Fluoride ingestion in children: a review of 87 cases.

All cases of fluoride ingestion in children younger than 12 years old reported to the Rocky Mountain Poison Center between January 1 and December 31, 1986, were retrospectively reviewed. Eighty-seven cases were identified. Eighty-four cases involved accidental ingestion of dental fluoride products in the home (tablets, drops, rinses) in children 8 months to 6 years old. Two older children (8 and 9 years old) became symptomatic after fluoride treatment by a dentist. A 13-month-old child died after ingesting an unknown amount of sodium fluoride insecticide, the only insecticide exposure in our series. Postmortem total serum calcium value was 4.8 mg/dL (normal 8.8 to 10.3). No other patients had serious symptoms or sequelae. Twenty-six (30%) of 87 became symptomatic, with gastrointestinal symptoms (nausea, vomiting, diarrhea, abdominal pain) in 25 patients and drowsiness in 1. Only 3 patients became symptomatic later than 1 hour after ingestion. Analysis of data from 70 cases with sufficient information revealed that as the amount of fluoride ingested increased, the percentage of patients with symptoms increased. Not including the fatal case, 6 patients had serum calcium levels measured, and all were normal. Children who ingested up to 8.4 mg/kg of elemental fluoride in dental products had mild and self-limited symptoms, mostly gastrointestinal.

Drug- and toxin-induced seizures.

Seizure is an omnimous sign when it occurs in relation to drugs or toxins. Knowledge of those drugs or toxins that have a predilection to cause seizures may prove invaluable when one is treating such a patient. Aggressive treatment with the appropriate therapy may have a significant impact on outcome. As seen from this article, many drugs and toxins are associated with seizures. Fortunately, the majority of these seizures can be managed with supportive care, using the standard anticonvulsant drugs. Management of the seizure in a few drugs and toxins requires additional intervention. It is the addition of these specific treatment modalities that may prove to be lifesaving despite drug- or toxin-induced seizures.

Iron poisoning: report of three cases and a review of therapeutic intervention.

Although the acute ingestion of iron-containing preparations can produce very serious consequences, the majority of reported exposures are not associated with significant morbidity or mortality. We present 3 cases of acute iron ingestion and review the aspects of general management, with an emphasis on the appropriate choice of a gastrointestinal decontamination procedure.

Theophylline toxicity from an over-the-counter preparation.

The clinical presentation of theophylline poisoned patients has been well described in the literature. These individuals may develop severe and potentially fatal cardiac, neurologic, and gastrointestinal manifestations. While patients may present following an intentional over-dose, a significant percentage become toxic accidentally or iatrogenically, as a result of theophylline's narrow therapeutic index. Another factor, not well known or described in the literature, is the availability of theophylline in a variety of over-the-counter formulations. We present a case of theophylline toxicity from a nonprescription combination product containing theophylline, ephedrine, and phenobarbital. Clinicians should be aware of the potential for serious toxicity from over-the-counter medications, particularly those commonly thought of as "prescription only."

Chlorophyllum molybdites--severe mushroom poisoning in a child.

The case of a 6-year-old female who developed hypovolemic shock from mushroom poisoning is discussed. The mushroom ingested, Chlorophyllum molybdites, is considered to be a benign gastrointestinal irritant. This case emphasizes that the gastrointestinal irritant mushrooms can produce severe toxicity and that pediatric patients have a limited capacity for fluid loss before becoming hypovolemic.

Captopril overdose resulting in hypotension.

We present a case in which a patient took an overdose of captopril (Capoten) and alprazolam (Xanax) in a suicide attempt. The patient presented with hypotension (systolic blood pressure of 80 mm Hg) and drowsiness. The hypotension initially responded to administration of intravenous fluids and dopamine; however, it recurred twice at 18.5 and 24.5 hours after ingestion. These episodes again responded to administration of fluids and dopamine. A plasma captopril level of 27,391.1 nmol/L (5982 ng/mL) was documented, as well as a depressed level of angiotensin converting enzyme. Captopril is an angiotensin converting enzyme inhibitor used in the management of hypertension and ventricular failure; to our knowledge, this is the first case of an acute captopril overdose reported in the English-language literature. The role of captopril in inducing hypotension is discussed herein.

Acetaminophen overdose: a 48-hour intravenous N-acetylcysteine treatment protocol.

STUDY OBJECTIVE: To determine the safety and efficacy of a 48-hour IV N-acetylcysteine (IV NAC) treatment protocol for acute acetaminophen overdose. DESIGN: Nonrandomized trial open to all eligible patients. SETTING: Multicenter; hospitals included moderate- and high-volume private, university, and municipal hospitals in urban and suburban settings. TYPE OF PARTICIPANTS: Two hundred twenty-three patients were entered. Of these, 179 met inclusion criteria: acute acetaminophen overdose, plasma acetaminophen concentration above the treatment nomogram line, treatment with IV NAC according to the protocol, and sufficient data to determine outcome. INTERVENTIONS: IV NAC treatment consisted of a loading dose of 140 mg/kg followed by 12 doses of 70 mg/kg every four hours. MEASUREMENTS AND MAIN RESULTS: Patients were grouped for analysis according to risk group based on the initial plasma acetaminophen concentration. Hepatotoxicity (aspartate aminotransferase or alanine aminotransferase of more than 1,000 IU/L) developed in 10% (five of 50) of patients at "probable risk" when IV NAC was started within ten hours of acetaminophen ingestion and in 27.1% (23 of 85) when therapy was begun after ten to 24 hours. Among "high-risk" patients first treated 16 to 24 hours after overdose, hepatotoxicity occurred in 57.9% (11 of 19). There were two deaths (two of 179, 1.1%). Adverse reactions resulting from NAC occurred in 32 of 223 cases (14.3%), consisting in 29 of 32 patients (91% of reactions) of transient, patchy, skin erythema or mild urticaria during the loading dose that did not require discontinuation of therapy. CONCLUSION: This 48-hour IV NAC protocol is safe and effective antidotal therapy for acetaminophen overdose. Based on available data, it is equal to 72-hour oral and 20-hour IV treatment protocols when started early and superior to the 20-hour IV regimen when treatment is delayed. Further study will be required to determine its relative efficacy in the high-risk patient treated very late.

Hydrofluoric acid dermal exposure.

A retrospective review of 237 consecutive cases of dermal exposure to dilute (6-11%) hydrofluoric acid (HF)- containing rust stain remover consumer products reported to the Rocky Mountain Poison and Drug Center during 1986 was done to evaluate the toxicity of these agents and the efficacy of topical treatment with calcium gluconate gel. In 148 cases (62%), failure to follow manufacturers' recommended safety procedures was the likely cause of exposure. 219 patients developed the following symptoms: dermal swelling, redness, or both (131, 55%); blistering (12, 5%); black discoloration under fingernails (12, 5%); or pain without reported dermal changes (64, 27%). Local complications were noted in 7 cases (3%) (infection, 4 cases; fingertip dermal necrosis, 3 cases). No systemic toxicity was noted. 116 patients (49%) received treatment with topical calcium gluconate gel; 53 were followed until complete resolution of symptoms. There appeared to be a relationship between earlier initial gel application and more rapid resolution of signs and symptoms. Some degree of dermal injury may be quite common following exposure to dilute (6-11%) HF-containing rust stain remover consumer products. Failure to follow manufacturers' recommended safety procedures may be responsible for many exposures. Treatment with topical calcium gluconate gel may be effective, and more rapid resolution of signs and symptoms may occur with earlier initiation of this therapy.