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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes insipidus following cardiac arrest and hypoxemic encephalopathy occurred in two patients. In both, severe hypoxemic brain damage was followed within three days by clinical and laboratory features of diabetes insipidus, which were corrected by administration of exogenous vasopressin. Hypothalamic injury resulting in diabetes insipidus should be considered in the differential diagnosis of polyuria and dehydration occurring in critically ill patients who have suffered cardiorespiratory arrest.
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PMID:Diabetes insipidus following cardiorespiratory arrest. 57 64

Acute fatty liver of pregnancy, with a case history where an early diagnosis could have been made, and a review of the French literature. Acute fatty liver of pregnancy, or Sheehan's syndrome is a rare but very serious complication of pregnancy. The disease is demonstrated by vomiting, abdominal pain and a high level of uric acid in the blood before jaundice is noted. Within a few days the triad of jaundice, pruritus and encephalopathy occur. These are often associated with toxaemia of pregnancy and with polyuria and polydipsia. A raised white blood count and a high level of bilirubinemia are almost always present. The outlook is very serious when haemorrhage appears. This malignant form of the disease is characterised by liver and kidney failure. Liver biopsy confirms the diagnosis. The prognosis is related to an early diagnosis and is good when labour is induced or caesarean section performed. Acute fatty liver of pregnancy is an emergency from the diagnostic as well as the therapeutic angles.
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PMID:[Acute fatty liver of pregnancy. Diagnostic value of hyperuricemia in the pre-jaundice stage]. 322 Oct 52

Diabetes insipidus is an uncommon condition characterized by polyuria and polydipsia. The symptoms and biochemical changes of this condition result from either a lack of antidiuretic hormone or renal insensitivity to its effect. Failure to produce or release antidiuretic hormone may result from cranial pathology, including trauma and surgery. The renal insensitivity to antidiuretic hormone that occurs in patients with nephrogenic diabetes insipidus may be caused by genetic factors, drugs (especially lithium) or specific disease processes. Patients may compensate for polyuria and nocturia by excessive water intake but show marked decreases in urine specific gravity and osmolality. Patients with severe and uncompensated symptoms develop marked dehydration, neurologic symptoms and encephalopathy. The water deprivation test is useful in diagnosing diabetes insipidus and in differentiating neurogenic from nephrogenic cases. Neurogenic diabetes insipidus may respond to nasal administration of desmopressin. Nephrogenic diabetes insipidus requires good hydration and monitoring of body chemistry. Thiazides and amiloride may relieve symptoms.
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PMID:Evaluation and management of diabetes insipidus. 914 42

We assessed the utility of fluid-attenuated inversion-recovery (FLAIR) and diffusion-weighted (DWI) images in investigation of tacrolimus (FK-506) encephalopathy, and to see whether we could predict its cause from clinical and imaging data. In seven patients with presumed FK-506 toxicity the areas involved on MRI were similar to those in cyclosporin A (CsA) toxicity. The abnormal signal was most evident on FLAIR in all cases. In three of four patients who underwent DWI, no diffusion abnormalities were detected; in the remaining patient, increased diffusion was seen in the deep white matter bilaterally on the apparent diffusion coefficient map, consistent with the findings on T2-weighted spin-echo and FLAIR images. Five of the six patients for whom we had clinical data showed sudden changes in electrolyte or fluid equilibrium due to diarrhoea, a polyuria or oliguria one day before or on the day of onset of the central nervous system disturbances. We speculate that FK-506 encephalopathy is triggered by the disturbance of the electrolyte and/or fluid equilibrium, given a certain serum level of FK-506.
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PMID:MRI in seven cases of tacrolimus (FK-506) encephalopathy: utility of FLAIR and diffusion-weighted imaging. 1154 66

A 9-year-old boy was admitted to our hospital with daytime urinary incontinence for the past one year. MRI showed craniopharyngioma occupying the third ventricle. The tumor was excised by interhemispheric approach. Because hyponatremia and polyuria with high renal loss of sodium were observed on postoperative day 3, hydrocortisone and DDAVP were replaced. On postoperative day 24, successive general convulsions and hyponatremia recurred, and MRI FLAIR imaging showed marked brain edema in the bilateral parieto-occipital lobes. This finding disappeared late in the course of treatment, and the case was diagnosed as posterior reversible encephalopathy syndrome. The pathophysiology of cerebral salt wasting and posterior reversible encephalopathy syndrome in a craniopharyngioma patient are also discussed in the article.
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PMID:[Prolonged cerebral salt wasting following craniopharyngioma surgery and posterior reversible encephalopathy syndrome: a case report]. 1578 2

