George M Bosse

Publications of George M Bosse

• Amlodipine Fatality in an Infant with Postmortem Blood Levels.

  Authors: Henry A Spiller, Beth A Milliner, George M Bosse

  Journal of medical toxicology : official journal of the American College of Medical Toxicology. 01/2012;

  INTRODUCTION: Amlodipine is a dihydropyridine calcium channel blocker used in the treatment of hypertension and angina pectoris. Toxic effects reported from amlodipine include hypotension, reflexINTRODUCTION: Amlodipine is a dihydropyridine calcium channel blocker used in the treatment of hypertension and angina pectoris. Toxic effects reported from amlodipine include hypotension, reflex tachycardia, metabolic acidosis, and pulmonary edema. We report a rare fatality in an infant after ingestion of amlodipine with benazepril, with postmortem blood concentrations. CASE REPORT: An 11-month-old, 10.88-kg boy ingested 10 to 45 mg amlodipine with 40 to 180 mg benazepril. No action was taken initially because the parents believed only one or two capsules had been ingested. A later count revealed a maximum of nine capsules missing. The child was observed at home and vomited once with possible capsule fragments. Forty-five minutes post-ingestion, the child was noted to be suddenly unresponsive and was brought the local emergency department by a private vehicle. Upon arrival (90 min post-ingestion), the child was unresponsive with the following vital signs HR 133 bpm, BP 67/42 mmHg, respiratory rate 40/min, and temperature 97.5°F. Pertinent abnormal laboratory values were HCO(3) 13 mmol/l and glucose 302 mg/dl. The child was placed on oxygen via a non-rebreather mask and was intubated 45 min post-arrival. The patient became progressively bradycardic, and 55 min after arrival, the patient was in asystole with no palpable blood pressure. Resuscitation measures included chest compressions, epinephrine atropine, sodium bicarbonate, and calcium gluconate. Rescue insulin therapy was begun with 4 units IVP followed by 10 units per hour. Resuscitation efforts persisted for 1 h without success. An autopsy revealed pulmonary edema and no gross or microscopic evidence of natural disease. Stomach contents revealed food matter with small white fragments. Analysis of postmortem heart blood showed amlodipine 1,300 ng/ml (therapeutic <20 ng/ml). Benazepril levels were not available. DISCUSSION: We believe this is the first reported fatality in an infant from amlodipine. While benazepril may have contributed, ACE inhibitors have not been previously associated with rapid cardiovascular collapse. CONCLUSION: Small doses of amlodipine (0.9 to 4.1 mg/kg) may produce rapid and fatal cardiovascular collapse in an infant.

• Necrotizing peripheral vasculitis/vasculopathy following the use of cocaine laced with levamisole.

  Authors: Russell W Farmer, Paula S Malhotra, Michael P Mays, Michael E Egger, Jason W Smith, Saeed A Jortani, Henry Spiller, George M Bosse, Jeffrey P Callen, Glen A Franklin

  Journal of burn care & research : official publication of the American Burn Association. 12/2011; 33(1):e6-e11.

  The objective of this study was to describe a novel presentation of peripheral vasculitis associated with levamisole-adulterated cocaine. Cocaine abuse is widespread in the United States with 5.3The objective of this study was to describe a novel presentation of peripheral vasculitis associated with levamisole-adulterated cocaine. Cocaine abuse is widespread in the United States with 5.3 million people using cocaine in 2008. Over the past decade, drug enforcement officials have noticed the presence of levamisole in confiscated cocaine samples as an adulterant. Known side effects of cocaine-related levamisole ingestion have included agranulocytosis and a cutaneous acral purpura that is histopathologically characterized by a mixture of inflammation (vasculitis) and occlusion (vasculopathy). A 54-year-old man who nasally ingested cocaine laced with levamisole developed widespread necrotic/purpuric skin lesions on approximately 20% of his body with an acral accentuation. These lesions were complicated by multiple areas of sloughing and necrosis. He was initially treated with topical silver sulfadiazine dressing changes but progressed to require debridement and split-thickness skin grafting. Peripheral vasculitis/vasculopathy with severe necrosis resembling Coumadin necrosis is a relatively recently recognized sequelae from levamisole-adulterated cocaine use.

• Acute oral potassium overdose: the role of hemodialysis.

  Authors: George M Bosse, Melissa A Platt, Stephen D Anderson, Michael W Presley

  Journal of medical toxicology : official journal of the American College of Medical Toxicology. 03/2011; 7(1):52-6.

