Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-eight children with acute purulent meningitis were treated at The Hospital for Sick Children, Toronto, in 1962; nine deaths occurred. Hemophilus influenzae type B and meningitis in which no organism was cultured accounted for 35 and 17 cases, respectively. A number of other etiological agents caused six or fewer cases each.The principal presenting complaints were fever and vomiting, the more familiar symptoms of meningeal irritation occurring in 20% or less. A short duration of onset suggested a more severe illness and graver prognosis. Seven of the nine fatal cases had a presenting history of less than 24 hours' duration. Persisting high fever, convulsions, cyanosis and abdominal distension were also associated more specifically with the fatal cases.The laboratory examination of the initial spinal fluid sample, while of value in the identification of the causative organism, was not of prognostic value.The value of general treatment measures, as well as specific therapy, was evident in all cases.
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PMID:ACUTE PURULENT MENINGITIS IN CHILDREN: EXPERIENCE AT THE HOSPITAL FOR SICK CHILDREN, TORONTO. 1412 87

OBJECTIVE: To study the changes in methemoglobinemia of 17 children admitted with acute exposure to dapsone complicated by a methemoglobin concentration greater than 20% of the total hemoglobin. The children were treated with multiple doses of activated charcoal with or without the administration of methylene blue.PATIENTS AND METHODS: Seventeen patients (ages 1-13 y, median 3 y), were admitted 1-72 h after the ingestion of 100-1200 mg (median 350 mg, 10 patients) or an unknown amount of dapsone (7 patients). The methemoglobin blood concentrations upon admission ranged from 23.5%-49.7% (median 37.8%), and the main clinical features were cyanosis (17), tachycardia (17), vomiting (11) and tachypnea (8). All of the children received multiple doses of activated charcoal orally or via nasogastric tube (1g/kg, 10% solution, 4-6 times/day, 3-16 doses with a median of 8 doses). Twelve of the 14 patients with methemoglobin levels greater than 30% were also treated with a single dose of methylene blue (1-2% solution, 1-2 mg/kg) infused IV over 5 min.RESULTS: There was a progressive decrease in the methemoglobin levels after the beginning of both treatments (multiple doses of activated charcoal alone or associated with methylene blue), and only one dose of methylene blue was necessary. There were no significant statistical differences between the results of the two treatments according to the time-course decrease in methemoglobinemia (p=0.49 Wilcoxon test).CONCLUSIONS: Multiple doses of activated charcoal given when methemoglobin levels were greater than 20% can be considered as a possible treatment for pediatric patients, with or without the administration of methylene blue, after acute dapsone exposure.
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PMID:[Acute dapsone exposure and methemoglobinemia in children: treatment with multiple doses of activated charcoal with or without the administration of methylene blue] 1464 58

Medetomidine is a relatively new sedative analgesic drug that is approved for use in dogs in Canada. It is the most potent alpha2-adrenoreceptor available for clinical use in veterinary medicine and stimulates receptors centrally to produce dose-dependent sedation and analgesia. Significant dose sparing properties occur when medetomidine is combined with other anesthetic agents correlating with the high affinity of this drug to the alpha2-adrenoreceptor. Hypoventilation occurs with medetomidine sedation in dogs; however, respiratory depression becomes most significant when given in combination with other sedative or injectable agents. The typical negative cardiovascular effects produced with other alpha2-agonists (bradycardia, bradyarrhythmias, a reduction in cardiac output, hypertension +/- hypotension) are also produced with medetomidine, warranting precautions when it is used and necessitating appropriate patient selection (young, middle-aged healthy animals). While hypotension may occur, sedative doses of medetomidine typically raise the blood pressure, due to the effect on peripheral alpha2-adrenoreceptors. Anticholinergic premedication has been recommended with alpha2-agonists to prevent bradyarrhythmias and, potentially, the reduction in cardiac output produced by these agents; however, current research does not demonstrate a clear improvement in cardiovascular function. Negatively, the anticholinergic induced increase in heart rate potentiates the alpha2-agonist mediated hypertension and may increase myocardial oxygen tension, demand, and workload. Overall, reversal with the specific antagonist atipamezole is recommended when significant cardiorespiratory complications occur. Other physiological effects of medetomidine sedation include; vomiting, increased urine volumes, changes to endocrine function and uterine activity, decreased intestinal motility, decreased intraocular pressure and potentially hypothermia, muscle twitching, and cyanosis. Decreased doses of medetomidine, compared with the recommended label dose, should be considered in combination with other sedatives to enhance sedation and analgesia and lower the duration and potential severity of the negative cardiovascular side effects. The literature was searched in Pubmed, Medline, Agricola, CAB direct, and Biological Sciences.
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PMID:A review of the physiological effects of alpha2-agonists related to the clinical use of medetomidine in small animal practice. 1466 51

