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Toxic shock syndrome (TSS) is a serious, potentially life-threatening condition resulting from an exotoxin of Staphylococcus aureus. Presenting symptoms include high fever, diarrhea, nausea, and vomiting progressing to hypotension, oliguria, conjunctival hyperemia, and an erythematous rash over the trunk, abdomen, and extremities. TSS has been associated both with and without the use of tampons during menstruation, postsurgical infections, and stab wounds, and can occur in postrhinoplasty patients with and without nasal packing. There has been one case reported in the literature of TSS associated with suction-assisted lipectomy (SAL). This article discusses the diagnosis and treatment of two cases in which the patients developed TSS after outpatient use of SAL. In the first case, an abdominoplasty and SAL were performed in a healthy young female. The second case involved the harvesting of abdominal fat via syringe suction and subsequent facial fat injection in a female with systemic lupus erythematosus and severe facial atrophy.
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PMID:Toxic shock syndrome associated with suction-assisted lipectomy. 801 20

An analysis was made of the clinical course of 20 transurethral resections of the prostate performed under epidural analgesia in which between 676 and 3,600 ml of irrigating fluid containing glycine had been absorbed by the extravascular route. Symptoms consisted in arterial hypotension (n = 14), postoperative oliguria (n = 11), nausea (n = 10), bradycardia (n = 7), abdominal discomfort (n = 5) and visual disturbances (n = 2). There was a significant correlation between hypotension and postoperative oliguria. The hyponatraemia at the end of the operation was only one third of the values obtained if the same amount of irrigating fluid had been absorbed by the intravascular route. Suprapubic drainage of the absorbed fluid (n = 8) did not reduce the hyponatraemia and prolonged the postoperative stay in hospital. Diuretics is an alternative to surgical drainage in all but the most severe cases of extravasation, but should be postponed until normovolaemia is restored and the circulation is stable.
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PMID:Transurethral resection syndrome from extravascular absorption of irrigating fluid. 829 Sep 19

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

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

Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.
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PMID:Tetracycline-induced acute interstitial nephritis as a cause of acute renal failure. 988 23

We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
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PMID:[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus (MRSA) presenting as acute renal failure]. 1036 25

A 43-year-old man, with a history of central diabetes insipidus diagnosed 3 years previously, complained about reduced libido. An MRI scan showed a suprasellar lesion just below the supraoptic recess of the third ventricle. A stereotactically guided biopsy revealed fibrous glia, but no other specific tissue and no inflammatory cells. Two months later the patient presented with fatigue and muscular weakness. Tertiary adrenal failure and hypothyroidism were diagnosed by endocrine function tests and therapy with levothyroxine and hydrocortisone was started. Another 2 months later the patient was admitted with giddiness, nausea, peripheral oedema and oliguria. Radiological imaging and an open transperitoneal kidney exploration showed severe fibrosis around both ureters. Histological examination confirmed the diagnosis of idiopathic retroperitoneal fibrosis. Presumably the suprasellar tumour was the first manifestation of retroperitoneal fibrosis. Once the diagnosis 'idiopathic retroperitoneal fibrosis' is confirmed, fibrotic manifestations and complications involving extra-retroperitoneal tissues including the endocrine system, should be sought.
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PMID:Panhypopituitarism associated with severe retroperitoneal fibrosis. 1120 44

We report tamoxifen-induced hypertriglyceridemia and asymptomatic acute pancreatitis in a 51 year-old women with type 2 diabetes mellitus and stage III-b infiltrative ductal carcinoma, admitted to the hospital with weakness, oliguria and glucose dysregulation. On admission, there was no fever, abdominal or back pain, rebound tenderness, nausea, or vomiting. Following 1 year of tamoxifen treatment, triglycerides increased from 400 to 1344 mg/dl (blood urea nitrogen 52 mg/dl, creatinine 2.0 mg/dl, glucose 341 mg/dl). Hypertriglyceridemia was considered to be due to either diabetic dyslipidemia and/or tamoxifen. On computerized tomography, pancreatic enlargement, heterogenity, hypodensity and a pancreatic pseudocyst (5 x 7.5 cm diameter) were found. Acute pancreatitis was suspected, and serum amylase level was found to be increased (273 IU/L). Tamoxifen was discontinued and gemfibrozil was started. Triglycerides decreased to 301 mg/dl and amylase decreased to 66 IU/L a week later and remained normal thereafter. This case indicates that tamoxifen-induced hypertriglyceridemia may cause acute pancreatitis without classical symptoms which might be due to autonomic neuropathy in diabetic patients. Effects on lipid metabolism should be considered and triglycerides should be closely followed in patients on tamoxifen.
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PMID:Asymptomatic acute pancreatitis due to tamoxifen-induced severe hypertriglyceridemia in a patient with diabetes mellitus and breast cancer. 1212 Aug 88

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


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