Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

To determine the prognostic factors for leptospirosis, we conducted a retrospective study of data collected in the emergency department of our hospital between 1989 and 1993. Sixty-eight patients, for whom the diagnosis of leptospirosis was based on pertinent clinical and epidemiological data and positive serology, were included in this study. Fifty-six patients (82%) were discharged from the hospital, and 12 (18%) died. Multivariate logistic regression demonstrated that five factors were independently associated with mortality: dyspnea (odds ratio [OR], 11.7; 95% confidence interval [CI], 2.8-48.5; P < .05), oliguria (OR, 9; CI, 2.1-37.9; P < .05); white blood cell count, >12,900/mm3 (OR, 2.5; CI, 1.8-3.5; P < or = .01), repolarization abnormalities on electrocardiograms (OR, 5.9; CI, 1.4-24.8; P < or = .01), and alveolar infiltrates on chest radiographs (OR, 7.3; CI, 1.7-31.7; P < or = .01). Identification of these factors on admission might provide useful selection criteria for patients who need early transfer to the intensive care unit.
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PMID:Leptospirosis: prognostic factors associated with mortality. 931 67

Ascites is a clinical manifestation of severe ovarian hyperstimulation syndrome (OHSS) which may complicate the induction of ovulation using exogenous gonadotrophins. In severe OHSS severe ascites may occur and can lead to dyspnoea, abdominal discomfort and oliguria. To relieve ascites paracentesis is performed two to three times weekly as needed. We report three cases where an indwelling peritoneal catheter was used to decrease the need for repeated paracentesis. Under ultrasound guidance a closed system Dawson-Mueller catheter with 'simp-loc' locking design was inserted to allow continuous drainage of the ascitic fluid. A total of 23 l of the ascitic fluid were drained from the first, 20 l from the second and 28 l from the third patient with significant decrease in abdominal discomfort and improvement in the urine output. No complications or adverse reactions were noted. Continuous drainage of the ascitic fluid is efficient. It quickly decreases the abdominal discomfort, improves the urine output and prevents the need for multiple abdominal paracenteses which some patients may require.
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PMID:A novel approach to the treatment of ascites associated with ovarian hyperstimulation syndrome. 945 23

A 22 year-old woman with a seven year history of (SLE) was readmitted because of oliguria, edema, dyspnea and arterial hypertension. She had a previous biopsy diagnosis of focal glomerulonephritis, (WHO III b), and had been treated with immunosuppressors and steroids. Laboratory data showed lupus activity, AHM with thrombocytopenia, nephrotic-range proteinuria and renal failure. A second renal biopsy was performed showing diffuse proliferative nephritis, (WHO IV), in association with noninflammatory necrotizing vasculopathy with luminal obliteration. She started with hemodialysis and was subsequently treated with methylprednisolone pulses, plasmapheresis, cyclophosphamide and oral steroids. During the inpatient period, she had generalized seizures, acute lung injury and pulmonary hemorrhage. These complications, the AHM and the thrombocytopenia receded totally. Renal function was never resumed. We emphasize that this association of diffuse proliferative nephritis with noninflammatory necrotizing vasculopathy is not infrequent and has a poor renal prognosis. The AHM with thrombocytopenia was interpreted as secondary to endothelial cell damage due to vasculopathy.
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PMID:[Renal vascular lesion and microangiopathic hemolytic anemia in systemic lupus erythematosus]. 953 30

A 2-year-old boy was hospitalized with the chief complaint of oliguria and dyspnea. Bilateral hydronephrosis and obstruction of the pyeloureteral junction were detected by ultrasonography. Pulmonary edema was also found on chest radiographs. The clinical diagnosis was acute post renal failure due to bilateral pyeloureteral obstruction and pulmonary edema due to overtransfusion. After we performed bilateral percutaneous nephrostomy, the patient recovered from renal failure and pulmonary edema. Both nephrostomies were removed after we confirmed a non-obstructing pattern using the Whitaker test.
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PMID:[Acute renal failure due to over-infusion in a child with bilateral obstruction of the pyeloureteral junction]. 1054 Jul 11

The risk factors for death and changes in clinical patterns in leptospirosis (Weil's disease) have not been well studied. We retrospectively studied 110 patients with Weil's disease hospitalized in Brazil between 1985 and 1996. Univariate statistical analysis showed that nonsurvivors were older than survivors, and had higher frequency of oliguria, cardiac arrhythmia, dyspnea, and pulmonary rales. Logistic regression showed that the only independent factor associated with death was oliguria (odds ratio [OR] = 8.98). The presence of arthralgia (OR = 4.71), dehydration (OR = 6.26), dyspnea (OR = 17.7), and pulmonary rales (OR = 9.91) increased after 1994. These data suggest that in Weil's disease the clinical patterns have changed and the presence of oliguria is a risk factor for death.
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PMID:Risk factors for death and changing patterns in leptospirosis acute renal failure. 1054 99

