Intravenous Paraquat Poisoning-Induced Multiple Organ Failure and Fatality—A Report of Two Cases

Paraquat poisoning is the most common cause of fatal herbicide intoxication, mostly through oral ingestion. This work reports two cases of death following intravenous paraquat injection. The clinical courses of the two cases were fulminated and fatal. Toxic symptoms and severe organ function impairment developed soon after paraquat injection. Timely treatment with activated charcoal hemoperfusion with pulse steroid and cyclophosphamide was attempted in both cases; however, both cases died within five days owing to multiple organ failure. In cases of intravenous paraquat intoxication, toxic signs develop more quicker than with oral ingestion. The prognosis of intravenous paraquat intoxication is extremely poor.     

Mercury oxycyanide and mercuric cyanide poisoning: Two cases

Background Although cyanide poisoning can be serious or fatal, it is typically described as mild when the cyanide is ingested in the form of either mercuric cyanide or mercury oxycyanide.Methods We studied two patients with acute cyanide poisoning following ingestion of one of these two agents in each case.Results Both patients demonstrated features of life-threatening cyanide poisoning, including hemodynamic instability, severe lactic acidosis, and high blood cyanide concentration. One of the patients died, while the second demonstrated signs of mercury intoxication (acute renal failure and severe gastrointestinal symptoms), in addition to cyanide intoxication.Conclusion Ingestion of either mercuric cyanide or mercury oxycyanide can result in life-threatening cyanide intoxication.     

The successful use of "high level" PEEP in near fatal Endrin poisoning.

The insecticide Endrin is a highly toxic chlorinated hydrocarbon which can cause severe CNS and respiratory derangement. Death usually follows intoxication within 24 hours. A 19-year-old male developed convulsions and gross pulmonary edema after the ingestion of Endrin. His trachea was intubated and constant positive pressure ventilation with PEEP of up to 28 cm H2O was instituted. The patient survived and recovery appeared to be complete. Severe pulmonary edema is not a common finding in patients who have Endrin poisoning. The use of PEEP above 15 cm H2O is a controversial issue; however, we believe that it contributed significantly to the survival of our patient.     

Delayed Dystonia Following Pimozide Overdose in a Child

Background: Pimozide overdose has rarely been reported in children. In adults, pimozide intoxication may cause seizures, extrapyramidal and anticholinergic effects, hypotension, QTc prolongation and torsades de pointes. We report dystonia, hypotension and drowsiness following pimozide ingestion in a child. Case Report: An alert 18‐month‐old presented to hospital 40 minutes after ingesting up to 6 mg (0.5 mg/kg) of pimozide. Vital signs: BP 91/62 mmHg, HR 130/min, RR 26/min, temperature 97.2°F (36.2°C). She received gastric lavage and activated charcoal. One hour later, her QTc interval was 420 msec, HR 150. She remained asymptomatic until 12 hours post‐ingestion, when she developed drooling, tongue thrusting and drowsiness. BP was 75/40, HR 150, QTc 440 msec. BP increased to 95/50 after a bolus of normal saline. Her dystonia subsided over the next 12 hours without treatment. Drowsiness and tachycardia persisted until 40 hours post‐ingestion. QTc interval at this time was 370 msec. Patient recovered without sequelae. Conclusion: Pimozide overdose in children may be associated with delayed onset of symptoms, including dystonia.     

A Rare Ingestion of Black Locust Tree

Background: The Black Locust (Robinia Pseudoacacia) tree contain toxalbumins, robin and phasin, that exert their toxic effects by inhibition of protein synthesis. Despite the potential dangers of Black Locust intoxication, reports of human toxicity after ingestion are rare. We report the first human intoxication of Black Locust bark in North America in over one hundred years. Case Report: An eight‐year‐old male was brought to the emergency department 6 hours after chewing and expelling the Black Locust bark. He presented with emesis, which began approximately 2.5 hours after exposure. His vital signs were as follows: oral temperature, 97.5° F; blood pressure, 128/75 mmHg; heart rate, 114 beats per minute; respiratory rate, 15 breaths per minute. Initial treatment included 4 mg IV ondansetron, which resolved the vomiting, one dose of activated charcoal, and intravenous fluids. He was then admitted to the intensive care unit (ICU) for observation of signs of toxicity. Laboratory findings were unremarkable except for a white blood cell of 18.4 K/uL and an elevated alkaline phosphatase of 183 U/L. The patient remained asymptomatic throughout his stay in the ICU and was discharged on the fifth day of admission with a normal white blood cell of 4.1 K/uL and an alkaline phosphatase of 251 U/L. Conclusion: Patients with clinical toxicity following the ingestion of Black Locust are expected to do well with supportive care and observation.     