  Hyperkalemia is a common condition, particularly in the setting of renal dysfunction. Hyperkalemia due to intentional oral potassium overdose is not commonly reported. We present a case of acuteHyperkalemia is a common condition, particularly in the setting of renal dysfunction. Hyperkalemia due to intentional oral potassium overdose is not commonly reported. We present a case of acute intentional potassium overdose in a patient with normal renal function resulting in significant hyperkalemia, with a maximum serum potassium concentration of 11 mEq/L. Despite an initial course complicated by various unstable cardiac rhythms, including ventricular tachycardia, ventricular fibrillation, and pulseless electrical activity, the patient was discharged from the hospital neurologically intact. Treatment for hyperkalemia included hemodialysis. The role of dialysis in potassium overdose is poorly defined. Based on this case and a review of the medical literature, we recommend hemodialysis for cases of potassium overdose with hemodynamic instability and significantly elevated serum potassium concentrations that do not respond promptly to medical therapy. Hemodialysis should also be considered in cases with underlying renal dysfunction.

• Is elevated creatinine a reliable marker for methanol toxicity in nitromethane-containing model fuel ingestions in children?

  Authors: Pradeep Padmanabhan, Henry A Spiller, Mitchell P Ross, George M Bosse

  Clinical toxicology (Philadelphia, Pa.). 01/2011; 49(1):45-7.

  In the absence of a rapid serum methanol level estimation, it is difficult to assess the risk from unintentional childhood ingestion of model fuels containing methanol and nitromethane (MFNM).In the absence of a rapid serum methanol level estimation, it is difficult to assess the risk from unintentional childhood ingestion of model fuels containing methanol and nitromethane (MFNM). Previous reports have documented false elevations of serum creatinine from the nitromethane in these fuels, suggesting its utility as a readily available marker of significant methanol ingestion. We performed a 2-year retrospective chart review of cases of ingestion of MFNM in children, with both a methanol level and measured creatinine level. Seven children, ages 19 months to 3 years, ingested MFNM. All seven children were seen in a hospital and had measured methanol and creatinine levels. All blood samples for methanol and creatinine were drawn within 3 hours of ingestion with methanol estimation delayed up to 24 hours. Creatinine ranged from 0.39 (0.034 mmol/l) to 10.7 mg/dl (0.95 mmol/l). All methanol levels were <10 mg/dl (0.31 mmol/l) or reported as negative. Fomepizole was initiated empirically in two patients due to delay in obtaining methanol analysis results. Transient elevations of creatinine occurred in five of the seven children. Blood urea nitrogen was within normal limits, and there was no history of renal impairment in these children, suggesting the elevated creatinine was mostly related to nitromethane ingestion. No child had a significantly elevated methanol level. Elevated creatinine level, as measured by Jaffe colorimetric method, is not a reliable marker for elevated methanol levels after unintentional ingestion of MFNM.

• Use of antivenom for snakebites reported to United States poison centers.

  Authors: Henry A Spiller, George M Bosse, Mark L Ryan

  The American journal of emergency medicine. 09/2010; 28(7):780-5.

  In 2001, a new antivenin was introduced to the United States and became widely available in the snakebite season of 2002. We investigated what impact this may have had on snakebite treatment andIn 2001, a new antivenin was introduced to the United States and became widely available in the snakebite season of 2002. We investigated what impact this may have had on snakebite treatment and medical outcome. The study used a retrospective review of all snakebites to humans reported to the National Poison Center Database System from 2000 to 2007. During the 8 years, there were 37,760 snakebites, with a mean of 4720 bites per year. There was a 27% increase in bites reported to a Poison center for the 8-year period and an overall 13.5% increase in the use of antivenin. The 2 categories primarily responsible for the increased use of antivenin were copperhead and crotaline-unknown. Rattlesnake bites remained the category most frequently treated with antivenin with a mean 52.5% treatment rate and only moderate increase for the 8 years. There was no change in the percentage or number of patients with a major outcome (mean, 3.8%) or death (mean, 0.5%). There was a decrease in patients with a minor outcome and an increase in patients with a moderate outcome. The new antivenin is reported to have a reduced potential for adverse reactions. This may have had a role in the decision of which snakebite victims received antivenin. With the introduction of a new antivenin, there has been a dramatic increase in the number of snakebite patients treated with antivenin. This has been most noticeable in snake bite categories that were less frequently treated with antivenin in the past.

