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Rate of absorption of iron from chewable tablets
iodine adsorb to activated charcoal. The in vitro findings for arsenic, bromide, and silver have not been reported in the literature. There is documented in vitro analysis of iodine, mercuric chloride, and boric acid with results similar to those reported in our study. In vitro Studies may vary significantly from in v i v o findings, therefore, in vivo research should be used to guide clinical practices. When this is not possible due to the impracticality of the toxin being studied, current in vitro work should guide our recommendations for activated charcoal use.
47 Activated Charcoal and Sodium Polystyrene Sulfonate (Kayexalate ®) in Gastric Decontamination for Lithium Intoxication: An Animal Model JG Linakis, PG Lacouture, MS Eisenberg, TJ Maher, WJ Lewander, JL Driscoll, AD Woolf/Division of Emergency Medicine, The Children's Hospital; Massachusetts Poison Control System; Massachusetts College of Pharmacy, Boston; Department of Pediatrics, Rhode Island Hospital; The Rhode Island Poison Center, Providence To determine whether sodium polystyrene sulfonate is effective in decreasing the absorption of lithium and to test the assumption that lithium is poorly adsorbed by activated charcoal, 128 mice were administered an orogastric dose of lithium chloride (250 mg/ kg) followed immediately by orogastric sodium polystyrene Sulfonate (10 g/kg SPS group), activated charcoal (8.68 g/kg, AC group), or water in an equivalent volume (control group). Subgroups of each of the three groups were sacrificed at one, two, four, and eight hours after treatment and serum analyzed for lithium concentration.
Time After=LithiumAdministration(hr) 1 2 4 8 Control (Lithium mEq/L) 2.69 Activated charcoal (Lithium mEq/L) 2.51 Sodium polystyrene sulfonate (lithium, mEq/L) 1.63 P (Sodium polystyrene Sulfonate versus control) < .01 P (Sodium polystyrene sulfonate versus activated charcoal) < .01
1.75
1.36
1.26
1.74
1.83
1.06
1.04
0.57
0.76
< .01
< .01
< .01
< .01
< .01
< .05
Statistical analysis revealed no overall difference between the AC group and the control groups; however, the SPS group differed from both the control and the AC groups at each time interval, with lithium concentrations significantly lower in the SPS group. These results demonstrate that sodium polystyrene sutfonate effectively reduces the systemic absorption of lithium in an in v i v o model, and that lithium is not effectively bound by activated charcoal.
48 Rate of Absorption of Iron From Chewable Tablets CS Hornfeldt, JP Winter, LJ Ling/Hennepin Regional Poison Center, Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, Minnesota The treatment of iron poisonings (11,846, 71% chewable form, 1987) is based on serum iron levels. The literature offers many times for drawing levels, from two to six hours, based on adult tablets such as ferrous sulfate. The iron from such tablets is slowly and erratically absorbed. Because the ability to draw a single iron level would mean savings in laboratory tests and emergency time, we hypothesized that iron from chewable vitamins is readily absorbed and an optimal drawing time for a single serum iron level can be determined. Healthy, fasted adults chewed and ingested 10 and 5 mg/kg of iron in a chewable vitamin form in two separate studies. Iron levels were drawn serially over eight to 12 hours. At 10 and 5 mg/kg, the average peak was 321.2 and 243.4 gg/dL, with mean time to peak at 270.0 minutes (4.5 hours) and 252.0 minutes (4.2 hours). Student's t test for paired data showed mean times to peak to not be significantly different (P >. 1). Mean initial total ironbinding capacities were 334.2 and 332.4. Iron absorbed after chewable vitamin ingestion reached maximum levels four to five hours after ingestion, and a three-hour level was within 90% and 94% of peak, respectively. All subjects had moderate symptoms. A single serum iron level after four hours gives a strong indication of whether toxicity may occur when moderate amounts of iron have been ingested.
