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152


Elemental mercury neurotoxicity from self-injection [Case Report]

Schaumburg, H H; Gellido, C; Smith, S W; Nelson, L S; Hoffman, R S
PMID: 19171837
ISSN: 0028-3878
CID: 107797

Multisystem organ failure after large volume injection of castor oil [Case Report]

Smith, Silas W; Graber, Nathan M; Johnson, Rudolph C; Barr, John R; Hoffman, Robert S; Nelson, Lewis S
We report a case of multisystem organ failure after large volume subcutaneous injection of castor oil for cosmetic enhancement. An unlicensed practitioner injected 500 mL of castor oil bilaterally to the hips and buttocks of a 28-year-old male to female transsexual. Immediate local pain and erythema were followed by abdominal and chest pain, emesis, headache, hematuria, jaundice, and tinnitus. She presented to an emergency department 12 hours postinjection. Persistently hemolyzed blood samples complicated preliminary laboratory analysis. She rapidly deteriorated despite treatment and developed fever, tachycardia, hemolysis, thrombocytopenia, hepatitis, respiratory distress, and anuric renal failure. An infectious diseases evaluation was negative. After intensive supportive care, including mechanical ventilation and hemodialysis, she was discharged 11 days later, requiring dialysis for an additional 1.5 months. Castor oil absorption was inferred from recovery of the Ricinus communis biomarker, ricinine, in the patient's urine (41 ng/mL). Clinicians should anticipate multiple complications after unapproved methods of cosmetic enhancement
PMID: 19131711
ISSN: 1536-3708
CID: 96657

Solanaceous steroidal glycoalkaloids and poisoning by Solanum torvum, the normally edible susumber berry

Smith, Silas W; Giesbrecht, Esther; Thompson, Margaret; Nelson, Lewis S; Hoffman, Robert S
Ingestion of immature, environmentally stressed, or cultivar-specific Solanum species (particularly the potato) has been previously associated with gastrointestinal and neurological symptoms caused by solanaceous steroidal glycoalkaloids (SGAs). We report on two geographically, temporally disparate outbreaks of poisoning by susumber berries (Solanum torvum- Solanaceae) and on detection of alkaloids not present in non-toxic berries. Five family members in New York City participated in a traditional evening meal containing Jamaican susumber berries. All those consuming berries were symptomatic the following morning with varying degrees of gastrointestinal distress, dizziness, slurred speech, cranial nerve deficits, and ataxia. The most seriously afflicted patient developed hypertension, confusion, proximal upper extremity weakness, and hypercapnic respiratory failure requiring prolonged mechanical ventilation. A separate cohort of six patients in Toronto ate unripe Jamaican susumber berries. They presented 14h post-ingestion with varying degrees of diarrhea, weakness, facial paralysis, slurred speech, ataxia, early hypertension, and proximal weakness. Two patients had ventilatory decompensation; one required intubation. Poisonous berries appeared indistinguishable from non-toxic varieties. We isolated solasonine, larger amounts of solamargine, and other steroidal glycoalkaloids in the toxic berry strains. S. torvum poisoning can produce significant neurological and gastrointestinal effects which appear to be mediated by SGAs present in the berries
PMID: 18725244
ISSN: 0041-0101
CID: 91970

Altered Acetaminophen Pharmacokinetics and Hepatotoxicity Associated with Premature Cessation of Intravenous N-Acetylcysteine Therapy (September) [Case Report]

