Saralyn R Williams

Publications of Saralyn R Williams

• A prospective evaluation of shortened course oral N-acetylcysteine for the treatment of acute acetaminophen poisoning.

  Authors: David P Betten, F Lee Cantrell, Stephen C Thomas, Saralyn R Williams, Richard F Clark

  Annals of emergency medicine. 10/2007; 50(3):272-9.

  STUDY OBJECTIVE: Treatment with a shortened duration of oral N-acetylcysteine (20 to 48 hours) after acute acetaminophen poisoning is effective in the prevention of subsequent hepatic failure andSTUDY OBJECTIVE: Treatment with a shortened duration of oral N-acetylcysteine (20 to 48 hours) after acute acetaminophen poisoning is effective in the prevention of subsequent hepatic failure and death when administered to individuals meeting appropriate laboratory criteria. METHODS: Individuals with a potentially toxic acetaminophen ingestion according to serum acetaminophen levels were identified prospectively using a large statewide poison control system database throughout a 12-month period. N-acetylcysteine was administered for a minimum of 6 doses (20 hours), after which laboratory studies were obtained. Discontinuation of N-acetylcysteine was recommended by the poison center when 2 criteria were met: serum acetaminophen was undetectable (<10 microg/mL) and liver test results were normal (serum aminotransferase, international normalized ratio). A follow-up questionnaire was administered to individuals treated with N-acetylcysteine for 48 hours or less to ascertain the presence of symptoms consistent with progressive hepatotoxicity. RESULTS: Of 205 acutely poisoned individuals treated with N-acetylcysteine for 48 hours or less, 195 were successfully contacted after discharge, and 187 of 195 (95.9%) reported no symptoms consistent with hepatic failure. Eight individuals (4.1%) reported abdominal pain or vomiting; however, none received further N-acetylcysteine treatment or additional hospitalization. CONCLUSION: A shortened duration of treatment with N-acetylcysteine (20 to 48 hours) may be an effective treatment option in individuals considered to be at no further risk of developing liver toxicity according to the fulfillment of appropriate laboratory criteria before N-acetylcysteine discontinuation.

• Phenytoin-potentiated hepatotoxicity following acetaminophen overdose? A closer look.

  Authors: Matthew D Cook, Saralyn R Williams, Richard F Clark

  Digestive diseases and sciences. 02/2007; 52(1):208-9.

• Vasopressin treatment for cyclic antidepressant overdose.

  Authors: James David Barry, David W Durkovich, Saralyn R Williams

  The Journal of emergency medicine. 08/2006; 31(1):65-8.

  Due to neurotransmitter reuptake inhibition, peripheral alpha receptor blocking effects, and sodium channel blockade, severe cyclic antidepressant poisoning may lead to intractable hypotension. WeDue to neurotransmitter reuptake inhibition, peripheral alpha receptor blocking effects, and sodium channel blockade, severe cyclic antidepressant poisoning may lead to intractable hypotension. We report a case of severe amitriptyline toxicity, with hypotension unresponsive to direct alpha receptor agonists after pH manipulation, but improved with intravenous vasopressin. Vasopressin use in the setting of cyclic antidepressant toxicity has not been previously reported. Vasopressin may be a beneficial agent in the treatment of recalcitrant hypotension associated with poisoning or overdose. The anecdotal nature of this report must be emphasized and the use of vasopressin requires further research to define efficacy, dose, and potential side effects.

• North American coral snake antivenin for the neutralization of non-native elapid venoms in a murine model.

  Authors: William H Richardson, David A Tanen, Tri C Tong, David P Betten, Shaun D Carstairs, Saralyn R Williams, Frank L Cantrell, Richard F Clark

  Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 02/2006; 13(2):121-6.

