Cases reported "Dehydration"

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1/20. Cerebral bleeding, infarcts, and presumed extrapontine myelinolysis in hypernatraemic dehydration.

    The neuroimaging findings in an infant with hypernatremic dehydration are presented. Brain parenchymal haemorrhage and extensive multiple infarcts were present in the acute stage. Follow-up CT showed bilateral, symmetrical changes presumed to indicate extrapontine myelinolysis in the thalamus and globus pallidus. MRI confirmed sparing of the pons. Only three previous cases of neuroimaging abnormalities due to hypernatraemia have been described in the radiological literature.
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keywords = haemorrhage
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2/20. Cranial MRI in neonatal hypernatraemic dehydration.

    Severe neonatal hypernatraemia is a life-threatening electrolyte disorder because of its neurological complications. These are brain oedema, intracranial haemorrhages, haemorrhagic infarcts and thromboses. There are few reports concerning the radiological findings in the central nervous system in severe neonatal hypernatraemia. Cranial MRI findings in hypernatraemia have been reported in an older child, but have not been described in newborn infants. We report the cranial MRI findings in a newborn infant with acute renal failure and severe hypernatraemia.
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ranking = 9.7515816914644
keywords = intracranial haemorrhage, haemorrhage, brain
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3/20. Hyponatremic hypertensive syndrome.

    We report on a 4-year-old girl with hyponatremic-hypertensive syndrome (HHS), a rare entity in childhood. The girl was referred to us from a local hospital with a history of recurrent fever, vomiting, and seizures. On admission she was markedly dehydrated. Initial investigations revealed severe hyponatremia (serum Na 120 mmol/l), hypochloremia (serum Cl 68 mmol/l), and mild hypokalemia (serum K 3.3 mmol/l), while serum calcium and magnesium were normal. serum urea was 5 mmol/l and serum creatinine was 62 mumol/l. Despite hyponatremic dehydration, her urine output was high (2050 ml/24 h), as was her urinary sodium (168 mmol/24 h). She had massive transient proteinuria (maximal 1642 mg/24 h) while being severely hypertensive (blood pressure 210/160 mmHg). Further investigations revealed right kidney scarring, hyper-reflexive bladder dysfunction, massive brain infarcts, and myocardial left ventricular hypertrophy. Renal arteries were normal on arteriography. blood pressure control resulted in normalization of serum and urinary electrolytes and decrease of proteinuria. hyponatremia and transient massive proteinuria in this patient seem to be caused by high-pressure-forced diuresis due to malignant renoparenchymal hypertension.
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ranking = 0.031500791350086
keywords = brain
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4/20. A case of hypopituitarism with diabetes insipidus and loss of thirst. role of antidiuretic hormone and angiotensin ii in the control of urine flow and osmolality.

    A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin ii (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.
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ranking = 0.031500791350086
keywords = brain
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5/20. Prognostic value of evoked potentials and sleep recordings in the prolonged comatose state of children. Preliminary data.

    OBJECTIVES: sleep recordings and evoked potentials (EPs) were used in five comatose children to evaluate their predictive value for outcome following a severe comatose state. methods AND SUBJECTS: The protocol included EEG, Brainstem Evoked Responses (BERs), Somatosensory evoked potentials (SEPs) and polysomnography. From 10 to 15 days post-coma (D10 to D15), EEG and clinical examinations were carried out every second day, then one day in four from 15 to 30 days post-coma (D15 to D30), and one day in seven from D30 to six months (M6). evoked potentials and polysomnography were recorded on D10-D15 or D30 in the second month (M2) and in M6. Of the five children, three were in anoxic coma and two in traumatic coma. All had extensive lesions and a glasgow coma scale (GCS) score of less than five. The results of the EEG, polysomnographic and EP recordings were compared to the clinical outcome. RESULTS AND CONCLUSION: In the three anoxic comas we observed BER abnormalities and the absence of SEP N20 associated with wide cortical lesions with brainstem extension. sleep recordings showed major alterations of the wake-sleep cycle without any improvement in M6. Abnormalities included loss of the normal REM-sleep pattern associated with alteration of NREM sleep and periods of increase in motor activity without EEG arousal. This sleep pattern appeared to be associated with involvement of the brainstem. In the two traumatic comas, alterations of the early cortical SEP responses were less severe and the BERs were normal. Some sleep spindles were observed as well as the persistence of sleep cycles in the first weeks post-coma. The combined use of EEG, EPs and polysomnography improved the outcome prediction in comparison with the use of just one modality. EPs and sleep recordings were far superior to clinical evaluation and to GCS in the appreciation of the functional status of comatose children. The reappearance of sleep patterns is considered to be of favorable prognosis for outcome of the coma state, as is the presence of sleep spindles in post-trauma coma. This study showed that EPs and sleep recordings help to further distinguish between patients with good or bad outcomes.
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ranking = 0.063001582700171
keywords = brain
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6/20. Water-deprivation headache: a new headache with two variants.

