Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and five patients with Plasmodium falciparum were included, forty-three with cerebral malaria and sixty-two without cerebral manifestations. The main clinical presentations in cerebral malaria patients were fever (76.4%), pallor (72%), splenomegaly (60.5%), deep coma (39.5%), jaundice (18.6%), pulmonary oedema (13.9%), subconjunctival haemorrhage (13.9%), severe anemia (Hb<5mg/l) (53.5%), hypoglycemia (glucose<40mg/dl) (67.4%) and haemoglobinuria (6.9%) while in non cerebral malaria patients the clinical presentations were fever (83.8%), pallor (67.7%), splenomegaly (66%), jaundice (9.7%), severe anemia (Hb<5gm/dl) (51.6%) and hypoglycemia (glucose<40mg/dl) (3.2%). Nine patients from cerebral malaria group died after admission. Serum level of nitric oxide (nitrite plus nitrate) were assayed for all patients, serum level of nitric oxide were highly significant in patients with cerebral malaria than those without (34.6 +/- 2.3n. mol/ml VS 12.9 +/- 1.3n. mol/ml; P<0.01). In cerebral malaria, nitric oxide levels were highly elevated in patients with deeper coma than those with lighter coma (48.2 +/- 3.1n. mol/ml VS 24.4 +/- 1.3n. mol/ml; P<0.001) and also higher among patients with longer duration of coma (>72 hours) than among patients with shorter duration of coma (<72 hours) (54.5 +/- 2.8 n. mol/ml V.S. 23.6 +/- 3.1n. mol/ml; P<0.001). Also, nitric oxide levels were correlated with clinical outcome, fatal cases (9 patients) having significantly higher nitric oxide levels than survivors (56.2 +/- 3.1 n. mol/ml VS 32.5 +/- 1.3 n. mol/ml; P<0.001). Thus, higher levels of nitric oxide are associated with indices of disease severity and may predict outcome in-patients with cerebral malaria. These data are consistent with the hypothesis that nitric oxide is involved in the pathogenesis of cerebral malaria.
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PMID:Plasma levels of nitric oxide in association with severe Plasmodium falciparum in Yemen. 1256 1

The study objective was to describe the morbidity of patients presenting with heroin overdose (HOD)-induced noncardiogenic pulmonary edema (NCPE) at an urban ED. A retrospective chart review of patients presenting between 1996 and 1999 with the diagnosis of HOD was conducted. Using a standardized data abstraction form, information on prehospital care, ED care, demographics, and cointoxications was collected. One hundred twenty-five charts (78%) were available for review. Of these, 13 (10%) were diagnosed with NCPE and all were male. In the field, NCPE patients had an average relative risk of 6, a Glasgow Coma Scale of 4, and all needed naloxone. The average admitted duration of use was 2.9 years for those who developed NCPE compared with 13.2 years for those who did not. Five (42%) NCPE patients tested positive for cocaine use and 7 (58%) tested positive for alcohol. In this cohort, the NCPE patients were male and less experienced users with initial low relative risk and Glasgow Coma Scale which demanded prehospital naloxone use. (Am J Emerg Med 2003;21:32-34.
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PMID:Patterns of presentation in heroin overdose resulting in pulmonary edema. 1525 78

(1) Check for severe malaria (coma, shock, pulmonary oedema), and take account of drug resistance in the region. (2) Mefloquine and quinine are first-line options for uncomplicated P. falciparum malaria. The atovaquone + proguanil combination can be used in patients at high risk of side effects with mefloquine
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PMID:Treatment of imported uncomplicated malaria: a medical emergency. 1260 3

Three cows fed Chenopodium album hay died 30 min after showing ataxia, bluish-brown mucous membranes, rapid and difficult breathing, increased heart rates, tremors and coma. Brown-colored and badly coagulated blood was the prominent necropsy finding. Slight pulmonary edema was prominent and all visceral organs were hyperemic. The hay contained 2,500 ppm nitrate-nitrogen and 11 ppm nitrite nitrogen.
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PMID:Nitrate poisoning in cattle fed Chenopodium album hay. 1267 93

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.
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PMID:Human health effects of sodium azide exposure: a literature review and analysis. 1285 Nov 50

Falciparum malaria affect all ages with multiple-systemic complications which varies in different age group. We studied 242 children with complicated Falciparum malaria with a median age of 6.5 years to look for occurrence of different complications in younger and older age groups and overall mortality picture. Unarousable coma (40.5%), severe anemia (26.03%), repeated seizures (46.2%) and hepatopathy (32.2%) were commonest complications. Under five children had higher risk of development of cerebral malaria (P<0.01), severe anemia (P<0.05) and seizures (P<0.001); whereas above five children had higher risk of acute renal failure (P<0.05) and malarial hepatopathy (P<0.02). Over all mortality was 9.9%, cerebral malaria being the commonest cause (6.6%). Multi-system involvement was seen in 58.4% cases of death. Children having pulmonary edema, shock and cerebral malaria had high case fatality rate.
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PMID:Severe falciparum malaria. 1505 76

HUS was recently described following scorpion sting. We report 2 cases of HUS in the intensive care unit of a university hospital. Two children aged respectively 10 months and 1 year were admitted in the ICU after severe scorpion envenomation (with coma and pulmonary oedema) having required dobutamine and mechanical ventilation. Evolution was marked with acute anaemia without bleeding requiring blood transfusion, acute renal failure, low platelets and signs of haemolysis. Our experience and the previously reported case suggest that scorpion sting could be added to the list of causes of the HUS.
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PMID:[Hemolytic-uremic syndrome secondary to scorpion envenomation (apropos of 2 cases)]. 1511 20

This review focuses on the epidemiology, clinical description, pathophysiology, treatment, and prevention of high altitude cerebral edema (HACE). HACE is an uncommon and sometimes fatal complication of traveling too high, too fast to high altitudes. HACE is distinguished by disturbances of consciousness that may progress to deep coma, psychiatric changes of varying degree, confusion, and ataxia of gait. It is most often a complication of acute mountain sickness or high altitude pulmonary edema. The current leading theory of its pathophysiology is that HACE is a vasogenic edema; that is, a disruption of the blood-brain barrier, and we review possible mechanisms to explain this. Treatment and prevention of HACE are similar to those for the other altitude illnesses, but with greater emphasis on descent and steroids. We conclude the review with several case histories to illustrate key clinical features of the disorder.
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PMID:High altitude cerebral edema. 1526 35

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

In a 33-weeks pregnant patient with a head injury, neurological status severely deteriorated after introduction of tocolytic treatment with ritodrine. On admission to the intensive care unit she scored 10 points on the Glasgow coma scale. She gradually recovered and on day 7 there was no neurological deficit, apart from slight confusion. The same day tocolytic treatment with ritodrine was recommended because of imminent premature labour. Fourteen hours after ritodrine infusion was started, the neurological status deteriorated severely. Urgent CT scan showed signs of transtentorial herniation. Ritodrine infusion was stopped and therapy for brain oedema was introduced. The patient made a good neurological recovery. A caesarean section was performed on day 11, because of placenta praevia, and a healthy girl was delivered. The patient was discharged without neurological sequelae. The clinical course and CT findings imply that tocolytic treatment with ritodrine can worsen brain oedema in a patient with a disrupted blood-brain barrier, as in head injury. The mechanism is probably analogous to the one by which ritodrine causes pulmonary oedema, a well-known complication.
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PMID:Tocolysis with ritodrine worsens cerebral oedema in a patient with brain injury. 1532 63


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