Cyanide poisoning from laetrile ingestion: role of nitrite therapy.

A 4-year-old child ingested laetrile and almost died of cyanide poisoning. Treatment with the Lilly cyanide antidote kit resulted in rapid, complete recovery. Extremely high whole blood cyanide levels were documented. The necessity for use of the antidote kit in serious cyanide poisoning has recently been questioned. This case demonstrates benefit from antidotal treatment.

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.

Superwarfarin poisoning in children: a prospective study.

This prospective study was undertaken to determine the incidence, severity, time of onset, and duration of coagulopathy in children following accidental ingestion of long-acting anticoagulant rodenticides, often called "superwarfarins." Of 110 children, who ingested superwarfarins and in whom one or more prothrombin time values were obtained, 8 had a prothrombin time ratio (patient to control) of greater than or equal to 1.2, indicative of anticoagulation. Prothrombin time values obtained 48 hours after ingestion were more likely to be prolonged (6/34, 17.6%) than values obtained 24 hours after ingestion (2/104, 1.9%) (P less than .005). The occurrence of an abnormal prothrombin time could not be predicted based on the history of amount ingested or on the presence of the characteristic green-blue product dye in or around the child's mouth. Acute toxicity was evidenced by transient abdominal pain, vomiting, and heme positive stools in 2 patients. The duration of prothrombin time prolongation could not be determined because of the few values obtained after 48 hours. To detect all possible abnormal prothrombin time values, 24- and 48-hour determinations are recommended after a child has ingested a superwarfarin.

The other alcohols. Methanol, ethylene glycol, and isopropanol.

The alcoholic patient, in an attempt to maintain an altered mental status, may ingest ethanol substitutes containing methanol, ethylene glycol, or isopropanol. The subsequent clinical presentation in the Emergency Department is highly variable and depends on the ethanol substitute ingested, the time since ingestion, and concomitant ethanol abuse. This article describes the clinical features of intoxication by the ethanol substitutes. Early diagnosis and therapeutic intervention may prevent irreversible sequelae. The rationale for treatment interventions is discussed.

Cimetidine as adjunctive treatment for acetaminophen overdose.

The aim of this study was to determine if cimetidine in addition to N-acetylcysteine and standard supportive care provide additional hepatoprotection following acute acetaminophen poisoning. It was designed as a prospective study with alternate month treatment protocol, and the work was carried out at a regional certified poison information centre. For a 2-year period, consultations received by the Rocky Mountain Poison Center involving acute acetaminophen overdose patients with a serum level above the nomogram line, but who would not receive N-acetylcystine therapy until at least 8 h postingestion, were prospectively evaluated for adjunctive treatment with cimetidine. All patients received standard supportive therapy and N-acetylcysteine treatment. During odd numbered months, cimetidine 300 mg was administered intravenously every 6 h for the duration of N-acetylcysteine therapy. Forty-one cimetidine treated patients were compared to 66 patients in the control group. The peak measured AST levels (+/- s.e.) were 1259+/-330 and 1301+/-451 for the control and cimetidine treatment groups, respectively (P = 0.94). Fourteen of 64 patients (21%) in the control group and 8/41 patients (20%) in the cimetidine group developed an AST > 1000 IUL-1. There were no statistical differences between the cimetidine-treated and control groups when classified by AST < 100 IUL-1, 100-1000 IUL-1, or > 1000 IUL-1. The addition of cimetidine therapy to standard N-acetylcysteine treatment did not provide additional hepatoprotection in acutely acetaminophen poisoned patients when treatment was started later than 8 h post overdose.(ABSTRACT TRUNCATED AT 250 WORDS)

Human ivermectin exposure.

Ivermectin is a veterinary antiparasitic medication for domestic animals. Two cases of human exposure to veterinary preparations of ivermectin are reported. Patient number one accidentally self-injected ivermectin and developed nausea, pallor, and transient pain and numbness in the affected extremity. Patient number two, a 4-year-old child, ingested an unknown amount of the paste preparation and remained asymptomatic. As ivermectin is being used with increasing frequency in veterinary medicine, more human exposures may be anticipated.

