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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxic shock syndrome (TSS) is a recently recognized condition associated with toxin-producing strains of Staphylococcus aureus. Patients affected with this syndrome are frequently young and have multisystemic complaints such as fever, headache, edema, myalgia, scarlatiniform rash, conjunctival injection, confusion, diarrhea, oliguria, hypotension and shock, This is followed by desquamation of the skin, especially the palms and soles. The majority of cases reported have been in menstruating women who used vaginal tampons regularly. Because similarities exist between toxic shock syndrome and Kawasaki's disease (mucocutaneous lymph node syndrome), as well as other conditions, proper diagnosis and management are of the utmost importance.
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PMID:Toxic shock syndrome. Possible confusion with Kawasaki's disease. 726 71

We report on a 25-year-old man who had scrub typhus with the unusual complication of acute renal failure. The clinical features of fever, headache, high Weil-Felix OX-K agglutination and Rickettsia tsutsugamushi immunofluorescence titers confirmed the diagnosis of scrub typhus. Acute renal failure was proven by oliguria, urinary diagnostic indices and renal biopsy. The patient had a complete recovery after adequate medical treatment.
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PMID:Acute renal failure associated with scrub typhus: report of a case. 810 4

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

We report on 10 patients with acute renal involvement in Hantaan virus infection observed at the Department of Nephrology, Faculty of Medicine, Skopje, Republic of Macedonia, during a period of 3 years (October 1987-July 1990). Eight patients were male and 2 were female, aged 37.5 +/- 4.8 years. The diagnosis of Hantaan virus infection was proven by an indirect immunofluorescent and ELISA test with a significant increase of the titer after a week to ranges from 1:512 to 1:2,048. Percutaneous renal biopsy was performed in 3 cases using standard procedures for optical and immunofluorescent microscopy. Fever, weakness, headache, conjunctival injection, hematuria, and lumbar pain were clinical features all patients had in common. Complete anuria was noted in 7 out of 10 and oliguria in the other 3 of the 10 cases with serum levels of creatinine 967 +/- 152.6 mumol/L. Other following laboratory findings were leukocytosis in 10 out of 10 patients, with neutrophylia, and reduction of serum sodium and potassium in 8 out of 10, and a decrease in serum complement C3 in 3 out of 10 patients. Percutaneous renal biopsy confirmed interstitionephritis in 2 out of 3 biopsied patients and acute diffuse proliferative glomerulonephritis in the third. Interstitial mononuclear infiltration with dominant T cells proven with monoclonal antisera (direct immunoperoxidase method) was present in all 3 cases. The outcome of the disease was good in 8 of the 10 patients with a development of polyuric phase and complete recovery of renal function later. One patient with interstitial lesions on biopsy developed chronic renal failure, and the other with a concomitant brucellosis died during the polyuric phase of the disease.
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PMID:Hantaan virus infection with acute renal failure. 857

The aim of our study was to analyze the clinical course and outcome of acute renal failure (ARF) in patients with hemorrhagic fever with renal syndrome (HFRS). From 1983 to 1995, we treated 33 patients (27 males, 6 females) aged from 16 to 71 years. Half of patients were connected with work at a farm or in a forest. The disease was confirmed serologically with indirect immunofluorescence test (IFT) and enzyme-linked immunosorbent assay (ELISA). In 18 patients percutaneous kidney needle biopsies were analyzed. In 85% of the cases, the disease broke out from June to October. The most frequently expressed clinical signs and symptoms were fever, nausea/vomiting, headache, backache, abdominal pain, myalgia, diarrhea, conjunctival injection, and hemorrhages. Four patients had concomitant pancreatitis. In 25 patients, oliguria was present, and transient hemodialysis treatment was needed in 19 patients. Infection with Hantaan virus was established in 20 patients and with Puumala virus in 13 patients. At renal biopsy, acute interstitial nephritis accompanied with hemorrhages and necrosis was found, and at a later biopsy there were also signs of interstitial fibrosis. All patients were cured, but renal function was not completely recovered in some. We conclude that ARF is a serious complication in patients with HFRS. Although not lethal in our group of patients, many of them showed severe signs and symptoms of illness. Transient hemodialysis was necessary in two-thirds of the patients. Some degree of functional defects and morphological changes might persist.
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PMID:Acute renal failure due to hemorrhagic fever with renal syndrome. 887 90

Nephropathia epidemica (NE) is a prevalent zoonosis throughout Europe and is caused by the Puumala type of hantavirus. The incidence of NE varies in a cyclic fashion, with peaks occurring every 3rd to 4th year, coinciding with peaks in vole populations. The clinical course of NE is generally milder than haemorrhagic fever with renal syndrome caused by hantaviruses in other parts of the world. Typically, NE has a sudden onset with fever, headache, backpain and gastrointestinal symptoms. However, severe complications, e.g. gastrointestinal haemorrhage, occur and fatal cases have been reported. Renal involvement is prominent and manifests as initial oliguria and later as marked polyuria. Tests of renal function show pronounced glomerular and tubular involvement. Vaccine against Puumala virus infection as well as specific treatment for NE are still lacking.
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PMID:Clinical aspects of nephropathia epidemica (Puumala virus infection) in Europe: a review. 1082 95

