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Carson R Harris

Publications and source records attributed to Carson R Harris.

6 recordsLinked to original sources

Deadly ingestions.

More than 50% of the toxic-exposure calls to US poison centers involve children. Although most of these exposures are nontoxic, there are several products and medications that are widely available to the pediatric population that can lead to severe toxicity or even death. With some of these medications, death or severe symptoms can occur with the ingestion of only a small amount. It is important that the clinician be familiar with presenting signs and symptoms of potentially toxic ingestions and is able to initiate a therapeutic and life-saving intervention. This article reviews some of the deadlier ingestions that children may be exposed to.

Alcohols↗

A comparison of vasopressin and glucagon in beta-blocker induced toxicity.

OBJECTIVE: We compared the efficacy of vasopressin and glucagon in a porcine model of beta-blocker toxicity. Our primary outcome was survival over 4 hours. METHODS: Sixteen pigs received a 1-mg/ kg bolus of propranolol IV followed by continuous infusion at 0.25 mg/kg/minute. Toxicity was defined as a 25% decrease in the product of heart rate (HR) and mean arterial pressure (MAP), at which point 20 mL/kg normal saline was rapidly infused. Each pig was randomly assigned to receive either vasopressin or glucagon after the saline bolus. The vasopressin group received a continuous infusion at 0.0028 U/kg/minute, titrated up to a maximum of 0.014 U/ kg/minute. The glucagon group received a 0.05-mg/kg bolus followed by continuous infusion at 0.15 mg/kg/hour. The HR, MAP, systolic BP (SBP), cardiac output (CO), glucose, and pH were monitored for 4 hours from toxicity or until death. RESULTS: One pig survived at 4 hours (vasopressin group). Analysis of the 4-hour Kaplan-Meier survival curves found no differences between the groups (log-rank test 0.059, p = 0.81). No overall differences were identified in MAP, systolic BP, cardiac output, glucose, pH, or HR. However, over the first hour MAP and SBP were significantly higher in the vasopressin group (p = 0.004, p = 0.006, respectively). CONCLUSION: In this beta-blocker toxicity model, there were no differences in the survival curves between vasopressin- and glucagon-treated pigs during a 4-hour analysis period. No overall differences were noted in MAP, systolic BP, CO, HR, pH, or glucose levels, although vasopressin treatment yielded higher MAP and systolic BP early in resuscitation.

Adrenergic beta-Antagonists↗

Methanol ingestion: prevention of toxic sequelae after massive ingestion.

Methanol ingestion, a rare but potentially fatal poisoning, is often difficult to diagnose in the emergency department (ED) and historically has been difficult to treat. In this article, we report a methanol ingestion with a blood concentration of 692 mg/dL, which was treated with 4-methylpyrazole (Fomepizole) and dialysis, without sequelae. To our knowledge, such a massive ingestion has never been treated with this modality without development of long-term disability. Another unusual feature of this case is the significantly elevated serum osmolal gap at presentation without elevation in anion gap, demonstrating the effects of co-ingestion of ethanol. Additionally, there was a marked disparity between the patient's breath alcohol analyzer level and the blood ethanol concentration, illustrating the inability of the breath alcohol analyzer to differentiate between volatile alcohols. Treatment of the methanol-poisoned patient with Fomepizole is discussed.

Adult↗

Cardiotoxicity and late onset seizures with citalopram overdose.

A 31-year-old man ingested 400 mg of citalopram (Celexa) after an argument with his parents and girlfriend 13 h before presentation. Paramedics witnessed the patient having a generalized clonic seizure. The electrocardiogram (EKG) revealed a wide QRS complex, prolongation of the QTc interval, and left bundle branch pattern. He was treated with sodium bicarbonate with resolution of these changes. The patient was continued on a sodium bicarbonate infusion and demonstrated no further EKG abnormalities. Sodium bicarbonate should be considered as a treatment modality in patients with EKG abnormalities of prolongation of QRS or QTc interval after citalopram overdose.

Adult↗

Repeated ingestion of 2-butoxyethanol: case report and literature review.

BACKGROUND: Ethylene glycol monobutyl ether (2-butoxyethanol) is not commonly associated with significant human poisoning. Exposures are usually through occupational contact and typically involve inhalation injury. Animal studies report severe hemolysis occurring in rats and mice. Rare published human cases give varied descriptions of the clinical course associated with 2-butoxyethanol poisoning including reports of metabolic acidosis, ethylene glycol production, oxaluria, renal failure, and anemia. We report a case of two separate ingestions (80 to 100 grams) of a glass cleaner concentrate containing 22% 2-butoxyethanol, and its primary metabolite butoxyacetic acid. CASE REPORT: An 18-year-old male ingested 360-480 mL of 22% 2-butoxyethanol on two separate occasions. Approximately 10hours after the first ingestion, the patient developed severe CNS depression, metabolic acidosis, hematuria, and mild elevation of hepatic enzymes. He was treated initially with ethanol therapy but continued to deteriorate and was started on hemodialysis. Approximately 10 days after discharge, the patient ingested 480 mL of the same product and received ethanol and hemodialysis within four hours of ingestion. During his second admission the patient did not develop the delayed severe CNS depression or profound metabolic acidosis. Clinically significant hemolytic anemia, oxaluria, ethylene glycol production, and renal failure were not noted in either episode. The patient recovered on both occasions without sequelae. CONCLUSION: Hemodialysis may be an effective treatment intervention for managing severe acute 2-butoxyethanol intoxication, however, further investigation is warranted.

Adolescent↗

Physostigmine, sodium bicarbonate, or hypertonic saline to treat diphenhydramine toxicity.

Diphenhydramine (DPH) is a commonly reported overdose that shares similar toxicities with other agents. such as tricyclic antidepressants, that interact with the fast sodium channels. Although physostigmine is considered an acceptable antidote for severe DPH toxicity, adverse effects such as seizures and cholinergic crisis may occur. We hypothesized that hypertonic saline or bicarbonate is equivalent or are better antidotes in an animal model of DPH toxicity. In a preliminary study. Sprague-Dawley rats were given toxic doses of DPH while continuous ECG, EEG, and blood pressure monitoring was performed. Seizures were the common toxic effect observed and was chosen. Four groups of 10 rats each were established as control physostigmine, hypertonic sodium bicarbonate, and hypertonic saline(3%) treatment. Control had initial "drop-off" seizure burst rates over time; seizure bursts in the treatment groups were compared to these rates. Hypertonic sodium bicarbonate was the most effective treatment, followed closely by hypertonic saline. Hypertonic sodium bicarbonate may interact with DPH neuronal sodium channels and may be considered adjuvant therapy in humans with DPH-induced seizures.

Animals↗