The diagnostic utility of flumazenil (a benzodiazepine antagonist) in coma of unknown etiology.

The use of flumazenil, a benzodiazepine antagonist, was studied in two patients with coma of unknown etiology. One patient ingested 20.5 mg alprazolam before crashing his truck into parked automobiles. The patient was awakened by flumazenil administration, and the severity of his injuries was evaluated reliably. A second patient ingested 7.5 mg triazolam and attempted suicide with carbon monoxide from car exhaust. His coma resolved completely after the administration of the double-blind study drug, obviating treatment with hyperbaric oxygen. Flumazenil had a clear diagnostic and therapeutic role in the treatment of these patients and should be a useful tool for emergency physicians and toxicologists.

Cyanide and methemoglobin kinetics in smoke inhalation victims treated with the cyanide antidote kit.

STUDY OBJECTIVE: To evaluate serial cyanide, methemoglobin, and carbon monoxide levels in smoke inhalation patients. SETTING: Regional poison center and regional toxicology treatment center. PARTICIPANTS: Seven critically ill smoke inhalation patients referred to the regional poison center. INTERVENTIONS: Peak level and half-life were determined by obtaining serial carboxyhemoglobin, cyanide, and methemoglobin levels. RESULTS: The mean observed half-life of cyanide was 3.0 +/- 0.6 hours. Methemoglobinemia was evaluated in four patients after sodium nitrite administration. The peak measured methemoglobin levels (mean, 10.5% +/- 2%; range, 7.9% to 13.4%) did not occur until a mean of 50 minutes (range, 35 to 70 minutes) following administration of sodium nitrite. The total oxygen-carrying capacity reduced by the combination of carboxyhemoglobin and methemoglobin was never more than 21% (range, 10% to 21%) in this series. CONCLUSION: The administration of sodium nitrite to smoke inhalation patients in the presence of concomitant carbon monoxide poisoning may be relatively safe.

Drug- and chemical-induced methaemoglobinaemia. Clinical features and management.

Methaemoglobin is haemoglobin with the iron oxidised to the ferric (Fe ) state from the normal (or reduced) ferrous (Fe++) state. Methaemoglobinaemia refers to the presence of greater than the normal physiological concentration of 1 to 2% methaemoglobin in erythrocytes. Methaemoglobin is incapable of transporting oxygen. It has an intense dark blue colour; thus, clinical cyanosis becomes apparent at a concentration of about 15%. The symptoms are manifestations of hypoxaemia with increasing concentrations of methaemoglobin. Concentrations in excess of 70% are rare, but are associated with a high incidence of mortality. Methaemoglobinaemia may be congenital but is most often acquired. Congenital methaemoglobinaemia is of two types. The first is haemoglobin M disease (several variants) which is due to the presence of amino acid substitutions in either the alpha or beta chains. The second type is due to a deficiency of the NADH-dependent methaemoglobin reductase enzyme. This deficiency has an autosomal dominant transmission, and both homozygous and heterozygous forms have been reported. The heterozygous form is not normally associated with clinical cyanosis, but such individuals are more susceptible to form methaemoglobin when exposed to inducing agents. A wide variety of chemicals including several drugs, e.g. the antimalarials chloroquine and primaquine, local anaesthetics such as lignocaine, benzocaine and prilocaine, glyceryl trinitrate, sulphonamides and phenacetin, have been reported to induce methaemoglobinaemia. An intense 'chocolate brown' coloured blood and central cyanosis unresponsive to the administration of 100% oxygen suggests the diagnosis. A simple bedside test using a drop of the patient's blood on filter paper helps to confirm the clinical suspicion. Methaemoglobin can be quantitated rapidly by a spectrophotometric method.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute toxic blindness: unrecognized quinine poisoning.