Post-infectious acute glomerulonephritis with hypertensive encephalopathy is characterized by episodic hypertension with headache, vomiting, and hematuria. The association between hypertensive encephalopathy and cortical blindness in children with acute glomerulonephritis is extremely rare. We report the case of a 10-year-old boy with acute glomerulonephritis who presented with gross hematuria, headache, vomiting, and oliguria, and developed transient cortical blindness as a complication of hypertensive encephalopathy. No occurrence of seizure was observed during the clinical course. T2-weighted cranial magnetic resonance imaging showed a high-intensity signal over cortical and subcortical areas of bilateral occipital regions. His vision recovered fully, 2 days after receiving antihypertensive therapy. The patient was well without complaint at 1-year follow-up. This case highlights the possibility that cortical blindness may develop as a complication of acute glomerulonephritis in children. Prevention of the occurrence of neurological deficits in children with acute glomerulonephritis and hypertensive encephalopathy requires careful evaluation and appropriate management of hypertension.
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PMID:Cortical blindness in a boy with acute glomerulonephritis. 1268 14

Among many viral hemorrhagic fevers, only hemorrhagic fever with renal syndrome (HFRS) occurs in Croatia. HFRS is a natural focus zoonosis with sudden onset, characterized by high fever and other clinical symptoms, renal insufficiency and hemorrhages. In Croatia, HFRS is caused by two types of hantaviruses--Puumala (PUU) and Dobrava (DOB). The basic pathologic and patophysiologic disorder in HFRS is capillary damage (vasculitis). Incubation of HFRS has not been precisely determined, it is most frequently around two weeks. The disease onset is usually abrupt. At the beginning, general symptoms include high fever and myalgias, especially in the lumbar region, and abdominal pain, as well as strong headaches, malaise and nausea, and often vomiting or diarrhea. In half of the patients respiratory symptoms occur. Later on, some patients may experience hypotension, oliguria and other signs of renal failure, and apart from petechial, severe hemorrhages may also occur in other organs. During typical clinical presentation of the disease, some characteristic symptoms are clearly distinguished in particular stages of the disease. Therefore, the course of HFRS is usually divided into five distinct stages (febrile, hypotensive, oliguric, polyuric and convalescent). Such a course of the disease is more commonly present in case of DOB virus than PUU virus infection. The febrile stage with sudden onset usually lasts from 3 to 7 days, when thrombocytopenia and hemoconcentration, as well as albuminuria and hematuria are almost always recorded. The hypotensive stage lasts from one to 2 days on an average and is characterized by lower blood pressure and signs of renal failure. The oliguric stage usually starts at the beginning of the second week of the disease, when extensive hemorrhage may occur and urea and creatinine reach their highest values. The oliguric stage is followed by the polyuric stage which can last for up to two weeks, and is characterized by excretion of a large quantity of urine of low specific gravity (up to 15 liters during 24 hours). The convalescence (convalescent stage) is slower, may last for several weeks or months, but usually resolves without complications. During the infection caused by PUU virus, the course of disease is usually milder with only two stages. The first one is febrile, followed by the second stage with renal symptoms, and rare and mild hemorrhagic manifestations. This type of disease is mostly encountered during epidemics. The mortality in severe cases of the disease (DOB virus) is 5% to 10%, whereas in PUU virus infection it is less than 1%.
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PMID:[Clinical picture of hemorrhagic fever with renal syndrome in Croatia]. 1501 67

Reversible posterior leukoencephalopathy syndrome is a recently described disorder with typical radiologic findings in the posterior regions of the cerebral hemisphere and cerebellum. The symptoms include headache, nausea, vomiting, visual disturbances, focal neurologic deficits, and seizures. A 10-year-old male was hit on his back, resulting in backache. He was medicated with sodium diclofenate and mefenamic acid. The next day, he had edema and oliguria. By the third day, his blood pressure increased and he began to experience restlessness and worsening mental status. He then complained of headache and visual disturbances and had a seizure. A magnetic resonance imaging scan revealed abnormalities in the posterior regions of the cerebral hemisphere and cerebellum. The patient was treated with antiepileptics and calcium antagonists. His hypertension and seizures were well controlled. On the 22nd day, he was discharged without any neurologic or renal deficits. Reversible posterior leukoencephalopathy syndrome does not occur frequently in childhood, and this is the first case report of reversible posterior leukoencephalopathy syndrome related to nonsteroidal anti-inflammatory drugs. One should consider reversible posterior leukoencephalopathy syndrome as a side effect of nonsteroidal anti-inflammatory drug use in daily medical treatment.
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PMID:Pediatric posterior reversible leukoencephalopathy syndrome and NSAID-induced acute tubular interstitial nephritis. 1650 99

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 +/- 34 days). The time until death ranged from one to nine days (mean 3.3 +/- 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > or = 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.
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PMID:Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil. 1655 20


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