    OBJECTIVES: To describe a new type of headache induced by water deprivation. BACKGROUND: Two medical students experienced headache over the previous 7 (C.A.K.) and 9 (J.M.S.) years when deprived of drinking water. In a tutorial on headache, they mentioned this precipitant, not recognized by the tutor (J.N.B.) or described in the medical literature. dialysis and post-alcohol headaches are widely attributed to dehydration, but simple water deprivation has not been documented as a headache precipitant. methods: family members, colleagues, and acquaintances were asked whether they experienced a headache when deprived of fluids. If they had, information was obtained regarding the location and quality of the headache, whether activity or posture influenced the pain, and what amount of fluid and time was needed to relieve symptoms. RESULTS: Approximately 1 in 10 interrogated subjects experienced water-deprivation headache, aching in the majority and accentuated by head movement, bending down, or walking. The 34 subjects were divided into 2 groups according to the time taken to relieve the headache by drinking water: total relief within 30 minutes by drinking 200 to 1500 mL (mean, 500) occurred in 22 subjects, and within 1 to 3 hours by drinking 500 to 1000 mL (mean, 750) in 11 subjects; 1 subject required sleep in addition to fluid intake. Surprisingly, the internet revealed many references to water deprivation inducing headaches. CONCLUSIONS: Water-deprivation headache is common, recognized by the public, but not described in the medical literature. Here we delineate it as a primary headache, postulating that the pain arises from the meninges; that the brain is also involved is indicated by impaired concentration and irritability, although not studied in detail in this preliminary survey. We speculate that water deprivation may play a role in migraine, particularly in prolonging attacks. Further studies of serum osmolality could prove illuminating.
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ranking = 0.031500791350086
keywords = brain
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7/20. May the best friend be an enemy if not recognized early: hypernatremic dehydration due to breastfeeding.

    Hypernatremic dehydration is a serious condition in the newborn period. We present 5 infants with hypernatremic dehydration due to breastfeeding; one of them died because of brain edema during treatment.Hypernatremic dehydration in breast-fed newborns is secondary to insufficient lactation and all mothers should be encouraged about breastfeeding, taught the signs of successful breastfeeding, and the warning signs of dehydration. Here, we discuss hypernatremic dehydration in breastfeeding neonates, its causes and treatment.
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ranking = 0.031500791350086
keywords = brain
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8/20. Brain apparent diffusion coefficient decrease during correction of severe hypernatremic dehydration.

    We report on the brain diffusion MR imaging findings in a neonate with severe hypernatremic dehydration, which resulted in cerebral edema (osmotic edema) and in apparent diffusion coefficient decrease, despite a careful and slow rehydration. This report provides in vivo insight into nervous cell response to osmotic challenge.
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ranking = 0.031500791350086
keywords = brain
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9/20. A case report of hypodipsic hypernatremia syndrome associated with suprasellar tumor.

    A 20-year-old woman was diagnosed as hypodipsic hypernatremia syndrome in association with a variety of hypothalamic syndromes. Computed brain tomography disclosed a space occupying lesion over the region of the hypothalamus, lateral ventricle and paraventricles. Evaluation revealed defective osmoregulation of thirst and AVP release and hypothalamic syndrome. She showed no desire to drink at a plasma osmolality of above 320 mOsm/kg. Dissociation in the plasma vasopressin response to osmotic change and hemodynamic change was demonstrated in this patient. Treatment with a vasopressin analogue, desamino-D-arginine vasopressin and forced intake of water restored plasma osmolality and serum sodium levels to normal. In this case, selective osmoregulating dysfunction was presumably associated with pathologic conditions in or around the hypothalamus.
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ranking = 0.031500791350086
keywords = brain
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10/20. Cerebral oedema complicating diabetic ketoacidosis.

    Four children presented with cerebral oedema secondary to diabetic ketoacidosis, each of whom had a different clinical picture and time of onset of neurological deterioration. No single factor emerged as the cause of the cerebral oedema, but disturbances in brain water balance appeared to be already operative at the time of presentation with ketoacidosis. Irregularities in treatment may exacerbate these disturbances, leading to frank cerebral oedema. diagnosis of this dangerous complication of diabetic ketoacidosis depends on clinical awareness; the diagnosis may be confirmed by CT scan. Management remains empirical.
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ranking = 0.031500791350086
keywords = brain
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