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)

Recently introduced chloroquine resistant malaria has altered the clinical picture and complicated the overall management of malaria. 113 adults with proved malaria admitted at Harare Central Hospital, Zimbabwe, were evaluated to determine the incidence, nature, relationship to morbidity and mortality and response to treatment of the complications due to malaria. 47.7 pc (52 of 109) patients had relatively chloroquine resistant malaria. 87.4 pc (99 of 113) had complications whose percentage frequency of occurrence were: Anaemia 51.2 pc, diarrhoea and/or vomiting 42.2 pc, cerebral malaria +/- fits 39.2 pc, renal insufficiency +/- hyperkalaemia 26.4 pc, hypoglycaemia 15.6 pc, jaundice 15.2 pc, neuro-psychiatric 15.0 pc, shock 10.6 pc, concurrent sepsis 8.9 pc, pulmonary oedema 3.5 pc and hyperpyrexia 1.7 pc. Multiple complications in the same patient were common. The combination of cerebral malaria and renal insufficiency had the worst mortality (p less than 0.001). All patients dialysed, however, survived. Non-iron deficiency anaemia, 91.7 pc (51 of 55) and diarrhoea and/or vomiting, were common, worsened morbidity but not mortality (p = 0.555). A seriously-ill patient with malaria should be suspected of having complications and chloroquine resistance and should be referred promptly to a centre with facilities for dialysis. Anti-malaria drugs should be mixed in a dextrose solution and iron supplements should not be given routinely.
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PMID:Complications of seasonal adult malaria at a central hospital. 209 79

Systemic mast cell disease (SMCD) is a rare disease often associated with symptoms of general malaise, pruritus, diarrhea, vomiting, fever, urticaria pigmentosa, hepatosplenomegaly and lymphadenopathy. We reported a case of SMCD associated with cutaneous xanthoma and serum hyper IgE. Skin biopsy revealed xanthomas and diffuse infiltration of mast cells in the dermis. The association of SMCD with xanthoma was reported in the literature for only one case. The hyper IgE could be due to the defect of IgE receptors on the cell membrane of mast cells of dysfunction of T and/or B cell. Any of the treatment using H1 and H2 receptor blockade, disodium cromoglycate, adrenocorticosteroid or chemotherapy (VEPA) were not effective. The patient died of pulmonary edema and multiple organ failure 7 months after the diagnosis was established. The crush method for the cytological examination of bone marrow was considered more useful than smear method for the diagnosis of SMCD.
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PMID:[Systemic mast cell disease associated with cutaneous xanthomas and markedly elevated serum IgE]. 224 20

Simple cardiopulmonary functions were studied serially in 26 mountaineers between sea level and an altitude of 25,200 ft. Up to 12,000 ft there was no altitude sickness, though there were complaints of leech bite (26.9%) and blisters (3.8%). One member died of exhaustion, two developed pulmonary oedema, one "flu" (at 15,600 ft) and one pleural rub (at 21,000 ft). Up to 16,000 ft altitude, 4 to 7.7% developed diarrhoea or epistaxis only, but at higher levels 25 to 50% subjects developed several symptoms, besides excessive dyspnea. These included diarrhoea (35-60%), vomiting (30%) abdominal pain (35-60%), rectal bleeding (15%), chest pain (10-40%), dry cough (40-60%), giddiness (30%) and poor memory (7.7%). A small rise in blood pressure was seen (for systolic at lower and diastolic at greater altitudes). After 18,200 ft the steady increase seen in VE slowed and the rise in heart rate and respiratory rate (f) became steeper. After a small rise at 7,800 ft, FVC and FEV1 showed a gradual decline at higher altitudes. After a large initial increase in PEFR up to 12,000 ft, a gradual decline was seen. The mean weight loss during the expedition was 8 +/- 2.7 kg. These changes seem to be due to an incomplete acclimatisation, which future mountaineering teams should take into consideration to avoid health problems and improve performance.
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PMID:Cardiopulmonary functional changes in acute acclimatisation to high altitude in mountaineers. 225 31