Dinitrotoluenes (DNTs) are nitroaromatic compounds appearing as pale yellow crystalline solids at room temperature. Dinitrotoluenes exist as a mixture of 2 to 6 isomers, with 2,4-DNT, and 2,6-DNT being the most significant. About 500 persons are estimated to be potentially exposed yearly to 2,4-DNT and 2,6-DNT during the production of munitions and explosives. The main route of human exposure at ammunition facilities is inhalation, but dermal contact and inadvertent ingestion can also be substantial. In factory workers, exposure to DNTs has been linked to many adverse health effects, including cyanosis, vertigo, headache, metallic taste, dyspnea, weakness and lassitude, loss of appetite, nausea, and vomiting. Other symptoms including pain or parasthesia in extremities, abdominal discomfort, tremors, paralysis, chest pain, and unconsciousness have also been reported. The primary targets of DNT toxicity are the hematopoietic system (pallor, cyanosis, anemia, and leukocytosis), the cardiovascular system (ischemic heart disease), the nervous system (muscular weakness, headache, dizziness, nausea, insomnia, and tingling pains in the extremities) and the reproductive system (reduction of sperm counts, alteration of sperm morphology, and aspermatogenesis). An association between DNT exposure and increased risk of hepatocellular carcinomas and subcutaneous tumors in rats, as well as renal tumors in mice, has been established. Epidemiologic studies of DNT toxicity have been limited to small groups of workers who had been occupationally exposed at various ammunitions production facilities. Clearly defining the health effects of DNTs with a high degree of confidence has therefore been difficult because of the multigenic nature of occupational exposure. In an attempt to update the toxicologic profile of the DNTs, we hereby provide a critical review of the environmental and toxicologic pathology of DNTs, with a special emphasis on their potential implications for public health.
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PMID:Environmental toxicology and health effects associated with dinitrotoluene exposure. 1467 15

There is widespread concern about gastroesophageal reflux (GER) in preterm infants. This article reviews the evidence for this concern. GER is common in infants, which is related to their large fluid intake (corresponding to 14 L/day in an adult) and supine body position, resulting in the gastroesophageal junction's being constantly "under water." pH monitoring, the standard for reflux detection, is of limited use in preterm infants whose gastric pH is >4 for 90% of the time. New methods such as the multiple intraluminal impedance technique and micromanometric catheters may be promising alternatives but require careful evaluation before applying them to clinical practice. A critical review of the evidence for potential sequelae of GER in preterm infants shows that 1) apnea is unrelated to GER in most infants, 2) failure to thrive practically does not occur with GER, and 3) a relationship between GER and chronic airway problems has not yet been confirmed in preterm infants. Thus, there is currently insufficient evidence to justify the apparently widespread practice of treating GER in infants with symptoms such as recurrent apnea or regurgitation or of prolonging their hospital stay, unless there is unequivocal evidence of complications, eg, recurrent aspiration or cyanosis during vomiting. Objective criteria that help to identify those presumably few infants who do require treatment for GER disease are urgently needed.
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PMID:Gastroesophageal reflux: a critical review of its role in preterm infants. 1475 82

Limitation of a bioterrorist anthrax attack will require rapid and accurate recognition of the earliest victims. To identify clinical characteristics of inhalational anthrax, we compared 47 historical cases (including 11 cases of bioterrorism-related anthrax) with 376 controls with community-acquired pneumonia or influenza-like illness. Nausea, vomiting, pallor or cyanosis, diaphoresis, altered mental status, and raised haematocrit were more frequently recorded in the inhalational anthrax cases than in either the community-acquired pneumonia or influenza-like illness controls. The most accurate predictor of anthrax was mediastinal widening or pleural effusion on a chest radiograph. This finding was 100% sensitive (95% CI 84.6-100.0) for inhalational anthrax, 71.8% specific (64.8-78.1) compared with community-acquired pneumonia, and 95.6% specific (90.0-98.5) compared with influenza-like illness. Our findings represent preliminary efforts toward identifying clinical predictors of inhalational anthrax.
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PMID:Clinical predictors of bioterrorism-related inhalational anthrax. 1565