  OBJECTIVES: North American coral snake antivenin (CSAV; Wyeth Antivenin [Micrurus fulvius], equine origin) is approved for the treatment of coral snake envenomations in the United States. The coralOBJECTIVES: North American coral snake antivenin (CSAV; Wyeth Antivenin [Micrurus fulvius], equine origin) is approved for the treatment of coral snake envenomations in the United States. The coral snake is the only elapid that is native to North America, but envenomations from non-native elapids are occurring more commonly in this country. This study was designed to evaluate the efficacy of CSAV in the neutralization of two exotic elapid envenomations: Naja naja (Indian cobra) and Dendroaspis polylepsis (black mamba). METHODS: A randomized, blinded, placebo-controlled murine model of intraperitoneal venom injection was employed. Venom potency was determined in preliminary dosing studies. Study animals then were divided into five groups: 1) N. naja venom + CSAV, 2) N. naja venom + 0.9% normal saline (NS), 3) D. polylepsis venom + CSAV, 4) D. polylepsis venom + NS, and 5) CSAV + NS. The venom dose was chosen to be twice the estimated LD50. The amount of CSAV injected was ten times the amount necessary for neutralization of a 2 x LD50 dose of M. f. fulvius venom in a murine model. Statistical analysis included Fisher's exact and log-rank testing to compare survival rates and times. RESULTS: Preliminary studies estimated the venom LD50 to be 2.58 mg/kg and 0.45 mg/kg, respectively, for the N. naja and D. polylepsis. A significant difference was shown in comparison of survival times between CSAV-venom groups and normal saline-venom groups despite all animals in both treatment and control arms dying. Animals receiving CSAV and N. naja venom survived (mean +/- SD) 24.4 +/- 3.0 minutes, versus 17.8 +/- 1.3 minutes in the control group (p < 0.001), whereas those receiving CSAV and D. polylepsis venom survived 203.8 +/- 37.0 minutes versus 130.0 +/- 42.6 minutes in the control group (p < 0.001). All animals in the CSAV + NS group survived to the conclusion of the study. CONCLUSIONS: When premixed with venom, CSAV increased survival time in a murine model of intraperitoneal N. naja and D. polylepsis venom injection. The clinical implications of this are unclear, given unchanged mortality rates.

• Response to Latrodectus-associated compartment syndrome.

  Authors: Michael J Matteucci, Saralyn R Williams, Richard F Clark

  Annals of emergency medicine. 07/2005; 45(6):679-80; author reply 680-1.

• Crotalidae polyvalent immune Fab (ovine) antivenom is effective in the neutralization of South American viperidae venoms in a murine model.

  Authors: William H Richardson, David A Tanen, Tri C Tong, David P Betten, Shaun D Carstairs, Saralyn R Williams, Frank L Cantrell, Richard F Clark

  Annals of emergency medicine. 07/2005; 45(6):595-602.

  STUDY OBJECTIVE: Crotalidae polyvalent immune Fab (ovine) (CroFab; FabAV) is used in the treatment of symptomatic crotaline envenomations in North America. Unlike Antivenin (Crotalidae) Polyvalent,STUDY OBJECTIVE: Crotalidae polyvalent immune Fab (ovine) (CroFab; FabAV) is used in the treatment of symptomatic crotaline envenomations in North America. Unlike Antivenin (Crotalidae) Polyvalent, which is approved for treatment of crotaline envenomation in North and South America, FabAV is manufactured using only venoms from crotaline snakes native to the United States. This study was designed to evaluate the efficacy of FabAV in the neutralization of venom from 2 South American crotaline snakes: Crotalus durissus terrificus (tropical rattlesnake) and Bothrops atrox (fer-de-lance). METHODS: A randomized, blinded, placebo-controlled murine model of intraperitoneal venom injection was used. Venom potency was determined in preliminary median lethal dose (LD 50) dosing studies. Study animals were then divided into 7 groups: (1) C durissus terrificus venom (Sigma-Aldrich Co.)+FabAV, (2) C durissus terrificus venom (Sigma-Aldrich Co.)+0.9% normal saline solution, (3) C durissus terrificus venom (Biotoxins Inc.)+FabAV, (4) C durissus terrificus venom (Biotoxins Inc.)+normal saline solution, (5) B atrox venom+FabAV, (6) B atrox venom+normal saline solution, and (7) FabAV+normal saline solution. Twice the estimated LD 50 was the chosen venom dose, and the amount of FabAV injected was 10 times the amount needed for venom neutralization. Statistical analysis included Fisher's exact test and log-rank testing to compare survival rates and times. RESULTS: The venom LD 50 was found in preliminary studies to be 0.9 mg/kg and 1.35 mg/kg for the C durissus terrificus venom obtained from Sigma-Aldrich Co. and Biotoxins Inc., respectively. The LD 50 for B atrox venom was 5.0 mg/kg. All animals receiving venom only and saline solution died. Animals receiving FabAV together with either venom survived to the end of the 24-hour observation period ( P <.001). Comparison of survival times between groups demonstrated a significant difference in time to death between venom-only control groups and the FabAV+venom groups (P <.001). All animals in the FabAV+normal saline solution group survived to the conclusion of the study. CONCLUSION: FabAV, when premixed with venom, decreases lethality in a murine model of intraperitoneal venom injection of the South American pit vipers, C durissus terrificus and B atrox .