Subject Index to Abstracts

The authors report six patients with acute endosulfan intoxication. The symptoms of nausea, vomiting, headache, and dizziness began 2.7 ± 0.5?h after ingestion; in four cases the patients had been hospitalized but were asymptomatic. All had severe metabolic acidosis with high anion gap and hyperglycemia; five of six had decreased blood platelets. Three patients had pulmonary aspiration, and five required mechanical ventilation. The one fatality followed acute renal failure, disseminated intravascular coagulation, thrombi in the pulmonary arteries and aorta, and cardiogenic shock. In this patient the blood endosulfan was 2.85?mg/L versus a mean of 0.48?mg/L in the survivors.     

血液灌流对地高辛中毒患者治疗作用的临床研究

目的研究血液灌流对地高辛中毒患者的治疗作用。方法严重地高辛中毒患者6例,给予血液灌流治疗,观察血液灌流对血中地高辛浓度和中毒症状的影响。结果经过一次或两次血液灌流治疗可消除地高辛的中毒症状,非常显著地降低血中地高辛的浓度。结论血液灌流能有效地清除血中的地高辛。     

Survival after acute endosulfan intoxication

Abstract

The clinical course following endosulfan ingestion in a suicidal attempt is described. The clinical picture comprised three stages: the acute cardiac and convulsive stage followed by subacute pulmonary and convulsive stage and finally the slow recovery stage. This is the first known survivor of endosulfan ingestion.     

EFFECT OF ANAEROBICALLY PREPARED PNEUMOCOCCUS AUTOLYSATE TOXIN ON MICE AND EVALUATION OF PNEUMOCOCCUS AUTOLYSATE ANTITOXIN IN MICE

1. Certain anaerobically produced autolysates of pneumococcus injected intravenously kill mice in 0.1 to 0.2 cc. quantities in a few hours to 8 days. 2. The symptoms of mice inoculated with these autolysates are weakness and increasing prostration until death. Massive albuminuria is found, appearing 18 hours after injection. During the course of a prolonged intoxication ascites and edema of the subcutaneous tissues may develop. Large pale yellow or white kidneys are found in mice that survive 5 days. In these latter animals, emaciation is usually marked at death. 3. The antitoxin prepared in horses by immunization with the anaerobically prepared toxic autolysates of pneumococcus neutralizes the poisonous autolysates whether mixed in vitro before injection or injected separately after the autolysate. 4. The injection of pneumococcus autolysate toxin incompletely neutralized with autolysate antitoxin causes a protracted intoxication with symptoms and pathologic findings similar to those found in mice dying slowly after injections of the toxic autolysate alone.     

Transient myocardial dysfunction in a child with salicylate toxicity

Aspirin overdose may result in acid-base disturbances, electrolyte abnormalities, pulmonary edema, chemical hepatitis, seizures, and mental status alteration, but myocardial depression has not been reported following aspirin overdose in children. In addition to these more typical features, the 13-month-old boy reported here developed clinical, radiographic, and echocardiographic evidence of myocardial impairment with pulmonary edema and moderately severe global left ventricular dysfunction (estimated shortening fraction of 23%). Complete resolution of the myocardial dysfunction was demonstrated on follow-up echocardiography as the child recovered from the aspirin intoxication. This case suggests that myocardial dysfunction can occur as a result of toxic aspirin ingestion, and that it may contribute to salicylate-induced pulmonary edema.     