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

A neonate presenting to the emergency department can present a challenge to even the most experienced clinician. This article has focused on four deceiving and potentially devastating neonatal diseases. 1. Neonatal herpes is a potentially devastating illness without pathognomonic signs or symptoms. Early recognition and therapy can reduce mortality markedly. Although no specific sign or symptom is diagnostic,the diagnosis should be strongly considered in the presence of HSV risk factors, atypical sepsis, unexplained acute hepatitis, or focal seizure activity. Acyclovir therapy should be initiated before viral dissemination or significant CNS replication occurs. 2. Pertussis is a disease in which infants are at greatest risk of death or severe complication. Neonatal pertussis often presents in an atypical manner, lacking the classic signs and symptoms such as the "whoop."More common signs and symptoms include cough, feeding difficulty,low-grade fever, emesis, increasing respiratory distress, apnea, cyanosis,and seizures. Management should include hospitalization, supportive care, and antibiotics. 3. Congenital heart defects, particularly ductal-dependent lesions, may have an initial asymptomatic period that culminates in a rapidly progressive and fatal course. A neonate with CHD presents with shock refractory to volume resuscitation or pressor support. Resuscitative efforts are ineffective unless PGE, is administered. 4. Inborn errors of metabolism often are unsuspected because of their protean and heterogeneous nature. Signs and symptoms are subtle,are nonspecific, and often mimic other, more common diseases.An elevated index of suspicion, along with application and correct interpretation of a select few laboratory tests, is the key to making a diagnosis. Therapy is relatively straightforward and focused on resuscitation followed by prevention of catabolism and correction of specifically identified abnormalities. Although these disorders are relatively uncommon, prompt diagnosis and therapy can lead to a decrease in morbidity and mortality. The key is to maintain a high index of suspicion.
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PMID:Unsuspected neonatal killers in emergency medicine. 1547 77

The clinical presentations of laboratory-confirmed Bordetella pertussis infection in Chang Gung Children's Hospital during 1997 and 2001 were analyzed. Of the 46 cases, 25 (54.3%) were male. The patients ages ranged from 24 days to 37 years, with a mean and median of 4.3 years and 10.5 years, respectively. Forty four patients had vaccination records, among them 23 patients (52.2%) had received > or = 3 doses of pertussis vaccine. Of the patients who were partially vaccinated (received 1 or 2 doses vaccine) or unvaccinated, 16 (69.6%) presented with whooping cough, 5 (22.2%) with post-tussive vomiting, and 13 (59.1%) with cyanosis. Leukocytosis (white blood cells > or = 15,000 cells/microL) and lymphocytosis (lymphocytes > or = 10,000 cells/microL) were observed in 17 (47.2%) and 16 (44.4%) of the patients, respectively. Fourteen patients (30.4%) developed complications, among which pneumonia was the most common (92.3%). Among infants < or = 1 year of age, 95.2% were partially vaccinated (20/21), compared with 5% (1/20) of the patients > 1 year of age (p<0.05). The overall complication rate was 37.5%, compared with 18.2% for patients > 1 year of age (p<0.05). One 2-month-old patient required ventilatory support after the development of cardiopulmonary failure. There was no mortality in this study. In summary, pertussis most commonly occurred in infants who were unvaccinated or partially vaccinated. These patients usually presented with atypical symptoms such as cyanosis or apnea. The importance of vaccination still cannot be overemphasized because immunized patients usually present with milder disease than those who are not immunized.
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PMID:Bordetella pertussis infection in northern Taiwan, 1997-2001. 1549 10

Acute ingestion of copper sulfate has been reported to cause gastrointestinal injury, hemolysis, methemoglobinemia, hepatorenal failure, shock; or even death. The toxicity of organocopper compounds, however, remains largely unknown. A 40-y-old man attempted suicide by ingesting some 50 ml of Sesamine fungicide. He immediately developed headache, vomiting and abdominal pain, followed by progressive dyspnea, cyanosis, dark urine and diarrhea. Severe methemoglobinemia and hemolysis were documented, and treatment with ascorbic acid and hydration was commenced. He was referred to our service 3 d later for methylene blue treatment. Despite the above treatment, his symptomatology persisted and it was not until 5 d post-ingestion that the implicated fungicide was identified as copper-8-hydroxyquinolate. BAL therapy and plasma exchange were instituted, which decreased his plasma hemoglobin from 1,300 mg/dL to 29.1 mg/dL, and lowered his methemoglobin level from 20.9% to 1.1%. His serum and urine copper concentration dropped from 238 microg/dL to 96 microg/dL and from 112 microg/dL to 16 microg/dL, respectively. He was discharged uneventfully 18 d post-ingestion. Pre-existing glucose-6-phosphate dehydrogenase (G6PD) deficiency as well as copper-induced inhibition of G6PD activity was documented during hospitalization. Organocopper compounds may cause prolonged hemolysis and methemoglobinemia through oxidative stress, especially among patients with G6PD deficiency. Antidotal therapy with methylene blue is not likely to be effective in this setting: treatment with intensive supportive measures and other therapeutic options, such as plasma exchange, should be sought.
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PMID:Prolonged hemolysis and methemoglobinemia following organic copper fungicide ingestion. 1558 50


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