• Overdose of aripiprazole, a new type of antipsychotic.

  Authors: Shaun D Carstairs, Saralyn R Williams

  The Journal of emergency medicine. 05/2005; 28(3):311-3.

  Aripiprazole is the first member of a new class of antipsychotic medications. Unlike other antipsychotics, it acts as a partial agonist at dopamine D(2) and 5-HT(1A) receptors, thereby mitigatingAripiprazole is the first member of a new class of antipsychotic medications. Unlike other antipsychotics, it acts as a partial agonist at dopamine D(2) and 5-HT(1A) receptors, thereby mitigating most of the adverse reactions such as extrapyramidal side effects and hyperprolactinemia. Additionally, most research to date has suggested a low incidence of QTc prolongation and orthostatic hypotension at therapeutic doses. Experience in the setting of intentional overdose, however, is limited. We present a case of a 27-year-old woman who intentionally ingested 330 mg of aripiprazole in a suicide attempt. Clinical effects were limited to mild sedation. Serum levels performed by the drug's manufacturer confirmed a total level (parent drug and active metabolite) of 716 ng/mL, nearly six times the upper limit of accepted therapeutic levels. This suggests that aripiprazole's therapeutic index is quite high and reinforces the drug's known safety profile.

• Rattlesnake envenomation to the face of an infant.

  Authors: William H Richardson, James D Barry, Tri C Tong, Saralyn R Williams, Richard F Clark

  Pediatric emergency care. 04/2005; 21(3):173-6.

  BACKGROUND: Mortality from rattlesnake envenomation in the United States is rare. Despite approximately 8000 crotaline (pit vipers) bites annually, it is estimated that only 10 to 15 deaths occur.BACKGROUND: Mortality from rattlesnake envenomation in the United States is rare. Despite approximately 8000 crotaline (pit vipers) bites annually, it is estimated that only 10 to 15 deaths occur. Besides direct intravascular envenomation and anaphylaxis, bites to the head and neck may account for some of these rare fatalities. We report a pediatric case of severe facial envenomation requiring emergent intubation and antivenom administration. CASE REPORT: A 14-month-old female toddler was envenomated by a Southern Pacific rattlesnake (Crotalus viridis helleri) above the right upper lip while playing in her backyard. Rapid swelling and ecchymosis developed, and the patient was airlifted to a pediatric tertiary care hospital. Within 3 hours, stridorous respirations complicated by significant facial and oropharyngeal edema necessitated emergent orotracheal intubation. A total of 16 vials of FabAV [Crotalidae Polyvalent Immune Fab (ovine) antivenom] were administered over the next 24 hours. The child gradually improved and was successfully extubated 5 days later. A 3-month follow-up demonstrated no significant cosmetic facial abnormalities. CONCLUSION: Crotaline bites to the head and neck have the potential for significant swelling and airway compromise. Facial bites, anaphylaxis, and rare intravascular envenomation may account for many of the fatalities from rattlesnake envenomation. Early intubation may be required to maintain airway patency.

• Fatal unintentional overdose of diltiazem with antemortem and postmortem values.

