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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

20 children, diagnosed with scrub typhus who attended Chiang Rai Regional Hospital during a period of 6 months from June 2003 to December 2003, were studied prospectively. All cases were serologically proved to be scrub typhus by using Dipstick or indirect immunofluorescent antibody (IFA) technique. The most common clinical feature was eschar (75%). Others included hepatomegaly (65%), cough (60%), lymphadenopathy (40%), tachypnea (35%), constipation (25%), abdominal pain (20%), edema (20%), splenomegaly (15%), vomiting (15%), rash (15%) and petichia (5%) respectively. Chest radiography showed abnormalities in 85% with mostly bilateral interstitial infiltrations. Elevated of SGOT: SGPT were detected in 18 (90%) and 15 (75%) cases. Hypoalbuminemia was detected in 12 (60%) cases. Complete blood count showed PMN leukocytosis (> 60%) in 12 (60%) cases, lymphocytosis (> 40%) and atypical lymphocytosis (> 5%) in 1 (5%) case each and thrombocytopenia in 16 (80%) cases. The Weil-Felix test was positive in 1 (5%) case. Complications were pneumonia with or without pulmonary edema, meningitis and shock. Chloramphenicol and doxycycline were successfully treated and roxithromycin was not effective.
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PMID:Clinical study of 20 children with scrub typhus at Chiang Rai Regional Hospital. 1651 87

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.
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PMID:Two fatal cases of selenium toxicity. 1689 Oct 71

A 36-year-old woman, who had given birth once before, had an eclamptic epileptic seizure eight days after caesarean delivery of healthy premature twins. Severe headache and loss of vision, leading to blindness, had not been recognised as prodromal signs by the healthcare professionals involved. Thereafter, she suffered a generalised epileptic seizure with tongue bite. She recovered fully after treatment with magnesium sulphate and nifedipine. Eclampsia is a severe condition with high rates of maternal complications, such as abruptio placentae, disseminated intravascular coagulation, neurological problems, pulmonary oedema, acute renal insufficiency and even death. Recognition of prodromal symptoms like headache, visual disturbances and upper abdominal pain is of the utmost importance. Magnesium sulphate intravenously is the treatment of choice. About 25% of the cases of postpartum eclampsia develop 2-28 days after delivery. A history of pre-eclampsia before or during the delivery is often absent. There is a relative increase in the incidence of late postpartum eclampsia, possibly because of misinterpretation ofprodromal symptoms, as illustrated by this case report. Every physician should be able to recognise the symptoms of pre-eclampsia and be aware of the possible consequences.
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PMID:[Late postpartum eclampsia]. 1750 Mar 49

Morgagni-Larrey hernia (MH) is an unusual diaphragmatic hernia of the retrosternal region. Few cases of MH, treated laparoscopically, associated with Down's syndrome (DS) have been reported in literature. On October 2004, a DS 40-year-old male was admitted to our Department with mild abdominal pain and nausea. Hematochemical tests were within the normal range. Ultrasonography showed biliary sludge and multiple gallstones. Chest X-ray revealed a right-sided paracardiac mass that appeared as MH after a thoraco-abdominal computed tomography (CT). Four trocars were placed as a routinary cholecystectomy. Abdominal exploration confirmed the presence of a voluminous hernia through a wide diaphragmatic defect (12 cm) on the left side of the falciform ligament, containing the last 20 cm ileal loops and right colon with the third lateral of transverse. After retrograde cholecystectomy and reduction of the herniated ileo-colonic tract from multiple adherences, the defect was repaired with an interrupted 2/0 silk suture and then a running 2/0 polypropylene suture. Postoperative course was complicated by pulmonary edema but subsequently the patient was discharged without further complications and has no recurrence after 2 years. In conclusion, surgery is necessary for symptomatic MH and to prevent possible severe complications. We preferred laparoscopy for the reduced morbidity compared to laparotomy, even if in our case the postoperative course was not uneventful. There are still few comparative data about the modality of closure of the defect between primary repair with nonabsorbable suture material, in case of small defects, or continuous monofilament suture or prosthesis in case of large defects.
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PMID:Laparoscopic repair of Morgagni hernia and cholecystectomy in a 40-year-old male with Down's sindrome. Report of a case. 1751 46