We report a 67-year-old man with progressive disturbance of gait. He was well until the spring of 1993 (62 years of the age), when he noted an onset of unsteady gait. He also noted that he started to have a difficulty in playing tennis, in which he became unable to hit the ball with his racket. He also noted parkinsonian features such as bradykinesia and loss of hand dexterity. He was treated with levodopa, which did not improve his symptoms. His MRI revealed marked atrophy of the cerebellum and the pons. The criss-cross high signal lesion was seen in the center of the pons. The third ventricle was dilated. The putamen was unremarkable. His subsequent course was complicated by easy to fall, difficulty in swallowing with episodes of aspiration pneumonia. He also developed nocturnal apneustic episodes. He was admitted to our hospital on November 15, 1998, when he was 67 years of the age. He had low grade fever and low blood pressure (98/70). He was anemic but not icteric. Tumors were palpated in his jaw, anterior chest, and in the left arm. He was alert but unable to convey his desire because of dyspnea and tracheostomy. His gaze was slightly restricted in the horizontal direction and markedly so in the vertical direction. Motor functions were difficult to evaluate. His clinical course was complicated by atelectasis of the right lung and pleural effusion. He developed marked edema and oliguria. He developed sudden bradycardia and expired on December 26, 1998. He was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had multiple system atrophy. Majority of the audience agreed with this diagnosis. Post-mortem examination revealed a lung cancer in the right lung (undifferentiated adenocarcinoma) with metastases to the liver, kidneys, lymph nodes, pericardium, pleura, skin, bone marrow, and the brain. Neuropathologic examination revealed marked atrophy of the pons and the cerebellum. The putamen showed brownish discoloration and atrophic changes. The substantia nigra showed marked neuronal loss and gliosis. Oligodendrocytic inclusion bodies (alpha-synuclein positive) were seen in the putamen, globus pallidus, substantia nigra, pontine nucleus, cerebellar white matter, internal capsule, cerebral peduncle, and the spinal cord. These findings are consistent with the pathologic diagnosis of multiple system atrophy. What was interesting to us was the presence of neurofibrillary tangles in the substantia nigra, nucleus ruber, globus pallidus, and subthalamic nucleus. Tuft-shaped astrocytes were also seen. This patient appears to be a rare example of combination of MSA and PSP.
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PMID:[A 67-year-old man with progressive disturbance of gait]. 1093 28

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71

We report a case of multiple organ dysfunction following epididymitis. A 53-year-old male patient was admitted to our emergency room with bilateral clavicular fractures, multiple costal fractures and left hemopneumothorax due to a traffic accident. Open reduction of the right clavicular fracture was performed under general anesthesia on the sixth hospital day. A bladder balloon catheter was inserted after induction of anesthesia. The clinical course in the perioperative period was satisfactory and the bladder balloon catheter was removed on the seventh hospital day. However, spontaneous left scrotal pain with tenderness, intense heat with swelling developing on the tenth hospital day, and hypotension, dyspnea and oliguria were noted on the eleventh hospital day. Blood chemistry data showed severe inflammatory findings. Chest X-ray showed acute respiratory distress syndrome. Blood coagulation data showed pre-disseminated intravascular coagulation. The patient's condition continued to deteriorate and we suspected septic shock due to left epididymitis. Emergent left orchiectomy was performed under local anesthesia on the twelfth hospital day. Postoperatively he recovered rapidly. We consider that multiple organ dysfunction following postoperative epididymitis was caused by cytokines released due to systemic inflammatory response syndrome (SIRS) after the trauma, operation, and placement of the bladder catheter. In conclusion, it is important to note that patients with SIRS should undergo further examinations of septic shock immediately and resection of the causative tissue should be performed as soon as possible.
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PMID:[A case of multiple organ dysfunction following postoperative epididymitis]. 1205 38

Beriberi (BB), thiamine deficiency, has been described in the Asian literature in the 17th century and is characterized by peripheral neuropathy and muscle weakness, also called "dry" beriberi (BB) to differentiate it from "wet" BB, with essentially cardiovascular manifestations. Wet can be either "classic" wet BB in which signs and symptoms of right-sided heart failure with normal or high cardiac output are the presenting features or the "shoshin" BB variant with severe biventricular failure and metabolic acidosis, which must be treated early to prevent the rapid development of low cardiac output failure and sudden death. In this case, we report a 58 year old alcoholic woman who developed dyspnea, oliguria, edema, cardiac failure with high output, metabolic acidosis, renal tubular dysfunction and serum lactate level of 5.6 mEq/L. Neurological examination revealed peripheral neuropathy in the lower legs and cognitive alteration. She was treated with a loading dose of 100 mg of intravenous thyamine and responded with a marked increase in urine output, correction of acidosis, reduction in pulmonary-capillary wedge pressure and a change of the hemodynamic pattern. We conclude that shoshin-BB is uncommonly encountered but not widely recognized. In lactic acidosis and/or hyperdynamic circulation without any other apparent etiology in patients with possible vitamin B1 deficiency, the diagnosis of BB must be considered and thiamine should be administered.
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PMID:[Acute cardiovascular beriberi (shoshin-beriberi)]. 1232 90


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