  Authors: F Lee Cantrell, Saralyn R Williams

  Clinical toxicology (Philadelphia, Pa.). 02/2005; 43(6):587-8.

  BACKGROUND: Therapeutic errors involving calcium channel antagonists (CCA) resulting in death rarely have been reported in detail. We report a fatality from an unintentional overdose ofBACKGROUND: Therapeutic errors involving calcium channel antagonists (CCA) resulting in death rarely have been reported in detail. We report a fatality from an unintentional overdose of sustained-release (SR) diltiazem including antemortem and postmortem blood concentrations. CASE REPORT: A 65-year-old man with aortic stenosis mistakenly took six tablets of diltiazem 360 mg SR. He developed symptoms of toxicity by 7 hours after ingestion. By 10 hours, he went to the emergency department. Despite a prolonged resuscitative attempt, the patient died 17 hours postingestion. An antemortem blood sample drawn 11.5 hours after ingestion was 2.9 mcg/mL. Postmortem gas chromatography of central blood revealed a diltiazem level of 6 mcg/mL and the peripheral blood sample measured 5 mcg/ mL. CONCLUSION: This case suggests that an unintentional overdose with a CCA may be lethal if the patient's cardiovascular ability to compensate for the toxic effects is compromised.

• A picturesque reversal of antimuscarinic delirium.

  Authors: William H Richardson, Saralyn R Williams, Shaun D Carstairs

  The Journal of emergency medicine. 06/2004; 26(4):463.

• A reassessment of topical organic phosphorus insecticide exposures and permanent paralysis.

  Authors: Richard F Clark, Saralyn R Williams, Frederick Fung, Aaron B Schneir, Binh T Ly, David A Tanen, Stephen W Munday

  Journal of toxicology. Clinical toxicology. 02/2004; 42(7):991-2.

• Prevalence of autonomic signs and symptoms in antimuscarinic drug poisonings.

  Authors: Raj J Patel, Tim Saylor, Saralyn R Williams, Richard F Clark

  The Journal of emergency medicine. 02/2004; 26(1):89-94.

  Classically described antimuscarinic poisoning signs and symptoms include mydriasis, decreased secretions, ileus, urinary retention, hyperthermia, tachycardia, and altered mental status. TheseClassically described antimuscarinic poisoning signs and symptoms include mydriasis, decreased secretions, ileus, urinary retention, hyperthermia, tachycardia, and altered mental status. These features may be used clinically to assist in the diagnosis of patients with unknown poisonings. We sought to analyze the prevalence of antimuscarinic physical examination findings in evaluating patients presenting with acute poisoning from antimuscarinic agents. We conducted a retrospective, medical record review at two urban tertiary care teaching hospitals. The study population consisted of patients presenting to the Emergency Department with a diagnosis of acute poisoning secondary to medications with known antimuscarinic side effects during a 78-month period between January 1994 and July 2001. Cases were excluded for incomplete medical records or unreliable histories of ingestion, and when concomitant ethanol intoxication was present on laboratory analysis. Clinical information obtained from each patient included vital signs, pupillary size, electrocardiogram abnormalities, the presence of mucous membrane and axillary secretions, initial urine output after bladder catheterization, quality of bowel sounds, mental status changes, the occurrence of seizures and coma, need for orotracheal intubation, and time required for clinical resolution. Diagnostic and therapeutic information including laboratory tests, administration of sodium bicarbonate, and usage of physostigmine was also collected. We identified a total of 345 cases, 213 of which met inclusion criteria. Of these cases, the most common documented findings included decreased secretions in 75.1%, tachycardia in 68.1%, confusion in 49.3%, drowsiness in 48.2%, and hypoactive or absent bowel sounds in 44.6%. Combining signs and symptoms to predict this toxic syndrome was not very reliable. Tachycardia, decreased oral or axillary secretions, and mydriasis proved to be the most predictive trio of clinical signs, but were found in only 28.2% of cases. At least one of these three signs was documented in 94% of our patients. The combination of tachycardia and decreased secretions was the most common pair of findings, recorded in 55.4% of cases. We conclude that the clinical presentation of antimuscarinic syndrome is variable.

• A case of type F botulism in southern California.