49 Clonidine Poisoning in Young Children JF Wiley//, C Wiley, S Torrey, F Henretig/Departments of Pediatrics, Children's Hospital of Philadelphia and St Christopher's Hospital for Children, Philadelphia, Pennsylvania 18:4 April 1989
Case reports of clonidine ingestions suggest that such patients usually need intensive care. We reviewed 47 consecutive cases. Mean age of patients was 27 _+ 16 months (range, 9 to 84 months). The average time from ingestion to symptoms was 52 minutes with 75 % of patients displaying symptoms within one hour of ingestion. Delayed progression of symptoms did not occur, and duration of symptoms was 9.5 + 5.5 hours. Average length of stay was 33 _+ 11 hours. Depressed sensorium occurred in 94% of patients, and bradycardia, hypotension, or hypertension was seen in 79% of patients. Over one third of patients had apnea or depressed respirations. Therapy included supportive care (endotracheal intubation in 13 % ), gastric emptying (ipecac 38 % ), naloxone (40 %; dose range, .008 to .22 mg/kg), atropine ( 15 %), and dopamine (2%). Naloxone caused transient improvement in 13 of 19 patients. Three patients who responded later required intubation, and in three others, naloxone was associated with hypertension. Clonidine can cause major neurologic and cardiopulmonary effects. Ipecac is contraindicated due to rapid onset of lethargy. Naloxone is a poor antidote for clonidine and may induce hypertension. Few patients require ventilatory or pressor support.
50 DimethyI-PGE 2 Prolongs Survival From Alpha Amanitin EA Miche/son, SM Schneider/Montefiore Hospital, University of Pittsburgh Alpha amanitin (A) is the toxin believed responsible for deaths from ingestion of the toxic mushroom A m a n i t a phalloides. 1,16Dimethyl-PGE2 (PGE) is a prostaglandin with known hepatic cytoprotective effects against several toxins. The protective mechanism is uncertain. We investigated the effect of PGE on toxicity of A in our mouse model. Swiss female mice were divided into five groups and treated with A 0.63 mg/kg intraperitoneally. Group 1 received no further therapy while groups 2 through 5 received PGE 150 gg/kg intraperitoneally after delays of one and one half, two, three, and five hours from A injection. A sixth group received only PGE. Animals were given free access to food and water and followed daily for survival to one week. Survival data were analyzed by Kaplan-Meier and Breslow tests. There were no deaths in the PGE control group, and 18 of 20 (90%) deaths in the A control group. Only the mice in group 5 (five-hour delay until injection) experienced an increase in survival (P < .01). PGE failed to increase survival when given within three hours of A; however, it was effective after a delay of five hours. PGE presumably has a short half-life and is no longer effective two to three hours after administration. Our data suggest A toxicity is delayed due to either delayed absorption or time necessary for toxic conversion. We conclude that a single dose of 1,16-dimethyl-PGE~ prolongs survival after exposure to alpha amanitin in our mouse model, but only if given following a delay of five hours.
51 Empiric Use of Naloxone in Patients With Altered Mental Status: A Reappraisal JR Hoffman, JS Luol D Schriger/Emergency Medicine Center, UCLA Medical Center, Los Angeles, California This study was performed to test the hypothesis that the majority of opiate overdose patients with altered mental status can be identified by clinical signs and symptoms, and that empiric use of naloxone in all patients with altered mental status is therefore unnecessary, as well as extremely costly. We reviewed records of 730 patients who received naloxone for acute altered mental status. Only 25 patients (3.4%) had a complete response to this agent; 19 (76%) had a final hospital diagnosis of opiate overdose. Of these 19 patients, 18 (95%) had respiratory rates less than or equal to 12; 17 (90%) had constricted pupils; and 15 (79%) had a known history of drug abuse. These numbers were vastly different (P < .01 for all comparisons) for the great majority of patients who neither responded to .naloxone nor had an ultimate diagnosis of opiate