Two cases of acute blindness due to quinine poisoning are presented. In both cases, the diagnosis was initially unsuspected. In addition, tinnitus, decreased hearing, vomiting, abdominal pain, and confusion were noted in one patient, and the other experienced decreased hearing, headache, confusion, tachycardia, later bradycardia, and first-degree atrioventricular block. The onset of blindness was delayed more than 12 hours after ingestion in both cases. Quinine levels of 13.6 micrograms/mL and 18.6 micrograms/mL were demonstrated (therapeutic = 1 to 3 micrograms/mL). One patient developed marked constriction of visual fields and some residual decreased acuity, while the other regained normal visual acuity.

Intravenous theophylline poisoning and multiple-dose charcoal in an animal model.

Large overdoses of IV theophylline (50 to 100 mg/kg) were administered to five canines on two separate occasions. On day one, with no charcoal administered, theophylline levels were serially obtained between ten minutes and 12 hours after infusion and the animals were recovered from anesthesia. Three days later the same dose of theophylline was administered, but then 50 g activated charcoal was placed through a nasogastric tube into the duodenum every hour for eight doses. In all five animals tested, activated charcoal significantly decreased the area under the serum concentration-time curve, decreased the half-life of elimination, and increased the clearance of theophylline. This effect on pharmacokinetics was not seen when the nasogastric tube was put into the stomach instead of the small bowel because the charcoal administered did not pass beyond the pylorus. In a separate experiment in which bile theophylline concentrations were measured, it was demonstrated that enhanced elimination was not from interruption of enterohepatic circulation of theophylline. This suggests that the demonstrated physiologic mechanism is that of gastrointestinal dialysis.

Whole-bowel irrigation as treatment for zinc sulfate overdose.

A 16-year-old boy ingested approximately 50 zinc sulfate tablets (ZnSO4; 500-mg tablets). After spontaneous emesis, ipecac-induced emesis, and orogastric lavage, an abdominal radiograph performed four hours after ingestion still demonstrated approximately 50 ZnSO4 tablets within the stomach and three pills within the colon. Whole-bowel irrigation was begun with a polyethylene glycol lavage solution (PEG; Golytely) that was administered through a nasogastric tube; within one hour, the patient began producing a rectal effluent that contained pills. The patient remained asymptomatic throughout whole-bowel irrigation. Stool guaiac tests were negative. The serum chloride, however, increased from 105 to 127 mEq/L. Follow-up kidney, ureter, and bladder studies demonstrated the clearance of the zinc tablets from the gastrointestinal tract during the next 24 hours.

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.

Formate levels following a formalin ingestion.

Although formalin ingestions have previously been reported in the literature, technology has only recently been developed to measure both formaldehyde and formate levels in plasma. Methanol, formaldehyde, and formate levels were followed in the case reported here until the patient's death approximately 13 h after the ingestion. The clinical course was marked by an initial profound CNS depression followed by an apparent clinically quiescent period. Severe abdominal pain and retching preceded the development of seizures, DIC, severe hypotension, and cardiac arrest. Methanol levels rose throughout this 13-h course. Formate and formaldehyde levels increased until bicarbonate and ethanol therapy were instituted. The "fixing" of the stomach by formaldehyde may have produced delayed absorption following formalin ingestion. Therapeutic implications are discussed.

Intravenous epinephrine abuse.

A 19-year-old man with a history of intravenous cocaine and amphetamine abuse injected 1.1 mg of epinephrine intravenously from an over-the-counter bronchodilator inhaler. Within seconds, headache, nausea, numbness of hands and feet, precordial chest discomfort, and palpitations developed. The patient was given a sublingual nitroglycerin tablet by a bystander and promptly had a syncopal episode. Hypotension was observed in the emergency department 10 minutes later. Administration of 2 L of Ringer's lactate maintained blood pressure at 80-90 mm Hg systolic. An electrocardiogram showed ischemic changes in the precordial leads. Cardiac enzymes remained normal. Mild hypokalemia and hyperglycemia were observed. This case illustrates an unusual route of abuse of an over-the-counter epinephrine bronchodilator.