  Authors: William H Richardson, Shermane S Frei, Saralyn R Williams

  Journal of toxicology. Clinical toxicology. 02/2004; 42(4):383-7.

  BACKGROUND: Botulism caused by type F botulinum toxin accounts for less than 0.1% of all human botulism cases and is rarely reported in the literature. CASE REPORT: A 45-year-old woman presented toBACKGROUND: Botulism caused by type F botulinum toxin accounts for less than 0.1% of all human botulism cases and is rarely reported in the literature. CASE REPORT: A 45-year-old woman presented to an emergency department complaining of blurred vision, difficulty focusing, and dysphagia. The treating physician initially considered the possibility of paralytic shellfish poisoning due to a report of shellfish ingestion, which was later determined to be frozen shrimp and a can of tuna, but no gastroenteritis or paresthesias were present. During the emergency department observation, the patient developed respiratory distress with hypercapnea and required intubation and mechanical ventilation. Within hours, ptosis, mydriasis, and weakness in the arms and legs developed. Bivalent (A, B) botulinum antitoxin was administered approximately 24 h from the onset of initial symptoms, but over the next two days complete paralysis progressed to the upper and lower extremities. Shortly thereafter a stool toxin assay demonstrated the presence of type F botulinum toxin. The patient subsequently received an experimental heptavalent botulinum antitoxin on hospital day 7 but paralysis was already complete. Her three-week hospital course was complicated by nosocomial pneumonia and a urinary tract infection, but she gradually improved and was discharged to a rehabilitation facility. Anaerobic cultures and toxin assays have yet to elucidate the source of exposure. CONCLUSION: We report a rare case of type F botulism believed to be foodborne in etiology. Administration of bivalent botulinum antitoxin did not halt progression of paralysis.

• Complications of diagnostic physostigmine administration to emergency department patients.

  Authors: Aaron B Schneir, Steven R Offerman, Binh T Ly, Jefferey M Davis, Rachel T Baldwin, Saralyn R Williams, Richard F Clark

  Annals of emergency medicine. 08/2003; 42(1):14-9.

  STUDY OBJECTIVES: Literature exists describing the complications associated with therapeutic physostigmine administration. No series exists detailing strictly diagnostic use. Our objective was toSTUDY OBJECTIVES: Literature exists describing the complications associated with therapeutic physostigmine administration. No series exists detailing strictly diagnostic use. Our objective was to document the complications associated with diagnostic physostigmine administration in emergency department (ED) patients suspected of having antimuscarinic delirium. METHODS: Two reviewers blinded to the study purpose performed a retrospective chart review on all adult patients administered physostigmine diagnostically over a 79-month period at a tertiary-care hospital. Twenty percent of charts were reviewed by both abstractors. The data abstracted from the chart included total dose of physostigmine, effect on mental status, any subsequent complications, or any use of atropine. Discharge summaries, toxicology consultations, and urine drug screens were used to determine the cause of the altered mental status. RESULTS: Thirty-nine adult patients were administered varying doses of physostigmine (range 0.5 to 2 mg). The reviewers were able to determine the cause of the altered mental status in 35 patients. The cause was purely antimuscarinic in 19 patients, purely nonantimuscarinic in 10 patients, mixed antimuscarinic and nonantimuscarinic in 2 patients, psychiatric in 4 patients, and unknown in 4 patients. A total of 22 patients had full reversal of delirium, and this group comprised all 19 patients with a purely antimuscarinic cause and 3 patients in whom a cause was never determined. One (2.6%) in 39 patients had a brief convulsion without adverse sequelae. This patient was poisoned with an antimuscarinic drug. No patient had dysrhythmias, had signs of cholinergic excess, or was administered atropine. CONCLUSION: Diagnostic physostigmine administration was without significant complication when given to ED patients suspected of having antimuscarinic delirium. Although a relatively small series, it contributes to the safety profile of physostigmine.

• Dendrotoxin poisoning in a neurobiochemist.

  Authors: Stephen W Munday, Saralyn R Williams, Richard F Clark

  Journal of toxicology. Clinical toxicology. 02/2003; 41(2):163-5.