• Unintentional ingestion of bupropion in children.

  Authors: Henry A Spiller, George M Bosse, Michael Beuhler, Ted Gray, S David Baker

  The Journal of emergency medicine. 04/2010; 38(3):332-6.

  The incidence of seizures after unintentional bupropion ingestion in children aged < 6 years has been reported as 0.2%. However, in many poison centers, > 80% of these patients are referred to theThe incidence of seizures after unintentional bupropion ingestion in children aged < 6 years has been reported as 0.2%. However, in many poison centers, > 80% of these patients are referred to the Emergency Department (ED) for evaluation. To evaluate if all unintentional pediatric bupropion ingestions require referral to a health care facility (HCF), or what fraction of these could be managed safely at home. A retrospective chart review was conducted of all bupropion ingestions in children aged < 6 years for 2000-2006 from four regional poison centers. Exclusion criteria were lack of follow-up or multiple drug ingestion. Of 407 patients, 209 (51%) were male. Mean age was 2.2 years (SD +/- 1.0). There were 329 patients (81%) seen in a HCF, of which 143 (35%) were hospitalized; 77 patients (19%) were observed at home. Symptoms occurred in 73 patients (18%): sinus tachycardia (n = 50), nausea/vomiting (n = 32), hyperactivity (n = 17), seizure (n = 3), hallucinations (n = 2), and hypertension (n = 2). The mean heart rate of patients with sinus tachycardia (n = 50, 12.3%) was 137 beats/min (SD +/- 13), with a range of 112-172 beats/min. Mean dosage of those with tachycardia was 24 mg/kg. In the 2 patients with hypertension, the maximum recorded blood pressures were 145/80 mm Hg (2-year-old boy) and 137/90 mm Hg (2-year-old girl), with heart rates of 122 and 125 beats/min, respectively. Dose ingested and patient weight was known for 218 patients. Mean dosage ingested was 12.2 mg/kg, with a range of 2.6-64 mg/kg. Eighty-eight percent of patients with a known dosage ingested < 20 mg/kg. A high percentage of children continue to be seen in a HCF. Concern from the higher incidence of severe effects seen with intentional adult exposures may be one of the reasons for this cautious approach. Conclusion: Unintentional pediatric bupropion ingestions resulted in clinical effects that rarely required any HCF intervention. Isolated unintentional bupropion ingestion of <or= 10 mg/kg may not require referral to a health care facility.

• A case of hypercalcemia and gastric necrosis from hot pack ingestion.

  Authors: Pradeep Padmanabhan, Henry A Spiller, George M Bosse

  Journal of medical toxicology : official journal of the American College of Medical Toxicology. 04/2010; 6(2):139-42.

  Hot packs (instant hot compresses) are frequently used to relieve pain. We report a patient who had significant complications from ingestion of a hot pack containing calcium salts. A 35-year-old maleHot packs (instant hot compresses) are frequently used to relieve pain. We report a patient who had significant complications from ingestion of a hot pack containing calcium salts. A 35-year-old male swallowed three hot packs, and developed hematemesis, severe abdominal pain, and hypercalcemia (21.1 mg/dl). He developed diffuse gastric necrosis requiring gastrectomy and colonic interposition. Hypercalcemia was treated with intravenous fluids, pamidronate, and calcitonin. A Medline search revealed no prior report on hot pack ingestion though ingestion of calcium salts has been reported. Hot packs can potentially cause significant injury both from an exothermic reaction and hypercalcemia. Ingestions of calcium salts can result in necrosis of the stomach. Management includes aggressive treatment of hypercalcemia, supportive care and upper gastrointestinal endoscopy.

• A fatal case of venlafaxine overdose.

  Authors: George M Bosse, Henry A Spiller, Aaron M Collins

  Journal of medical toxicology : official journal of the American College of Medical Toxicology. 04/2008; 4(1):18-20.

  Introduction: Based on its primary action of serotonin reuptake inhibition, venlafaxine overdose would be expected to result in serotonergic effects. Case Report: A 40 year old male ingestedIntroduction: Based on its primary action of serotonin reuptake inhibition, venlafaxine overdose would be expected to result in serotonergic effects. Case Report: A 40 year old male ingested venlafaxine without co-ingestants in a suicide attempt. The patient developed refractory ventricular fibrillation and expired approximately 9 hours post-ingestion. ECG monitoring revealed significant QRS and QTC interval prolongation prior to his demise. Discussion: A literature review of venlafaxine overdose cases and investigation into its mechanism of action was conducted. The potential for sodium channel blockade and implications for therapy are discussed.