Vitamin D deficiency state is endemic to the Kashmir valley of the Indian subcontinent. Physicians often treat patients with high doses of vitamin D for various ailments and on occasion the prescribed doses far exceed the requirements of the patients. Ten cases of hypercalcemia due to vitamin D intoxication are presented with features of vomiting, polyuria, polydipsia, encephalopathy and renal dysfunction. All the patients had demonstrable hypercalcemia and vitamin D levels were high in nine of the 10 cases. The patients had received high doses of vitamin D and no other cause of hypercalcemia was identified. Treatment of hypercalcemia resulted in clinical recovery in nine cases. We conclude that hypervitaminosis D must be considered in the differential diagnosis of patients with hypercalcemia in endemically vitamin D deficient areas. A careful history and appropriate biochemical investigation will unravel the diagnosis in most of the cases.
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PMID:Vitamin d toxicity in adults: a case series from an area with endemic hypovitaminosis d. 2204 17

This descriptive report describes the case of a 50 year-old woman with bipolar disorder, whose maintenance therapy comprised risperidone, sodium valproato and lithium carbonate without any past occurrence of toxicity. Her past medical history was significant for hypertension, cardiopathy and obesity. She presented with a 1-week history of fever, increasing confusion and slurred speech. At presentation, the patient was somnolent. Laboratory investigations revealed a serum creatinine of 3,6 mg/dl, BUN 45 mg/dl serum lithium 3,0 mEq/L with polyuria defined as more than 3 litres a day. EEG and ECG were abnormal. CT brain scanning and lumbar puncture were negative for brain haemorrage or infection. Lithium toxicity causes impairment of renal concentration and encephalopathy due to lithium recirculation, a mechanism responsible for the so-called cerebro-renal syndrome, where dialysis plays an important role in treatment.The patient was treated with continous veno-venous haemodiafiltration (CVVHDF) over 35 hours with gradual improvement of her general condition and efficacy of renal concentration. Our case highlights a few important points. Lithium nefrotoxicity and neurotoxicity can cause a cerebro-renal syndrome even when serum lithium levels are not particularly raised (2,5-3,5 mEq/L). Haemodialysis is the treatment of choice to reduce the molecular mechanisms of lithium-related changes in urinary concentration and reinstate dopaminergic activity in the brain.
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PMID:[The acute renal and cerebral toxicity of lithium: a cerebro-renal syndrome? A case report]. 2383 81

Diabetes insipidus is an uncommon disorder of water-electrolyte balance characterized by the excretion of abnormally large volumes of diluted urine (polyuria) and increased fluid intake (polydipsia). The disease may result from the insufficient production of vasopressin, its increased degradation, an impaired response of kidneys to vasopressin, or may be secondary to excessive water intake. Patients with severe and uncompensated symptoms may develop marked dehydration, neurologic symptoms and encephalopathy, and therefore diabetes insipidus can be a life-threatening condition if not properly diagnosed and managed. Patients with diabetes insipidus require treatment with desmopressin or drugs increasing sensitivity of the distal nephron to vasopressin, but this treatment may be confusing because of the disorder's variable pathophysiology and side-effects of pharmacotherapy. This review summarizes the current knowledge on different aspects of the pathophysiology, classification, clinical presentation, diagnosis, and management of diabetes insipidus. The reader is also provided with some practical recommendations on dealing with patients suffering from this disease.
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PMID:[Diabetes insipidus]. 2595 3

Treatment with desmopressin diacetate arginine vasopressin (DDAVP) and its withdrawal are associated with side effects. We present a rare case of severe biphasic adverse reactions induced by DDAVP and its withdrawal in a 63-year-old female patient. A lump in the left axillary region was biopsied, and she received DDAVP after surgery. The following day, she lost consciousness, with foaming at the mouth and seizures. Hypotonic encephalopathy was considered. DDAVP was ceased, and she received electrolytes. On day 1, she displayed low blood pressure and increased urine output. She received DDAVP and dopamine as well as electrolytes. The patient was ambulatory on day 7 and was discharged without brain abnormalities on MRI. In conclusion, severe hyponatremia induced by DDAVP and massive polyuria and hypovolemic shock induced by DDAVP withdrawal are life-threatening conditions. This case underlines the need to be vigilant when administering DDAVP and to monitor for any side effects.
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PMID:Life threatening biphasic adverse reactions to desmopressin: case report and review of the literature. 2714 68

We describe 2 patients, a 52-year-old woman and a 57-year-old man, with rapidly progressive hypertension and marked elevation of brain natriuretic peptide who exhibited polyuria, natriuresis, hypokalemia, posterior reversible encephalopathy syndrome and left ventricular dysfunction together with retinopathy and nephropathy, which were attenuated in a short time span of 1-2 months with normalization of blood pressure after the antihypertensive treatment. The possible role of brain natriuretic peptide in the pathophysiology of accelerated malignant hypertension was discussed and a review of the literature was completed.
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PMID:Brain Natriuretic Peptide Counteracting the Renin-angiotensin-aldosterone System in Accelerated Malignant Hypertension. 2786 4


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