Smith, Silas W; Howland, Mary Ann; Hoffman, Robert S; Nelson, Lewis S
OBJECTIVE: To report a case of erratic absorption, double peak serum concentrations, and hepatotoxicity following premature cessation of intravenous Nacetylcysteine (NAC) treatment in the setting of a massive acetaminophen overdose. CASE SUMMARY: A 78-year-old man reportedly ingested approximately 96 immediate-release acetaminophen 500-mg tablets (48 g) over a one-hour period in an apparent suicide attempt. The acetaminophen concentration at 2.25 hours was 264 microg/mL. Intravenous NAC was initiated 5 hours postingestion. At 6.25 hours postingestion, the acetaminophen concentration was 281 microg/mL. Following administration of intravenous NAC for 21 hours, therapy was discontinued despite a residual acetaminophen concentration of 116 microg/mL. The patient experienced hepatotoxicity, coagulopathy, and renal injury. Pharmacokinetic analysis revealed significantly prolonged acetaminophen absorption and a second peak acetaminophen concentration of 228 microg/mL approximately 48 hours postingestion. Direct in-hospital monitoring of the patient made a second ingestion unlikely. DISCUSSION: Acetaminophen overdose is usually effectively managed with NAC. Patients with massive ingestions may have altered absorption kinetics due to acetaminophen's solubility being exceeded, physiologically or chemically altered gastrointestinal emptying or motility, or other factors. These patients may benefit from gastrointestinal decontamination and prolonged NAC therapy. CONCLUSIONS: In patients with massive acetaminophen ingestion, erratic absorption may occur, and toxic serum concentrations may persist beyond a standard 21-hour course of intravenous NAC therapy. Acetaminophen concentrations and aminotransferase levels should be evaluated at the completion of therapy intravenous NAC infusion to ensure complete elimination of acetaminophen and absence of hepatotoxicity and to exclude the need for prolonged treatment
PMID: 18628444
ISSN: 1542-6270
CID: 80581

Bedside Detection of Urine beta-Hydroxybutyrate in Diagnosing Metabolic Acidosis

Smith, Silas W; Manini, Alex F; Szekely, Tibor; Hoffman, Robert S
Objectives: While critically important, the rapid identification of the etiology of metabolic acidosis (MA) may be labor-intensive and time-consuming. Alcoholic, starvation, and severe diabetic ketoacidosis (AKA, SKA, and DKA, respectively) may produce beta-hydroxybutyrate (BOHB) in marked excess of acetone (ACET) and acetoacetate (AcAc). Unfortunately, current urine dipstick technology poorly detects ACET and cannot measure BOHB. The inability to detect BOHB might delay therapy for ketoacidoses or provoke unnecessary evaluation or empiric treatment of other causes of MA, such as toxic alcohol poisoning. The authors tested the previous assertion that commonly available hydrogen peroxide (H(2)O(2)) would improve BOHB detection. The effectiveness of alkalinization and use of a silver nitrate (AgNO(3)) catalyst was also assessed. Methods: Control and urine test specimens containing from 0.5 to 800 mmol/L ACET, AcAc, and BOHB were prepared. Urine specimens were oxidized with H(2)O(2) (3%) 1:9 (H(2)O(2):urine), alkalinized with potassium hydroxide (KOH; 10%), exposed to AgNO(3) sticks, or altered with a combination of these methods in a random fashion. Three emergency physicians (EPs) blinded to the preparation technique evaluated urine dipsticks (Multistix, Bayer Corp.) placed in the specimens for 'ketones.' Results: Multistix detected AcAc appropriately; ACET was detected only at high concentrations of >/=600 mmol/L. Multistix failed to measure BOHB at all concentrations tested. H(2)O(2) improved urinary BOHB detection, although not to clinically relevant levels (40 mmol/L). Alkalinization and AgNO(3) sticks did not improve BOHB detection beyond this threshold. Conclusions: Addition of H(2)O(2) (3%), alkalinization, or AgNO(3) sticks did not improve clinically meaningful urine BOHB detection. Clinicians should use direct methods to detect BOHB when suspected
PMID: 18637083
ISSN: 1553-2712
CID: 80582

Prolonged severe hypotension following combined amlodipine and valsartan ingestion [Case Report]