overdose. Six "complete responders" proved not to have opiate overdose; their assumed response was frequently due to spontaneous improvement during a postictal period. Partial or questionable response to naloxone also confused the diagnosis in 32 patients, none of whom proved to have opiate overdose, and only ten of whom had any clinical indicators or possible opiate use. Selective use of naloxone in patients in this series on the basis of easily defined clinical characteristics would have identified virtually all responders with opiate overdose and decreased use of the drug by 89%. Economic savings associated with widespread adoption of such a policy would be enormous with no apparent clinical detri-
Annals of Emergency Medicine
445/165
47 Activated Charcoal and Sodium Polystyrene Sulfonate (Kayexalate ®) in Gastric Decontamination for Lithium Intoxication: An Animal Model JG Linakis, PG Lacouture, MS Eisenberg, TJ Maher, WJ Lewander, JL Driscoll, AD Woolf/Division of Emergency Medicine, The Children's Hospital; Massachusetts Poison Control System; Massachusetts College of Pharmacy, Boston; Department of Pediatrics, Rhode Island Hospital; The Rhode Island Poison Center, Providence To determine whether sodium polystyrene sulfonate is effective in decreasing the absorption of lithium and to test the assumption that lithium is poorly adsorbed by activated charcoal, 128 mice were administered an orogastric dose of lithium chloride (250 mg/ kg) followed immediately by orogastric sodium polystyrene Sulfonate (10 g/kg SPS group), activated charcoal (8.68 g/kg, AC group), or water in an equivalent volume (control group). Subgroups of each of the three groups were sacrificed at one, two, four, and eight hours after treatment and serum analyzed for lithium concentration.
Time After=LithiumAdministration(hr) 1 2 4 8 Control (Lithium mEq/L) 2.69 Activated charcoal (Lithium mEq/L) 2.51 Sodium polystyrene sulfonate (lithium, mEq/L) 1.63 P (Sodium polystyrene Sulfonate versus control) < .01 P (Sodium polystyrene sulfonate versus activated charcoal) < .01
1.75
1.36
1.26
1.74
1.83
1.06
1.04
0.57
0.76
< .01
< .01
< .01
< .01
< .01
< .05
Statistical analysis revealed no overall difference between the AC group and the control groups; however, the SPS group differed from both the control and the AC groups at each time interval, with lithium concentrations significantly lower in the SPS group. These results demonstrate that sodium polystyrene sutfonate effectively reduces the systemic absorption of lithium in an in v i v o model, and that lithium is not effectively bound by activated charcoal.
48 Rate of Absorption of Iron From Chewable Tablets CS Hornfeldt, JP Winter, LJ Ling/Hennepin Regional Poison Center, Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, Minnesota The treatment of iron poisonings (11,846, 71% chewable form, 1987) is based on serum iron levels. The literature offers many times for drawing levels, from two to six hours, based on adult tablets such as ferrous sulfate. The iron from such tablets is slowly and erratically absorbed. Because the ability to draw a single iron level would mean savings in laboratory tests and emergency time, we hypothesized that iron from chewable vitamins is readily absorbed and an optimal drawing time for a single serum iron level can be determined. Healthy, fasted adults chewed and ingested 10 and 5 mg/kg of iron in a chewable vitamin form in two separate studies. Iron levels were drawn serially over eight to 12 hours. At 10 and 5 mg/kg, the average peak was 321.2 and 243.4 gg/dL, with mean time to peak at 270.0 minutes (4.5 hours) and 252.0 minutes (4.2 hours). Student's t test for paired data showed mean times to peak to not be significantly different (P >. 1). Mean initial total ironbinding capacities were 334.2 and 332.4. Iron absorbed after chewable vitamin ingestion reached maximum levels four to five hours after ingestion, and a three-hour level was within 90% and 94% of peak, respectively. All subjects had moderate symptoms. A single serum iron level after four hours gives a strong indication of whether toxicity may occur when moderate amounts of iron have been ingested.