• Ingestion of a denture cleanser: did it cause gastric perforation?

  Authors: Daniel M Ingram, George M Bosse, Richard Baldwin

  Journal of medical toxicology : official journal of the American College of Medical Toxicology. 04/2008; 4(1):21-4.

  Introduction: Human ingestion of denture cleansers leading to gastric perforation has not previously been described. Case Report: A 27-year-old male ingested three denture cleanser tablets in waterIntroduction: Human ingestion of denture cleansers leading to gastric perforation has not previously been described. Case Report: A 27-year-old male ingested three denture cleanser tablets in water over two days in an attempt to cause a false negative result on a workplace urine drug screen. Seven days later he presented to an emergency department with a perforated gastric ulcer. Discussion: A literature review of cases and the chemistry of the components of his ingestion was conducted to determine the possible relationship between these events. Ingestion of intact fragments of the tablets would be likely to result in significant gastric toxicity, but ingestion of dissolved tablets would be unlikely to have caused his illness.

• Fatal fluoxetine ingestion with postmortem blood concentrations.

  Authors: Russel Compton, Henry A Spiller, George M Bosse

  Clinical toxicology (Philadelphia, Pa.). 02/2005; 43(4):277-9.

  A 37-year-old male ingested 12 gm of fluoxetine approximately 2 hours prior to arrival at an emergency department. The patient developed tonic-clonic seizures, which resolved with diazepam andA 37-year-old male ingested 12 gm of fluoxetine approximately 2 hours prior to arrival at an emergency department. The patient developed tonic-clonic seizures, which resolved with diazepam and midazolam therapy. The patient then developed profound bradycardia that progressed to ventricular fibrillation and asystole. A postmortem toxicology analysis reported a fluoxetine concentration of 4500 mcg/L and diazepam of 500 mcg/L. No other drugs were detected. We report an unusual case of massive fluoxetine ingestion resulting in neurological and cardiovascular toxicity resulting in death.

• Retrospective review of Tizanidine (Zanaflex) overdose.

  Authors: Henry A Spiller, George M Bosse, Larry A Adamson

  Journal of toxicology. Clinical toxicology. 02/2004; 42(5):593-6.

  BACKGROUND: Tizanidine is a centrally acting muscle relaxant with a novel mechanism of action and structurally related to clonidine. There are no large case series of tizanidine exposure. METHODS:BACKGROUND: Tizanidine is a centrally acting muscle relaxant with a novel mechanism of action and structurally related to clonidine. There are no large case series of tizanidine exposure. METHODS: Retrospective review of all ingestions involving tizanidine reported to a poison control center from January 2000 through February 2003. Exclusion criteria were polydrug ingestion, no follow-up or lost to follow-up. RESULTS: There were 121 cases of which 45 patients met entrance criteria. Mean age was 32 years (range 1 to 80). Thirty-seven patients were evaluated in a health care facility of which 27 were admitted for medical care. Clinical effects included lethargy (n = 38), bradycardia (n = 14), hypotension (n = 8), agitation (n = 7), confusion (n = 5), vomiting (n = 3), and coma (n = 2). Mean dose ingested by history was 72 mg (S.D. + 86). The lowest dose associated with hypotension was 28mg, which occurred in a 63-year-old female with a BP of 88/52 and a HR of 54. The lowest dose associated with coma was between 60 mg and 120 mg, which occurred in a 30-year-old female with a HR of 30 and BP of 81/48. There were 6 patients < 6 yrs. The lowest dose with bradycardia and drowsiness in a small child was 16 mg in a 2 YO (weight unknown). All other cases in children < 6 yrs involved ingestion of a single tablet (2 or 4 mg) with only mild drowsiness reported. Therapy in this series was primarily supportive and included pressors in 3 cases and intubation in 3 cases. Naloxone was administered to 7 patients. There was no response to naloxone in 5 patients, poor documentation of response in one, and arousal in one patient. All patients recovered without residual complications. CONCLUSION: Clinical manifestations of tizanidine overdose include alterations of mental status, bradycardia, and hypotension. In this series, outcome was good with supportive therapy.

• Intermediate syndrome after exposure to chlorpyrifos in a 16-month-old girl.

  Authors: Jason E Mattingly, Janice E Sullivan, Henry A Spiller, George M Bosse

  The Journal of emergency medicine. 12/2003; 25(4):379-81.