Rare complication characterized by late-onset transient neurological symptoms without hyperperfusion after carotid artery stenting: A report of three cases

We experienced a rare complication after carotid artery stenting (CAS) characterized by transient neurological symptoms with no evidence of distal emboli or hyperperfusion. Using neuroimaging, we investigated the pathogenesis of the complication that occurred after CAS in three patients who developed neurological symptoms over a period of ten hours after CAS and improved within two days. None of the three patients showed signs of fresh infarctions on diffusion-weighted imaging or hyperperfusion on single-photon emission computed tomography. However, high signal intensity was observed in the leptomeningeal zone of the cerebral hemisphere on the stent side in all three patients and in the leptomeningeal zone of the contralateral anterior cerebral artery territory in one patient. These areas were assessed using fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging without gadolinium administration. The high signal intensity in the leptomeningeal zone disappeared as the symptoms improved. Based on the transient nature of the neurological disorders and the normalization of FLAIR imaging findings in these patients, the pathogenesis of this complication might have been vasogenic edema due to vasoparalysis of the local vessels caused by the hemodynamic changes occurring after CAS.     

Intermediate Syndrome After Malathion Ingestion Despite Continuous Infusion of Pralidoxime

Case Report: A 33-year-old female ingested an unknown quantity of malathion in a suicide attempt. Cholinergic signs consistent with severe organophosphate intoxication developed and were treated within 6 hours of ingestion. Intravenous atropine and a continuous infusion of pralidoxime (400 mg/h) were administered. Prolonged depression of plasma and red blood cell cholinesterases were documented. Despite an initial clinical improvement and the presence of plasma pralidoxime concentrations exceeding 4 μg/mL, the patient developed profound motor paralysis consistent with the diagnosis of Intermediate Syndrome. In addition to the dose and frequency of pralidoxime administration, other factors including persistence of organophosphate in the body, the chemical structure of the ingested organophosphate, and the time elapsed between ingestion and treatment may limit the effectiveness of pralidoxime as an antidote in organophosphate ingestions. This case study suggests that these factors should be taken into account in assessing the risk of Intermediate Syndrome after intentional organophosphate ingestions.     

Imipramine-provoked paradoxical pheochromocytoma crisis: A case of cardiogenic shock

The dramatic presentation of pheochromocytoma in crisis is uncommon and is classically associated with a state of hemodynamic and sympathetic hyperactivity. The case of a 35-year-old man with an occult pheochromocytoma presenting with hypotension and cardiogenic shock shortly after beginning imipramine therapy is presented. Retrospectively, there was a history of emergency department, inpatient, and outpatient evaluation of symptoms likely to be related to an occult pheochromocytoma. He presented with hypotension refractory to fluids and inotropes and in severe respiratory distress. The early differential diagnosis was extensive including acute myocardial infarction, pneumonia with sepsis, and toxic ingestion. Shortly after admission the patient's occult pheochromocytoma was discovered and subsequently specific therapy was initiated. The patient's symptoms resolved after surgical resection of the tumor, and he was ultimately discharged without signs of congestive heart failure. The clinical pathophysiology of cardiomyopathy secondary to pheochromocytoma, and possible mechanisms of pharmacological interactions with tricyclic antidepressants are discussed.     

Mad-honey intoxication confirmed by pollen analysis

Context. Despite numerous publications showing rhythm disturbance and hypotension caused by mad-honey intoxication, none of the findings are associated with ischemic heart disease. Case details. A 48-year-old patient was admitted to emergency service with acute anterior wall myocardial infarction after ingestion of mad-honey. Stent was implanted to the 99% stenosis lesion in the mid-portion of left anterior descending coronary artery. In this case, pollen analysis showed the suspected honey heavily contaminated with Rhododendron species pollen. Discussion. Mad-honey intoxication cases often apply to emergency service with similar signs and symptoms of acute coronary syndrome; therefore it may cause acute coronary syndrome to be bypassed. This also shows that in the cases of mad-honey intoxication, suspected honey pollen and/or toxin analysis should be done to confirm the diagnosis of mad-honey intoxication.     

Lithium intoxication: Manifestations and management

The clinical diagnosis of lithium intoxication can be elusive because of the slow onset and diversity of toxic manifestations. Mental status and neurologic symptoms often predominate. After the diagnosis is made, management depends on the clinical presentation and serum lithium level. Hemodialysis is the treatment of choice for severe lithium intoxication. Two cases of lithium intoxication are presented that demonstrate that predisposing factors and drug interactions play major roles. A review is given of the pathophysiology, presenting signs, symptoms, and approaches to treatment of lithium intoxication.     