  BACKGROUND: Dendrotoxin is a highly potent blocker of KV1.1, KV1.2, and KV1.6 potassium channels that is derived from the venom of the green mamba (Dendroaspis angusticeps). It is commonly used toBACKGROUND: Dendrotoxin is a highly potent blocker of KV1.1, KV1.2, and KV1.6 potassium channels that is derived from the venom of the green mamba (Dendroaspis angusticeps). It is commonly used to inhibit the function of whole nerve preparations in vitro. Despite the widespread use and potency of this compound, neurotoxicity in humans has not been described from refined toxin. We report a case of dendrotoxin toxicity from dermal exposure. CASE REPORT: A healthy 40-year-old female neurobiochemist presented with complaints of progressive numbness of the left malar region and lateral orbit that progressed to include the medial orbit and tongue. One hour prior to presentation she used her bare hands to remove residual petroleum jelly from a dish that had previously contained 500 nanoliters of 500 nanomolar dendrotoxin. She recalled rubbing her left eye prior to the onset of symptoms. Before touching the dish, she had washed it with running water and then 70% ethanol while using latex gloves. Physical examination was remarkable only for weakness to superior gaze and some mild tongue fasciculations. Within 12 hours of exposure, she was completely asymptomatic. CONCLUSION: Dendrotoxin is a highly potent neurotoxin that can cause localized impairment of nerve function after mucous membrane exposure.

• Massive OxyContin ingestion refractory to naloxone therapy.

  Authors: Aaron B Schneir, Tyler F Vadeboncoeur, Steven R Offerman, James D Barry, Binh T Ly, Saralyn R Williams, Richard F Clark

  Annals of emergency medicine. 11/2002; 40(4):425-8.

  OxyContin (oxycodone hydrochloride controlled release) is a long-acting preparation of oxycodone that is used as an opioid analgesic to treat chronic pain conditions. We report a patient who ingestedOxyContin (oxycodone hydrochloride controlled release) is a long-acting preparation of oxycodone that is used as an opioid analgesic to treat chronic pain conditions. We report a patient who ingested a massive quantity of OxyContin and had altered mental status, noncardiogenic pulmonary edema, and hypoventilation that proved refractory to naloxone administration. She required mechanical ventilation for 3 days before recovering completely. The severity and length of poisoning was likely related both to the quantity and formulation of the oxycodone ingested.

• A prospective study of acute, unintentional, pediatric superwarfarin ingestions managed without decontamination.

  Authors: Marianne Ingels, Chi Lai, Winnie Tai, Beth H Manning, Cyrus Rangan, Saralyn R Williams, Anthony S Manoguerra, Timothy Albertson, Richard F Clark

  Annals of emergency medicine. 08/2002; 40(1):73-8.

  STUDY OBJECTIVE: We determine the incidence of clinically important bleeding in children with superwarfarin rodenticide ingestions not treated with gastrointestinal decontamination or prophylacticSTUDY OBJECTIVE: We determine the incidence of clinically important bleeding in children with superwarfarin rodenticide ingestions not treated with gastrointestinal decontamination or prophylactic vitamin K. METHODS: We prospectively studied patients younger than 6 years of age who reported to our poison center with acute unintentional superwarfarin ingestions. Patients who received gastrointestinal decontamination or prophylactic vitamin K were excluded. Forty-eight- to 96-hour prothrombin time or international normalized ratio (INR) blood tests were recommended, and telephone contact was attempted at least 3 days after ingestion. RESULTS: A total of 595 consecutive patients were enrolled during the 16-month study period. Fifty patients were excluded: 8 who were known to have ingested 1 pellet or less; 25 who received activated charcoal; 15 who were treated with induced emesis; and 2 who received prophylactic vitamin K. The resulting study group contained 545 patients. Eighty-two patients were lost to follow-up. Follow-up was obtained for 463 patients, including 222 by telephone contact alone, 62 by 48- to 96-hour INR, and 179 by both methods. None of the patients had clinically important coagulopathy. Two patients had an INR of 1.5 or greater (1.5 and 1.8) without symptoms. Single nosebleeds were reported in another 2 patients with normal 48-hour INRs. Another child had a small amount of blood crusted in the nose with no other symptoms and no laboratory work available. One child with a normal 48-hour INR had blood-streaked stools that were thought to be caused by an anal fissure. CONCLUSION: Children with acute unintentional superwarfarin ingestions of less than 1 box may be managed without gastric decontamination or prophylactic vitamin K. Laboratory testing for coagulopathy should be reserved for cases involving clinically evident bleeding abnormalities.