49 Clonidine Poisoning in Young Children JF Wiley//, C Wiley, S Torrey, F Henretig/Departments of Pediatrics, Children's Hospital of Philadelphia and St Christopher's Hospital for Children, Philadelphia, Pennsylvania 18:4 April 1989
Case reports of clonidine ingestions suggest that such patients usually need intensive care. We reviewed 47 consecutive cases. Mean age of patients was 27 _+ 16 months (range, 9 to 84 months). The average time from ingestion to symptoms was 52 minutes with 75 % of patients displaying symptoms within one hour of ingestion. Delayed progression of symptoms did not occur, and duration of symptoms was 9.5 + 5.5 hours. Average length of stay was 33 _+ 11 hours. Depressed sensorium occurred in 94% of patients, and bradycardia, hypotension, or hypertension was seen in 79% of patients. Over one third of patients had apnea or depressed respirations. Therapy included supportive care (endotracheal intubation in 13 % ), gastric emptying (ipecac 38 % ), naloxone (40 %; dose range, .008 to .22 mg/kg), atropine ( 15 %), and dopamine (2%). Naloxone caused transient improvement in 13 of 19 patients. Three patients who responded later required intubation, and in three others, naloxone was associated with hypertension. Clonidine can cause major neurologic and cardiopulmonary effects. Ipecac is contraindicated due to rapid onset of lethargy. Naloxone is a poor antidote for clonidine and may induce hypertension. Few patients require ventilatory or pressor support.
50 DimethyI-PGE 2 Prolongs Survival From Alpha Amanitin EA Miche/son, SM Schneider/Montefiore Hospital, University of Pittsburgh Alpha amanitin (A) is the toxin believed responsible for deaths from ingestion of the toxic mushroom A m a n i t a phalloides. 1,16Dimethyl-PGE2 (PGE) is a prostaglandin with known hepatic cytoprotective effects against several toxins. The protective mechanism is uncertain. We investigated the effect of PGE on toxicity of A in our mouse model. Swiss female mice were divided into five groups and treated with A 0.63 mg/kg intraperitoneally. Group 1 received no further therapy while groups 2 through 5 received PGE 150 gg/kg intraperitoneally after delays of one and one half, two, three, and five hours from A injection. A sixth group received only PGE. Animals were given free access to food and water and followed daily for survival to one week. Survival data were analyzed by Kaplan-Meier and Breslow tests. There were no deaths in the PGE control group, and 18 of 20 (90%) deaths in the A control group. Only the mice in group 5 (five-hour delay until injection) experienced an increase in survival (P < .01). PGE failed to increase survival when given within three hours of A; however, it was effective after a delay of five hours. PGE presumably has a short half-life and is no longer effective two to three hours after administration. Our data suggest A toxicity is delayed due to either delayed absorption or time necessary for toxic conversion. We conclude that a single dose of 1,16-dimethyl-PGE~ prolongs survival after exposure to alpha amanitin in our mouse model, but only if given following a delay of five hours.
51 Empiric Use of Naloxone in Patients With Altered Mental Status: A Reappraisal JR Hoffman, JS Luol D Schriger/Emergency Medicine Center, UCLA Medical Center, Los Angeles, California This study was performed to test the hypothesis that the majority of opiate overdose patients with altered mental status can be identified by clinical signs and symptoms, and that empiric use of naloxone in all patients with altered mental status is therefore unnecessary, as well as extremely costly. We reviewed records of 730 patients who received naloxone for acute altered mental status. Only 25 patients (3.4%) had a complete response to this agent; 19 (76%) had a final hospital diagnosis of opiate overdose. Of these 19 patients, 18 (95%) had respiratory rates less than or equal to 12; 17 (90%) had constricted pupils; and 15 (79%) had a known history of drug abuse. These numbers were vastly different (P < .01 for all comparisons) for the great majority of patients who neither responded to .naloxone nor had an ultimate diagnosis of opiate overdose. Six "complete responders" proved not to have opiate overdose; their assumed response was frequently due to spontaneous improvement during a postictal period. Partial or questionable response to naloxone also confused the diagnosis in 32 patients, none of whom proved to have opiate overdose, and only ten of whom had any clinical indicators or possible opiate use. Selective use of naloxone in patients in this series on the basis of easily defined clinical characteristics would have identified virtually all responders with opiate overdose and decreased use of the drug by 89%. Economic savings associated with widespread adoption of such a policy would be enormous with no apparent clinical detri-
Annals of Emergency Medicine
445/165