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Journal of Modern Rehabilitation، جلد ۱۶، شماره ۲، صفحات ۶۴۲-۶۴۲
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| عنوان فارسی |
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| چکیده فارسی مقاله |
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| کلیدواژههای فارسی مقاله |
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| عنوان انگلیسی |
Gait Abnormalities in the Patient With Syndrome of Inappropriate Antidiuretic Hormone Secretion: A case studied with Gait Analysis. |
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| چکیده انگلیسی مقاله |
Background: Hyponatremia, defined as serum sodium concentration < 136 mEq/l, represents one of the most challenging clinical disorder both in geriatric and rehabilitative settings. It is associated with significant morbidity and mortality and often an accurate diagnostic protocol has to be performed in order to optimize the therapeutic approach. Hyponatremia can be often followed by neurological symptoms caused by cerebral oedema and can conduct to death if not appropriately treated. Unfortunately, even if we achive a rapid correct diagnosis we must be aware that a fast sodium correction could provoke an osmotic demyelination syndrome. In severe hyponatremia, patients frequently experience balance disorder and a high risk of falls
Case Report: We report the case of a female patient, followed at the Internal Medicine Unit of Hospital in Benevento (Italy). After an accurate diagnostic work-up a diagnosis of syndrome of inappropriate antidiuresis (SIAD) was made. Hyponatremia was initially treated with hypertonic saline infusion and then with fluid restriction. In consideration of the poor response to fluid restriction, treatment with tolvaptan was started. The patient experienced walking problems and was evaluated with an EMG computed Gait Analysis before and after that sodium level was normalized. During the days of hospitalization, headache and nausea, to which were added in increasing order of severe disorientation, mental confusion, sensory dullness, neurological focal deficits of the lower limbs and drowsiness. . Following gait analysis carried out with NA+ 127 mEq/l the patient highlighted neuromuscular instability with alteration of the time parameter (increased speed) and spatial postural deficit. Once corrected hyposodiemia at Na+ 135 mEq the patient showed a marked improvement in neuromuscular control with normalization of the temporal and spatial parameter of the step.
Clinical Rehabilitation Impact: Subjects potentially suffering from hyponatremia who have sudden disorders of consciousness and walking may be suffering from hyponatremia needing appropriate correction. The same are potentially at risk of syncope and need careful monitoring with ECG for QTC and PR study. The clinical manifestations of the patient with SIADH, beyond the cause that may have determined this clinical condition, are related to the severity of hyponatremia and the speed with which the sodium deficit is established. Generally neurological symptoms, due to cerebral edema caused by plasma hypotonicity, appear when the natremia becomes less than 120 mEq / l. Initially there may be headache and nausea, to which disorientation, mental confusion, dulling of the sensory, focal neurological deficits, convulsions can be added in increasing order of severity. With regard to the latter, when faced with a patient with a seizure of unknown origin, it is always necessary to think of hyponatremia as a possible trigger. Considering rehabilitation settings, it appears useful to recall that other cause such for example a chronic SSRI therapy can develop SIADH as well. The criteria for the diagnosis of SIADH in a patient with hypotonic hyponatremia remain those established by Bartter and Schwartz in 1967 : reduced plasma osmolarity (< 275 mOsm / kg); inappropriate urinary osmolarity (> 100 mOsm / kg in the presence of normal renal function), despite plasma hypotonicity; clinically euvolemic state; normal renal, adrenal and thyroid function; high urinary sodium elimination (> 30 mEql / l) in the presence of normal sodium and water intake. Our suggestions is so to and perform serial measurements of urine and serum osmolarity along with other laboratory parameters in order to prevent unbalance and falling. |
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| کلیدواژههای انگلیسی مقاله |
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| نویسندگان مقاله |
| Di Lorenzo Luigi
Department of NeuroScience, Rehabilitation Unit, AziendaOspedaliera DEA II SanPio Benevento, Italy.
| Falzarano Carmela
Department of NeuroScience, Rehabilitation Unit, AziendaOspedaliera DEA II SanPio Benevento, Italy.
| Cocozza Raimondo
Department of NeuroScience, Rehabilitation Unit, AziendaOspedaliera DEA II SanPio Benevento, Italy.
| Marano Paolo
Department of NeuroScience, Rehabilitation Unit, AziendaOspedaliera DEA II SanPio Benevento, Italy.
| Golini Vincenzo
PiedimonteMatese, Hospital, ASL Caserta, Italy.
| Ventre Itala
Department of Medicine, Internal Medicine Unit, FateeneFratelli Hospital Benevento, Italy.
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| نشانی اینترنتی |
https://jmr.tums.ac.ir/index.php/jmr/article/view/642 |
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