  We describe a case of intermediate syndrome after chlorpyrifos ingestion in a toddler, despite a continuous pralidoxime infusion. A 16-month-old girl ingested a pesticide containing chlorpyrifos. SheWe describe a case of intermediate syndrome after chlorpyrifos ingestion in a toddler, despite a continuous pralidoxime infusion. A 16-month-old girl ingested a pesticide containing chlorpyrifos. She was brought to an Emergency Department where she became lethargic and tachycardic, and subsequently developed pulmonary edema requiring mechanical ventilation. Pralidoxime 150 mg i.v. was administered twice, and an infusion begun at 15 mg/kg/h. At 24.5 h post-ingestion the child had a normal neurologic examination, showed no signs of cholinergic excess, and was extubated successfully. At 27.5 h post-ingestion the child became flaccid, bradycardic and apneic. She was emergently re-intubated. The child's delayed onset of respiratory arrest and flaccid paralysis after an asymptomatic period is consistent with Intermediate Syndrome. This is an unusual case in that it occurred in a young child, was related to chlorpyrifos, and occurred despite continuous and adequate oxime therapy.

• Prospective study of morbidity associated with snakebite envenomation.

  Authors: Henry A Spiller, George M Bosse

  Journal of toxicology. Clinical toxicology. 02/2003; 41(2):125-30.

  BACKGROUND: The morbidity associated with snakebite envenomation has not been well documented. METHOD: Using a standardized questionnaire all patients with snakebite reported to a regional poisonBACKGROUND: The morbidity associated with snakebite envenomation has not been well documented. METHOD: Using a standardized questionnaire all patients with snakebite reported to a regional poison center during the year 2001 were followed after hospital discharge by telephone until resolution of symptoms. RESULTS: One hundred and twenty-eight snakebite cases were reported, of which 16 (12.5%) were lost to follow-up and 31 (24.2%) reported no progression of symptoms beyond puncture and were deemed "dry bites." Eighty-one (63.3%) patients were followed for the duration of symptoms. Age ranged from 1 to 86 years with a mean of 32 years. There were 64 males (79%). The snakes were identified as copperhead (n = 57), unidentified venomous (n = 17), timber rattlesnake (n = 6), and cottonmouth (n = 1). All patients were initially evaluated in a hospital emergency department of which 51 were admitted. Nine patients received antivenin. Of the 37 patients who had a job, 33 lost a mean of 14 days of work (SD +/- 18.1). Mean duration of edema was reported as 11.4 days (S.D +/- 12). Recurrent edema frequently occurred with limb activity. Pain was scored on a scale of 1 to 10, with a mean score of 4.8 (SD +/- 2.7). Mean duration of pain was reported as 7.8 days (SD +/- 6.4). Thirty patients required accommodation for ambulation including crutches (n = 11), limp (n = 11), and no shoes or loose shoes (n = 14). Of the 26 patients bitten on the hand or finger, duration of reduced function persisted for a mean of 14.3 days (SD +/- 10.4) and reduction of hand strength persisted for a mean of 22 days (SD +/- 25.5). Five patients had poorly healing wounds at the bite site which persisted from 14 to 77 days with a mean of 45 days (SD +/- 22.8) CONCLUSION: In this study snakebite resulted in significant duration and extent of morbidity in a majority of patients.

• The safety of intravenously administered vitamin K.

  Authors: George M Bosse, Mary Nan S Mallory, Greg J Malone

  Veterinary and human toxicology. 06/2002; 44(3):174-6.

  Literature sources suggest that iv vitamin K is associated with significant adverse side effects. Systematic study and documentation is lacking. In this 2-y retrospective review, 100 sequential dosesLiterature sources suggest that iv vitamin K is associated with significant adverse side effects. Systematic study and documentation is lacking. In this 2-y retrospective review, 100 sequential doses of iv administered vitamin K in 45 patients were identified by computer-generated pharmacy utilization reports in an adult teaching hospital. Charts were reviewed for complications following infusion of vitamin K, including specific abnormalities during the 90-min period post-administration: systolic blood pressure <90, heart rate <60 or >120, rash, shortness of breath, and syncope. Complete post-administration data were available for 60/100 doses. One episode of clinically insignificant transient hypotension was identified. Progress notes, discharge summaries and a concurrent survey of adverse drug reaction reports identified no complications related to the use of iv vitamin K. In this series, the iv administration of vitamin K did not pose a clinically significant risk.