Fumonisins constitute a family of toxic and carcinogenic mycotoxins produced by Fusarium verticillioides (formerly F. moniliforme), a common fungal contaminant of corn. Contamination with fumonisin B(1) (FB(1)) is of concern as this mycotoxin causes various animal diseases. The gastrointestinal tract represents the first barrier against ingested chemicals, food contaminants, and natural toxins. Following ingestion of fumonisin-contaminated food or feed, intestinal epithelial cells could be exposed to a high concentration of toxin. In this review, we have summarized the data dealing with the impact of FB(1) on the intestine. Although FB(1 )is poorly absorbed and metabolized in the intestine, it induces intestinal disturbances (abdominal pain or diarrhea) and causes extra-intestinal organ pathologies (pulmonary edema, leukoencephalomalacia, or neural tube defects). The main toxicological effect of FB(1) reported in vivo and in vitro is the accumulation of sphingoid bases associated with the depletion of complex sphingolipids. This disturbance of the sphingolipid biosynthesis pathway could explain the other observed toxicological effects such as an alteration in intestinal epithelial cell viability and proliferation, a modification of cytokine production, and a modulation of intestinal physical barrier function.
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PMID:The intestine as a possible target for fumonisin toxicity. 1764 75

An obese body habitus may interfere with diagnosis of potentially life-threatening conditions. This report describes an obese woman who presented with acute hypoxemic respiratory failure and diffuse infiltrates. Her body habitus disguised her parturient abdomen and she could not provide a history because she was intubated and paralysed. Only after a urine pregnancy test was undertaken did it become apparent that she was pregnant and the diagnosis of pre-eclampsia with pulmonary oedema was considered. Urine pregnancy tests are part of the standard work-up for abdominal pain in women of childbearing age, but are not viewed as part of the work-up for respiratory distress or diffuse radiographic infiltrates. This case illustrates the value of obtaining a pregnancy test in all women, particularly those with obese body habitus, who present with respiratory failure of unclear aetiology.
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PMID:Unsuspected 34-week pregnancy presenting as acute hypoxaemic respiratory failure. 1802 28

A 49-year-old healthy woman was admitted after a horse-riding accident. On arrival to the emergency department she complained of lower abdominal pain. A CT-scan of the abdomen with non ionic contrast media (iomeprol, 150 ml 4 ml/s) was conducted. The patient died nine hours later due to an anaphylactoid reaction to radio contrast media. The autopsy showed pulmonary oedema and pleural effusion, but did not show any sign of trauma. Early interventions with appropriate therapy had no effect on the fatal outcome.
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PMID:[Lethal reaction after contrast medium administration]. 1846 29

Defined by the association of hemolysis, hepatic dysfunction and thrombocytopenia, the Hemolysis, Elevated Liver enzyme, Low Platelets (HELLP) syndrome can complicate preeclampsia and worsen maternal and fetal prognosis. It can be diagnosed in the immediate postpartum (30%) or in the absence of preeclampsia (10-20%). Clinical diagnosis can be difficult because there is no specific symptom. Abdominal pain or vomiting during the third trimester must lead to think about this diagnosis. Biological criteria are well defined: hemolysis by the presence of schistocytes, increased serum total bilirubin >12 mg/L or LDH >600 IU/L, hepatic dysfunction by increased transaminases and thrombocytopenia by a platelet count <100,000/microL. The evolution of those parameters is a major prognostic factor. With the HELLP syndrome, maternal morbidity is dramatically increased compared to isolated preeclampsia with complications such as eclampsia, placental abruptio, disseminated intravascular coagulation, pulmonary edema, acute renal insufficiency, subcapsular liver hematoma. The management of a HELLP syndrome requests level 3 hospital with intensive care units for neonate and mother. The treatment of this syndrome requires termination of the pregnancy as soon a possible, either by cesarean section or by vaginal delivery if cervical conditions are optimal (without any maternal or fetal complications). Before 32 weeks, a more expectative attitude could be acceptable with the prematurity permitting corticotherapy for fetal pulmonary maturation. This corticotherapy can improve temporary biological parameters but there are no proven benefits to consider improvement for long term maternal or fetal prognosis. During the postpartum, evolution is usually spontaneously favorable. Recurrences are not frequent.
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PMID:[Management of the HELLP syndrome]. 1900 44

Glyphosate-surfactant (GlySH) is a commonly used herbicide that has been used in attempted suicide. Most reports of GlySH toxicity in patients have followed ingestion of the commercial product "Round-up" (Monsanto Ltd; Melbourne, Victoria, Australia), which consists of a mixture of glyphosate (as a isopropylanine salt) and a surfactant (polyoxyethyleneamine). Ingestion of Round-up is reported to cause significant toxicity including nausea, vomiting, oral and abdominal pain. Renal and hepatic impairment and pulmonary oedema may also occur. Impaired consciousness and encephalopathy have been reported as sequelae but there are limited data on the central nervous system (CNS) effects of Round-up toxicity. We report a 71-year-old male who attempted suicide with GlySH and developed a prolonged but reversible encephalopathy suggestive of acute CNS toxicity.
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PMID:Glyphosate-surfactant herbicide-induced reversible encephalopathy. 2065 31


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