NACCT 2010 Abstracts - eapcct

[Pages:64]Clinical Toxicology (2010) 48, 604?667 Copyright ? Informa UK, Ltd. ISSN: 1556-3650 print / 1556-9519 online DOI: 10.3109/15563650.2010.493290

LACLT BSTRACTS

NACCT 2010 Abstracts

Clinical Toxicology Downloaded from by University of Zuerich on 10/04/10 For personal use only.

1.Abstracts Aluminum Testing in Children: What Do Results and Reference Ranges Mean?

Zeager MA,1 Woolf AD,1 Goldman RH.2 1Children's Hospital Boston, Boston, MA, USA; 2Cambridge Health Alliance, Cambridge, MA, USA

Background: Some parents of children with developmental issues are raising concerns about their child's aluminum exposure and requesting biological testing from health care providers. Aluminum can be measured in plasma, serum, or urine, but there is scant scientific information about the normal range of aluminum concentrations in the general population, let alone agerelated norms. Yet commercial laboratories offering aluminum testing provide reference ranges when reporting results. In this study, we sought to determine what scientific literature has been used to support the reference ranges provided, whether such literature sources specifically studied aluminum levels in otherwise normal infants and children, and how to interpret results of such testing. Methods: We obtained the names of 11 commercial laboratories in the United States that perform aluminum testing from texts, published lists, and Internet sources. Either telephone or emailed surveys were conducted with laboratory personnel or Internet searches were performed seeking current information regarding reference ranges and methods of testing for aluminum in biological samples. For a subset of seven laboratories the published scientific reports cited in determining the reference ranges were reviewed for details regarding the ages and health of the population sampled. Results: For laboratories using the AAS method, serum aluminum references ranged from 3 times concentration-time curve AUCs & prolonged elimination half-lives. Deficiency of CYP2D6 likely contributed to prolonged elevation of plasma TCA levels in our pt. While CYP2D6-deficient pts have been described who developed toxicity after therapeutic dosing, we couldn't find previous reports describing toxicokinetics after overdose in a deficient pt. Conclusion: CYP2D6-deficient pts may experience delayed rise in total [TCA]s & prolonged intoxication. References: 1. Spiker DG, Biggs JT. Tricyclic antidepressants: prolonged plasma levels after overdose. JAMA 1976; 236(15):1711?2.

10. Infant Gamma-Hydroxy Butyrate Intoxication: A Case Report

Rodriguez AM, McCreight A. University of Texas Southwestern, Dallas, TX, USA

Background: Gamma-hydroxybutyrate (GHB) is a well-known recreational drug that has also been used for illegal acts of drug-facilitated sexual assault and chemical submission. Unintentional ingestion of GHB has been documented in older children, but intentional GHB poisoning in young infants has not been reported in the literature. We report a case of child abuse in a 2-month-old infant due to intentional GHB poisoning. Case report: A 2-month-old female infant presented to the emergency department (ED) with coma and respiratory failure. According to the child's mother, the infant was found to have waxing and waning mental status. She attempted to feed the infant, which resulted in coughing, gagging, and respiratory distress. An ambulance was called and paramedics found the child lethargic, unresponsive, with small pupils. On arrival to the ED, vital signs demonstrated T 37.1?C, HR 83/min, BP 83/44 mm HG, RR 4/min, O2 saturation 97% on RA. The infant had small pupils, absent gag reflex, hypotonia of all extremities, no response to painful stimuli, and a Glasgow Score of 3. Narcan 0.1 mg/kg was administered IV without improvement in mental status or respiratory depression. The infant was intubated without sedatives or paralytics, but received one dose of atropine for bradycardia. Extensive evaluation did not reveal an etiology for the child's condition, including normal head CT scan, lumbar puncture, serum electrolytes, and glucose. Urine drugs of abuse screen, comprehensive toxicology screen, and ethanol were negative. The ED social worker received an anonymous telephone call stating that the infant was given GHB in the bottle to stop her crying. A quantitative serum GHB concentration obtained 5 h from the time of presentation was 240 mcg/ mL, consistent with sedation and coma. The infant was admitted to the intensive care unit for mechanical ventilation and supportive care. She awakened and was extubated within 24 h. Child protective services was consulted and the child was removed from the family and placed in protective custody. Further evaluation for

child abuse was negative, including a skeletal survey and retinal examination. Conclusion: We report a case of child abuse in a 2-month-old infant with an elevated serum GHB concentration due to intentional GHB poisoning.