Severe acute poisoning with homemade Aconitum napellus capsules: toxicokinetic and clinical data

Aconitum napellus is an extremely dangerous plant that contains various toxic diterpenoid alkaloids, mainly aconitine primarily concentrated in the roots. We report a case of acute intoxication of a 21-year-old man admitted to our Emergency Department after the ingestion, in order to sleep, of three homemade Aconitum napellus capsules. Capsules were measured to contain 237 mg of root and 19 microg of aconitine. The patient experienced the first symptoms on wakening 5 hours later with generalized paresthesia, nausea, diarrhea, vertigo, thoracic pain dyspnea, and dyschromatopsia. At admission, 7 hours after intake electrocardiographic analysis showed a sinusal bradycardia with polymorphic and bigeminal ventricular extrasystolia. Cardiovascular and neurological symptoms disappeared, respectively within 11 and 13 hours of ingestion. The patient was discharged from the ICU on day 2. Plasmatic concentrations at H7, H9, H14 H19, and after ingestion were, respectively, of 1.75, 0.75, 0.35, and 0.02 ng/mL. The calculated half-life of aconitine was 3 hours. To our knowledge, this is the first reported case with an aconitine toxicokinetic-effect relationship. The authors stress that clinicians must be aware of possible occurrence of acute poisoning with Aconitum napellus in European countries and in the United States as herbal medicine is becoming increasingly popular.     

Are One or Two Dangerous? Calcium Channel Blocker Exposure in Toddlers

Unintentional pediatric ingestions of calcium channel blockers are increasing in frequency due to increased use of this antihypertensive class. Potential toxic effects include severe refractory hypotension and death; however, the true toxicity of unintentional pediatric ingestions of 1-2 pills is poorly defined. A literature review was conducted to more closely determine toxic and lethal dosages of calcium channel blockers in the pediatric population under 6 years of age. Results indicate that, although most accidental pediatric ingestions are asymptomatic, a small number do result in cardiovascular instability or even death. The dihydropyridines, particularly nifedipine, and the phenylalkylamine verapamil are most often implicated in symptomatic ingestions. There are no adequate data to identify which children are predisposed to illness, or to determine cutoffs for toxic dosages. However, ingestions of only one pill have been documented to cause severe symptoms, including death. Thus, emergency evaluation to assess potential toxicity is necessary, and gastrointestinal decontamination and in-hospital observation of at least 6 h after toxic ingestion for regular release medications, and 12-24 h after toxic ingestion for sustained release medications is recommended for all cases of unintentional calcium channel blocker ingestion in children younger than 6 years of age.     

Methanol poisoning

Methanol poisoning is an uncommon but an extremely hazardous intoxication. Since methanol is a versatile fuel and is having increasing usage in an energy-conscious society, a high index of suspicion and swift laboratory confirmation is essential in managing this poisoning. Methanol poisoning may occur in sporadic or epidemic circumstances. Chronic exposure may occur in the occupational setting. Man is uniquely susceptible to methanol toxicity, perhaps dependent upon folate metabolism. Classic symptoms of methanol toxicity can only occur in laboratory animals who are rendered folate deficient. Folate may be useful in humans enhancing removal of the toxic products of methanol poisoning. The enzyme responsible for metabolism of methanol is alcohol dehydrogenase. Ethanol has a higher affinity for this enzyme and is preferentially metabolized. Simultaneous ethanol and methanol administration may confuse the onset of the intoxication. Pyrazoles may also be used to inhibit alcohol dehydrogenase thus preventing the intoxication. The most important initial symptom of methanol poisoning is visual disturbance. The symptoms may be delayed up to 24 hours after ingestion due to simultaneous alcohol administration and metabolic processes. Laboratory evidence of severe metabolic acidosis with increased anion and osmolar gaps strongly suggest the clinical diagnosis. There may be an important association between mean corpuscular volume which is significantly higher in cases of severe methanol poisoning than in mild cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute Intoxication Due to Ingestion of Vegetables Contaminated with Aldicarb

Three members of the same family ingested vegetables treated with aldicarb. All three developed signs and symptoms of acetylcholinesterase inhibition and all recovered a few hours after the ingestion. Reports of toxicity from the ingestion of aldicarb-contaminated food are uncommon. Aldicarb is a potent pesticide which can only be used safely if governmental and industry regulations are followed carefully.