• Delayed valproic acid toxicity: a retrospective case series.

  Authors: Marianne Ingels, Jon Beauchamp, Richard F Clark, Saralyn R Williams

  Annals of emergency medicine. 07/2002; 39(6):616-21.

  STUDY OBJECTIVE: We estimate how often an initially undetectable or nontoxic valproic acid (VPA) concentration misrepresents the potential toxicity of an acute VPA overdose. METHODS: All patientsSTUDY OBJECTIVE: We estimate how often an initially undetectable or nontoxic valproic acid (VPA) concentration misrepresents the potential toxicity of an acute VPA overdose. METHODS: All patients followed up by the San Diego and San Francisco Divisions of the California Poison Control System between January 1997 and June 1999 with a documented serum VPA concentration of 120 microg/mL or greater at any time were identified through a search of poison center databases. Cases involving patients who had serial VPA concentrations and an initial VPA concentration that was unmeasurable or less than 100 microg/mL were also identified. The methods of decontamination, clinical outcomes, highest measured concentration, and times after ingestion of the initial and highest measured concentration of VPA were determined by means of chart review for these cases. RESULTS: Of the 173 patients identified with VPA concentrations of 120 microg/mL or greater, 21 (12.1%) had a detectable initial concentration not in the toxic range, and 5 (2.9%) had initial concentrations of less than the limit of detection. These 26 cases involved acute ingestion of VPA preparations. Four of these 26 patients were discharged to home or to a psychiatric facility after the initial results were obtained. CONCLUSION: Delayed toxicity might occur in patients after an acute overdose of enteric-coated VPA. Initial serum VPA concentrations might be misleading. Serial measurements documenting declining VPA concentrations or prolonged observation are recommended to determine whether a patient is medically safe for discharge or psychiatric placement.

• Pharmacologic misadventure resulting in hypercalcemia from vitamin D intoxication.

  Authors: Sean Patrick Nordt, Saralyn R Williams, Richard F Clark

  The Journal of emergency medicine. 05/2002; 22(3):302-3.

• Mercuric oxide poisoning treated with whole-bowel irrigation and chelation therapy.

  Authors: Binh T Ly, Saralyn R Williams, Richard F Clark

  Annals of emergency medicine. 04/2002; 39(3):312-5.

  Most reported cases of inorganic mercury poisoning are from mercuric chloride. We report a case of mercuric oxide (HgO) powder ingestion. A 31-year-old man presented to an emergency department afterMost reported cases of inorganic mercury poisoning are from mercuric chloride. We report a case of mercuric oxide (HgO) powder ingestion. A 31-year-old man presented to an emergency department after ingestion of approximately 40 g of HgO. Soon after ingestion, he developed nausea, vomiting, and abdominal cramping. Abdominal radiograph revealed densely radiopaque material in the stomach. Gastrointestinal decontamination was accomplished with activated charcoal and whole-bowel irrigation with polyethylene glycol solution (Golytely) for 24 hours until repeat abdominal radiographs no longer demonstrated the substance in the gastrointestinal tract. He was also chelated with British anti-Lewisite for 5 days, followed by succimer for 10 days. He had markedly elevated urine and blood mercury levels after ingestion, but except for a mildly depressed serum bicarbonate (19 mEq/L), his chemistry results remained normal including blood urea nitrogen and creatinine. He had an uncomplicated hospital course and remained asymptomatic at 6 months postingestion. Despite elevated urine and blood mercury levels after ingestion of HgO, our patient did not develop the end-organ toxicity typical of inorganic mercury poisoning.