11. Diethylene Glycol: A Poison Center Review of 10 Years of Pediatric Exposures

Stellpflug SJ, Cole JB, Lintner CP, Kwon SK, Roberts DJ. Hennepin Regional Poison Center, Minneapolis, MN, USA

Introduction: Diethylene glycol (DEG), in brake fluid, can cause life threatening renal failure. Less is known about management of DEG as compared to the more commonly encountered toxic alcohols. In 2008, there were 1,292 DEG-related calls to poison centers. One issue that plagues providers is what to recommend for children who ingest small amounts. We report a 10-year poison center review of pediatric DEG exposures. Methods: A search was done of poison center cases from January 2000 through January 2010 for patients under 6 years old with oral exposures to DEG of small or unknown volumes. Cases were examined for location, symptoms, labs, treatment, and outcome. Results: Eighty-nine cases met initial inclusion criteria; nine were excluded (wrong fluid logged [1]; eye exposure only [2]; amount greater than a taste/mouthful [2]; potentially toxic but follow up not possible due to lack of parent/hospital cooperation [4]). Of the 80 cases left, 49 were observed at home, 23 sent home from the ED and 11 admitted. There were seven transferred to tertiary care. For outcomes, 69 were nontoxic/no effect, 10 minor effects (MiE) and 1 major effect (MaE). Of the MiE five had GI upset alone, one cough/GI upset, two oral irritation, one drowsy, and one eye irritation. The MaE child had cyanosis and AMS, but ingested antifreeze as well. No patients developed renal failure or death. Fomepizole was used in five cases (four no effects, one MiE). Supportive care only was provided in eight cases; the other 67 were observed only. Chem panels were done in 24 cases; all were normal except the anion gap in the MaE case. All 16 serum osmolalities done were normal. The three DEG levels obtained were negative. Discussion: Management of children exposed to tastes of DEG is a conundrum for poison centers. It ranges from obs to admission/fomepizole. In 79/80 cases there were no abnormal labs and no more than minor effects. The one variant ingestion included antifreeze. Limits of this data include sample size, retrospective data, and lack of extended follow up. However, this review argues that children with a taste of DEG will suffer no adverse outcomes. A large prospective cohort study would strengthen this conclusion. Conclusion: This 80 patient series indicates that children exposed to taste amounts of DEG will not have major adverse effects.

12. Critical Valproate Toxicity Reversed with Hemodialysis in a Toddler

Kostic MA,1 Pan CG,2 Leikin JB,1 Gummin DD.1 1Wisconsin Poison Center, Milwaukee, WI, USA; 2Medical College of Wisconsin, Milwaukee, WI, USA

Background: Traditional teaching is that valproic acid (VPA) is not amenable to extracorporeal removal by hemodialysis (HD), due to its affinity for serum proteins (85?90% bound in therapeutic dosing). However, beyond the therapeutic range, protein binding diminishes (70% when VPA level is 150 g/mL, 35% at 300 g/mL). Recent reports suggest that there is a role for HD in VPA poisoning, but few reports document the role of HD for toxicity in children. We report a case of a severely poisoned toddler with multisystem organ failure, who dramatically improved with hemodialysis. Case report: A previously healthy 20-month-old female was found unresponsive in her home on the morning after she ingested up to 10 g of VPA. She was endotracheally intubated and brought first to an outside ED, then to our PICU. On arrival, she was hypotensive (BP 68/31 mmHg) with a metabolic acidosis (lactate 4.6 mmol/L)