Smith, Silas W; Ferguson, Kathy L; Hoffman, Robert S; Nelson, Lewis S; Greller, Howard A
INTRODUCTION: Compared to other calcium channel blockers (CCBs), overdose with dihydropyridine CCBs are considered relatively benign due to their vascular selectivity. Although not a sustained-release preparation, amlodipine's prolonged duration of effect is concerning following overdose. In addition, angiotensin II receptor blocker blunting of vasoconstrictive and sympathetic compensatory responses could exacerbate calcium channel blocker toxicity. We describe severe toxicity associated with an overdose of amlodipine and valsartan. CASE REPORT: A 75-year-old woman presented to the ED 45 minutes after a witnessed suicidal ingestion of a 'handful' of amlodipine and valsartan tablets. Hypotension, which appeared two hours after ingestion, was refractory to crystalloids and colloids, calcium gluconate, epinephrine, norepinephrine, phenylephrine, and vasopressin infusions. High-dose insulin euglycemia (HIE) therapy, and treatment with glucagon and naloxone were successful in improving her hemodynamic status. In this combined overdose, right heart catheterization demonstrated both negative inotropic effects and decreased systemic vascular resistance. CONCLUSION: Co-ingestion of amlodipine with valsartan produced profound toxicity. Early institution of HIE therapy may be beneficial to reverse these effects
PMID: 18568804
ISSN: 1556-9519
CID: 80579

Case Files of the New York City Poison Control Center: Antidotal strategies for the Management of Methotrexate toxicity [Case Report]

Smith, Silas W; Nelson, Lewis S
A 10-year-old boy (37.5 kg; body surface area 1.26m2) with osteosarcoma of the right humerus received a planned 4-hour infusion of high-dose methotrexate (16 g, 12.7 g/m(2)). His previous medical history was notable for an implanted central venous catheter placement complicated by Horner's syndrome. Renal and hepatic functions were normal at baseline. A postinfusion methotrexate concentration was uninterpretable, but the significance of this result was not initially appreciated by the treating clinicians. Over the next 48 hours, the child developed blurry vision, painful mucositis, stomatitis, and facial blistering. Reported vital signs were: BP, 121/82 mm Hg; pulse, 111/minute; respirations, 16/minute. A physical examination was consistent with the reported symptoms. The 48-hour postinfusion serum methotrexate concentration at the time of poison control center (PCC) consultation was 171 micromol/L
PMCID:3550133
PMID: 18570175
ISSN: 1556-9039
CID: 80580

Rapid diagnosis of metabolic acidosis: Improving bedside detection of urine beta-hydroxybutyrate [Meeting Abstract]

Smith, SW; Manini, AF; Szekely, T; Hoffman, RS
ISI:000256917000276
ISSN: 1556-3650
CID: 86871

In response to Isbister et al.: Application of pharmacokinetic-pharmacodynamic modeling in management of QT abnormalities after citalopram overdose [Letter]

Manini, Alex; Smith, Silas; Moskovitz, Joshua; Nelson, Lewis
PMID: 17279361
ISSN: 0342-4642
CID: 80567

Resilience in the face of disaster: Accounting for varying disaster magnitudes, resource topologies, and (sub)population distributions in the PLAN C emergency planning tool

Narzisi, G; Mincer, JS; Smith, S; Mishra, B
PLAN C, an Agent-Based Model platform for urban disaster simulation and emergency planning, features a variety of reality-based agents interacting on a realistic city map and can simulate the complex dynamics of emergency responses in different urban catastrophe scenarios. Work reported here focuses on the incorporation of specific subpopulations of person agents, reflecting the existence of individuals with specific defining characteristics and needs, and their interactions with the available resources. Performance of these subpopulations are compared in both point-source attack and distributed disaster scenarios for disasters of different magnitudes. Specific ""recovery points"" can be derived both for total- and sub-populations, which estimate the duration of a response system's/city's vulnerability. The effect of varying topologies of available resources, i.e. different hospital maps, provides particular insight into the dynamics that can emerge in this complex system. PLAN C produces interesting emergent behavior which is often consistent with the literature on emergency medicine of previous events.
SCOPUS:37249026259
ISSN: 0302-9743
CID: 642742