Suspected cyanide poisoning in smoke inhalation: complications of sodium nitrite therapy.

A 78 year old man was found comatose, apneic, and asystolic after closed-space smoke inhalation. He was successfully resuscitated to pulse and blood pressure at the scene. A cyanide component to the poisoning was suspected and two 300 mg doses of sodium nitrite were administered, resulting in significant hypotension. Although high methemoglobin levels were not induced, when added to simultaneously obtained carboxyhemoglobin levels, the total amount of non-oxygen transporting hemoglobin remained nearly constant for about 4-1/2 hours before hyperbaric oxygen (HBO) therapy could be administered. The patient later died in multi-organ system failure. Admission whole blood cyanide level was only 0.34 mcg/mL. These sodium nitrite adverse effects can be avoided by slow intravenous infusion and by administering only recommended doses. In smoke inhalation victims with suspected cyanide poisoning, sodium thiosulfate should be administered first, and sodium nitrite withheld until after the patient is receiving HBO therapy. When available, hydroxocobalamin (which neither induces methemoglobinemia nor causes hypotension) may be the specific cyanide antidote of choice for victims of smoke inhalation.

Comparison of topical magnesium and calcium treatment for dermal hydrofluoric acid burns.

STUDY OBJECTIVE: To compare topical preparations of magnesium and calcium in the treatment of dermal hydrofluoric acid burns. DESIGN: A randomized, blinded, controlled animal model study. SETTING: Animal care facility. TYPE OF PARTICIPANTS: New Zealand rabbits. INTERVENTIONS: Each rabbit was burned with hydrofluoric acid at four sites along the thoracolumbar spine. Equimolar amounts of calcium gluconate, magnesium gluconate, and a magnesium hydroxide antacid were added into a lubricating jelly. The jelly alone was a control preparation. After a water rinse, the burns were massaged with the gels for 1 minute five times; at 4 and 20 minutes and at 1, 4, and 24 hours. Each rabbit served as its own control by receiving all four treatments. MEASUREMENTS AND MAIN RESULTS: Burn diameter and burn surface area diminished over time, but there were no statistically significantly differences among the treatments. Burn ranking and burn rating of severity also did not demonstrate differences. The histologic analysis of the burns, however, demonstrated that calcium gluconate-treated burns were less severe and more superficial than the control and magnesium gluconate-treated burns; the magnesium hydroxide antacid-treated burns were not statistically different compared to the calcium gluconate-treated burns. CONCLUSION: Topical calcium gluconate is an efficacious treatment for dermal hydrofluoric acid burns. Further research is needed to determine the role of magnesium-containing antacids in the treatment of hydrofluoric acid burns.

Acute ingestions of boric acid.

Four patients with elevated serum boric acid levels after single, acute ingestions of 10 to 297 grams were reported to the Rocky Mountain Poison and Drug Center (RMPDC) between January 1983 and August 1985. Systemic effects were absent. In 1983-4, 364 cases of boric acid exposure were reported to the RMPDC with only one fatality from a probable chronic ingestion. Vomiting, nausea, diarrhea, and abdominal cramps were rather common. Systemic effects were notably absent in acute ingestions. Five of three hundred sixty-four patients had measured serum levels and were the only ones hospitalized. These observations suggest that significant poisoning is unlikely to result from a single, acute ingestion of boric acid. Serum boric acid levels appear to correlate poorly with clinical toxicity following acute ingestion.

Tricyclic antidepressant overdose. A review.

Significant advances in diagnosis and management of tricyclic antidepressant overdose have occurred in recent years. This article reviews epidemiologic, pharmacologic, and therapeutic information to provide a systematic approach to these potentially life-threatening overdoses. The tricyclics are discussed as a group, with individual drugs specified when established differences exist.