Pre-HD Immediately post-HD

VPA (g/mL) 522 Arterial pH/serum 7.18/10.6

bicarb (mEq/L) Ammonia (M/L) 290

227 7.29/21

20

and respiratory acidosis (venous pH 6.99, pCO2 37 mmHg). Serum VPA was >600 g/mL. She became hypothermic (34.1?C), hyperammonemic, anemic (Hct 22%), thrombocytopenic (47,000/mm3), coagulopathic (PT 20 s), hypernatremic (151 mEq/L), and hypocalcemic. Her transaminases (AST 102 U/L), lipase (662 U/L), CK (829 U/L), BUN (31 mg/dL) and Cr (1.06 mg/dL) were all elevated. Approximately 24 h post-ingestion, she underwent 2.5 h of HD, resulting in rapid reduction of her VPA level and improved acid/base status. Pressors were weaned in the hours following HD, and she was awake and extubated 36 h later. All laboratory parameters normalized over the next 48 h. Case discussion: This child showed dramatic improvement with removal of VPA in a single session of HD, and prompt resolution of metabolic abnormalities. Her measured VPA half-life of 2 h during HD is comparable with other reports. This is the second documented case of HD for VPA poisoning in a toddler, and the first involving such a gravely ill child. Conclusion: Emergent HD should be considered in patients with severe VPA poisoning, especially if associated with acidemia. Whether HD improves outcome more than supportive care alone requires further investigation.

13. Overdose of Rivastigmine Patches Producing DUMBELS Toxicity Treated with Atropine Alone

Reedy SJD,1 Schwartz MD.2 1Emory University, Atlanta, GA, USA; 2Georgia Poison Center, Atlanta, GA, USA

Background: Rivastigmine (ExelonTM) is a non-competitive, reversible cholinesterase inhibitor approved in patch formulation for the treatment of Alzheimer's and dementia due to Parkinson's disease. The transdermal patch is thought to cause fewer muscarinic side effects and is the first patch treatment approved for dementia. It is a partial agonist at muscarinic receptors, blocks reuptake of 5HT, DA, and NE, inhibits MAO, and may block Na2+ and K+ channels. Toxicity from the application of multiple rivastigmine patches has been described only once and responded to pralidoxime. We report the first case of toxicity from multiple rivastigmine patches requiring atropine for potentially life-threatening muscarinic symptoms. Case report: A 71-year-old woman presented to the ED complaining of vomiting, diarrhea, abdominal cramps, weakness and diaphoresis for 1 day. Initial vital signs revealed bradycardia (40?50 bpm) and hypertension (160/105 mmHg). Physical exam revealed an elderly woman who appeared diaphoretic and drowsy, with miotic pupils, hyperactive bowel sounds, generalized 4/5 weakness without fasiculations, and nine rivastigmine patches (4.6 mg/24-h) adherent to her torso. The patches were removed immediately and the skin decontaminated with soap and water. During her evaluation, the patient displayed further decreases in heart rate into the 30s and received atropine 0.2 mg IV, with resultant increase in her heart rate to 100 bpm and improvement in her nausea, vomiting, and diaphoresis. One hour later, the patient developed recurrent cholinergic symptoms as well as bradycardia to the low 40s. A second dose of atropine 0.2 mg IV again increased her heart rate to 70 bpm and improved her GI symptoms and diaphoresis. Plasma cholinesterase was 1,775 IU/L and RBC cholinesterase was 5,936 IU/L; both values were near the lower end of normal reference ranges. The patient was admitted to the ICU for cardiac monitoring, required no further atropine, and was discharged the following day. Conclusions: Overuse of transdermal cholinergic medication used to treat dementia may precipitate predominantly muscarinic symptoms that were responsive to

Clinical Toxicology vol. 48 no. 6 2010

Abstracts

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Clinical Toxicology Downloaded from by University of Zuerich on 10/04/10 For personal use only.

atropine in our patient. Additionally, RBC and plasma cholinesterase levels were not predictive of clinical severity in this case.

14. Massive, Unintentional Pediatric Lamotrigine Overdose Resulting in Seizures

Lapoint J,1 Sullivan R,1 Rey L,2 Nelsen J.1 1SUNY Upstate Medical University, Syracuse, NY, USA; 2Albany Medical Center, Albany, NY, USA

Background: Lamotrigine (LTG), a phenyltriazine anticonvulsant, has been uncommonly associated with life-threatening toxicity. As its use for bipolar and other off-label use expands however, so does risk for potential poisoning. LTG exposures in patients ................
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