iron level falls below the iron-binding ca- pacity. Although the optimal length of therapy has not been well defined, one suggestion is to continue treatment for 24 hours following dis- appearance of the “vin rose color” in the urine. [Evan T. Wythe, MD] Editor’s Note: The emergency physician should remember that iron causes a visible bezoar on ab- dominal x-ray study. Persistence in lavage un- til the visible iron disappears is mandatory. On rare occasions it may be necessary to remove the iron surgically, as persistence can lead to mas- sive Gl hemorrhage. This should not preclude simultaneous treatment of toxic serum levels. I; COMPARISON OF CEFACLOR AhI) TRIMETHOPRIM-SL’LFAMETHOAZ0L.k: IN THE TREATMENT OF ACUTE OTITIS MEDIA. Blumer JL. Bertino JS Jr. Hujah \lP. PeclirrtsIt~,f>c~r Dis 1984; 3125-29. The author9 of thi$ propecti\c \~ucly C‘OIW pare the efficacy and safet!, of cefaclor and tri- tncthorprim-sulfamethosazole (TRIP-SMX) in the treatmenl of acute otitis media in children. Enrolled in the study \\ere 100 patients; 50 pa- ticnts were randomized into each group. Diag- nostic tympanozentesis \\as performed on all pa- tient5; the aspirate was cultured for aerobc\. Antibiotic therapy \bas prescribed for IO day’. Cefaclor \\a$ administered in a dose ol’ 10 mg/kg/day in three doses; TMP-SMX in a dos- age of 8 mg TMP per kilogram per day; and 40 mg SM?< per kilogram per day in two dosc$. The most common pathogen isolated in each group was S~reptocvmrs pneumoniae. Hemophihs it?- ,fluexye was the second most common organism isolated in the TMP-SMX group and S’lrep/o- coccusp_vovogenes in the cefaclor group. After IO day5 of therapy 46 of the 50 patients treated with

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Page 1: Chelation therapy in iron poisoning

Abstracts 149

ingestion of 150 mg/kg or more of acetamino- phen or (2) plasma acetaminophen level in the potentially toxic range on the nomogram by Rumack and Matthew. Patients were given ap- propriate emergency care, including gastric as- piration and lavage without administration of charcoal or cathartics. Acetylcysteine was ad- ministered in a loading dose of 140 mg/kg fol- lowed by up to 17 additional doses of 70 mg/kg every four hours. Serum electrolytes, liver func- tion tests, and clotting studies were serially measured. Fifty-five patients had documented toxic acetaminophen levels. Only three of these patients developed SGOT levels consistent with hepatotoxic effects. All of these patients received their loading dose of acetylcysteine more than 16 hours after ingestion. Patients with toxic acet- aminophen levels who had also ingested alcohol had significantly lower SCOT levels than those who had not, suggesting a hepato-protective role of alcohol in these cases. Concomitant ingestion of other substances (anticholinergics, antihista- mines, codeine, and propoxyphene) with aceta- minophen was associated with an increased in- cidence of lethargy and higher transient SGOT elevation. The author concludes that acetamino- phen ingestion rarely causes serious consequences in the age group studied. Acetaminophen re- mains the safest antipyretic for children.

[M. Jeff Slepin, MD]

Editor’s Note: All emergency physicians should be thoroughly familiar with the management of known or suspected acetaminophen ingestion because of both the increasing number of prep- arations that contain it and the documented long-term hepatocellular damage it may pro- duce. Although this study provides reassurance for physicians and parents that the likelihood of deleterious consequences from acetaminophen ingestion in young children is low, this should not alter the ED physician’s rapid and aggressive management of these patients.

U CHELATION THERAPY IN IRON Pot- SONING. Lovejoy FH Jr. J Tosicol: C/in Toxi- c-o/ 1983; 19:871-874.

This article reviews iron poisoning with par- ticular attention to treatment with high-dose intravenous deferoxamine. Toxicity of iron poi- soning occurs once plasma transferrin is satu- rated and serum iron exceeds the iron-binding capacity. Free iron damages blood vessels and is particularly toxic to the liver, kidney, lungs, and heart. Electron microscopic studies localize

iron to the mitochondrial membrane where, in toxic amounts, the Krebs cycle is substantially affected. Deferoxamine is a highly specific che- lator of iron and is the treatment of choice for iron overdose. It binds to free ferric iron circu- lating in the plasma; it has little effect on trans- ferrin or hemoglobin-bound iron. Recent studies indicate that deferoxamine also works intracel- lularly, binding ferritin iron in the hepatocyte. Toxicity of deferoxamine includes hypotension and gastrointestinal discomfort. Continuous in- travenous dosing of deferoxamine appears most efficacious with an initial dose of approximate11 15 mg/kg/h; total daily dose should not exceed 8 g. Subsequent reduction in dose should follow as the iron level falls below the iron-binding ca- pacity. Although the optimal length of therapy has not been well defined, one suggestion is to continue treatment for 24 hours following dis- appearance of the “vin rose color” in the urine.

[Evan T. Wythe, MD]

Editor’s Note: The emergency physician should remember that iron causes a visible bezoar on ab- dominal x-ray study. Persistence in lavage un- til the visible iron disappears is mandatory. On rare occasions it may be necessary to remove the iron surgically, as persistence can lead to mas- sive Gl hemorrhage. This should not preclude simultaneous treatment of toxic serum levels.

I; COMPARISON OF CEFACLOR AhI) TRIMETHOPRIM-SL’LFAMETHOAZ0L.k: IN THE TREATMENT OF ACUTE OTITIS MEDIA. Blumer JL. Bertino JS Jr. Hujah \lP. Peclirrts It~,f>c~r Dis 1984; 3125-29.

The author9 of thi$ propecti\c \~ucly C‘OIW pare the efficacy and safet!, of cefaclor and tri- tncthorprim-sulfamethosazole (TRIP-SMX) in the treatmenl of acute otitis media in children. Enrolled in the study \\ere 100 patients; 50 pa- ticnts were randomized into each group. Diag- nostic tympanozentesis \\as performed on all pa- tient5; the aspirate was cultured for aerobc\. Antibiotic therapy \bas prescribed for IO day’. Cefaclor \\a$ administered in a dose ol’ 10 mg/kg/day in three doses; TMP-SMX in a dos- age of 8 mg TMP per kilogram per day; and 40 mg SM?< per kilogram per day in two dosc$. The most common pathogen isolated in each group was S~reptocvmrs pneumoniae. Hemophihs it?- ,fluexye was the second most common organism isolated in the TMP-SMX group and S’lrep/o- coccusp_vovogenes in the cefaclor group. After IO day5 of therapy 46 of the 50 patients treated with