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

We present the case of a patient who attempted suicide by ingestion of the rodenticide zinc phosphide. Zinc phosphide manifests its immediate toxicity through production of phosphine gas. Signs and symptoms of toxicity include nausea, vomiting, dyspnea, and changes in mental status; immediate death results from pulmonary edema. Delayed effects are secondary to the absorption of phosphide, affecting primarily the liver, heart and kidneys. Delayed deaths are related to a direct cardiotoxicity. Treatment is mainly symptomatic and supportive; aggressive airway management and circulatory support are critical to a successful outcome.
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PMID:Zinc phosphide ingestion: a case report and review. 257 17

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64

We prospectively studied 56 consecutive patients with severe tricyclic antidepressant ingestion to determine the incidence of associated pulmonary complications. Among the patients meeting the entrance criteria, the mean antidepressant level was 1136 ng/ml. Other characteristics were a QRS duration of greater than or equal to 0.1 seconds in 35 (63%) and seizures in 19 (34%). Seventeen patients (30%) developed 18 abnormal chest X-ray findings which included pulmonary edema in 8 cases and aspiration pneumonia in 10. Using logistic regression, we evaluated the influence of tricyclic antidepressant level, blood pressure, QRS interval, seizures, drug co-ingestion and the use of gastric lavage vs. ipecac-induced emesis on pulmonary complications. For patients with pulmonary edema, the only significantly associated factor was hypotension on emergency department presentation. For aspiration pneumonia, no significant associations were found. Co-ingestion of another drug had no apparent influence on the development of pulmonary abnormalities. Our findings suggest that pulmonary edema and aspiration pneumonia are frequent complications of severe ingestions of tricyclic antidepressants. Pulmonary edema appears to result from hypotension or its treatment. The etiology of aspiration pneumonia is unclear. A chest X-ray should be obtained in all victims of tricyclic antidepressant overdose.
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PMID:Pulmonary consequences of severe tricyclic antidepressant ingestion. 289 71

The interest in mountain tracking and climbing has increased and there is a need for knowledge of altitude-related diseases. About one million non-acclimatized individuals annually frequent areas around 2,000 to 3,000 m above sea level and incur unpleasant symptoms in the form of acute altitude sickness or potentially fatal conditions such as pulmonary and/or cerebral oedema. Headache is the most prominent sign of acute altitude sickness but fainting fits, loss of appetite, hesitant gait, euphoria, or confusion also occur. Dyspnoea, cyanosis at rest, and a dry cough are signs of pulmonary oedema. Cerebral oedema may be feared when inexperienced climbers are afflicted by severe headaches, vomiting, and hesitant gait. Coma ensues relatively soon. Treatment consisting in descent to lower altitude, administration of oxygen, and possible medicinal therapy is effective if immediately introduced.
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PMID:[Altitude sickness]. 291 57

Two fatal cases of Japanese pieris poisoning in goats are reported. The clinical symptoms of the two animals consisted in vomiting, salivation, excitation and depression. Despite rumenotomy and symptomatic treatment, the goats died within four days after the onset of the symptoms. Pulmonary oedema accompanied by lobular aspiration pneumonia was found to be present in one goat at autopsy. Hyperaemia, pulmonary oedema and acute tubular nephrosis were observed in the other animal.
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PMID:[Pieris japonica pieris poisoning in 2 goats]. 337 72

Clinical studies were performed in 27 consecutive patients with high-altitude pulmonary edema who were transported from the mountains to Shinshu University Hospital, Matsumoto, Japan. The altitude of onset was 2,680 m to 3,190 m above sea level. Symptoms included marked dyspnea, cough, and stridor. Physical findings included cyanosis, tachycardia, and rales. Neurologic disturbances, which were seen in 17 patients, included headache, vomiting, memory disturbance, clouding of consciousness, or coma. Chest roentgenograms revealed patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern, and enlargement of the right ventricle. Hemodynamic studies by right cardiac catheterization showed that high-altitude pulmonary edema was noncardiogenic. Scintiscans of the lungs with technetium-99m-macroaggregated albumin (99mTc-MAA) performed in one patient showed decreased perfusion of 99mTc-MAA in the area of infiltrates. Pulmonary edema fluid collected through the endotracheal tube in two patients was rich in protein. Computerized tomograms of the brain showed small ventricles and cisterns, disappearance of sulci, and diffuse low density of the cerebrum, indicating cerebral edema in eight of nine cases. Retinal hemorrhage and papilledema were observed in five patients.
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PMID:Clinical features of patients with high-altitude pulmonary edema in Japan. 366 94


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