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Læknablaðið - 15.10.2008, Blaðsíða 23

Læknablaðið - 15.10.2008, Blaðsíða 23
SJÚKRATILFE FRÆÐIGREINAR LLI O G YFIRLIT 16. Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med 1992; 117: 891-7. 17. Stems RH, Cappuccio JD, Silver SM, Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: a multicenter perspective. J Am Soc Nephrol 1994; 4:1522-30. 18. Stems RH, Thomas DJ, Herndon RM. Brain dehydration and neurologic deterioration after rapid correction of hyponatremia. Kidney Int 1989; 35: 69-75. 19. Verbalis JG, Martinez AJ. Neurological and neuropathological sequelae of correction of chronic hyponatremia. Kidney Int 1991; 39:1274-82. 20. Stems RH. The treatment of hyponatremia: first, do no harm. Am J Med 1990; 88: 557-60. 21. Melton JE, Patlak CS, Pettigrew KD, Cserr HF. Volume regulatory loss of Na, Cl, and K from rat brain during acute hyponatremia. Am J Physiol 1987; 252(4 Pt 2): F661-9. 22. Videen JS, Michaelis T, Pinto P, Ross BD. Human cerebral osmolytes during chronic hyponatremia. A proton magnetic resonance spectroscopy study. J Clin Invest 1995; 95: 788-93. 23. Verbalis JG, Gullans SR. Hyponatremia causes large sustained reductions in brain content of multiple organic osmolytes in rats. Brain Res 1991; 567: 274-82. 24. Lien YH, Shapiro JI, Chan L. Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis. J Clin Invest 1991; 88: 303-9. 25. McManus ML, Churchwell KB, Strange K. Regulation of cell volume in health and disease. N Engl J Med 1995; 333: 1260- 6. 26. Strange K. Regulation of solute and water balance and cell volume in the central nervous system. J Am Soc Nephrol 1992; 3:12-27. 27. Baker EA, Tian Y, Adler S, Verbalis JG. Blood-brain barrier disruption and complement activation in the brain following rapid correction of chronic hyponatremia. Exp Neurol 2000; 165: 221-30. 28. DeLuca GC, Nagy Z, Esiri MM, Davey P. Evidence for a role for apoptosis in central pontine myelinolysis. Acta Neuropathol 2002; 103: 590-8. 29. Ellis SJ. Severe hyponatraemia: complications and treatment. QJMed 1995; 88: 905-9. 30. Rosenbloom S, Buchholz D, Kumar AJ, Kaplan RA, Moses H, 3rd, Rosenbaum AE. Evolution of central pontine myelinolysis on CT. AJNR Am J Neuroradiol 1984; 5:110-2. 31. Thompson AJ, Brown MM, Swash M, Thakkar C, Scholtz C. Autopsy validation of MRI in central pontine myelinolysis. Neuroradiology 1988; 30:175-7. 32. Chua GC, Sitoh YY, Lim CC, Chua HC, Ng PY. MRI findings in osmotic myelinolysis. Clin Radiol 2002; 57: 800-6. 33. Kumar SR, Mone AP, Gray LC, Troost BT. Central pontine myelinolysis: delayed changes on neuroimaging. J Neuroimaging 2000; 10:169-72. 34. Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. AJNR Am J Neuroradiol 2004; 25: 210-3. 35. Arieff AI, Llach F, Massry SG. Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. Medicine (Baltimore) 1976; 55:121-9. 36. Berl T. Treating hyponatremia: damned if we do and damned if we don't. Kidney Int 1990; 37:1006-18. 37. Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. N Engl J Med 2005; 352:1550-6. 38. Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med 2000; 342:1581-9. 39. Decaux G, Soupart A. Treatment of symptomatic hyponatremia. Am J Med Sci 2003; 326: 25-30. 40. Decaux G, Unger J, Brimioulle S, Mockel J. Hyponatremia in the syndrome of inappropriate secretion of antidiuretic hormone. Rapid correction with urea, sodium chloride, and water restriction therapy. JAMA1982; 247: 471-4. 41. Van Reeth O, Decaux G. Rapid correction of hyponatraemia with urea may protect against brain damage in rats. Clin Sci (Lond) 1989; 77: 351-5. 42. Soupart A, Stenuit A, Perier O, Decaux G. Limits of brain tolerance to daily increments in serum sodium in chronically hyponatraemic rats treated with hypertonic saline or urea: advantages of urea. Clin Sci (Lond) 1991; 80: 77-84. 43. Trachtman H, Futterweit S, Tonidandel W, Gullans SR. The role of organic osmolytes in the cerebral cell volume regulatory response to acute and chronic renal failure. J Am Soc Nephrol 1993; 3:1913-9. 44 Soupart A, Silver S, Schrooeder B, Stems R, Decaux G. Rapid (24-hour) reaccumulation of brain organic osmolytes (particularly myo-inositol) in azotemic rats after correction of chronic hyponatremia. J Am Soc Nephrol 2002;13:1433-41. 45. Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intem Med 1997; 126: 57-62. 46. Oh MS, Kim HJ, Carroll HJ. Recommendations for treatment of symptomatic hyponatremia. Nephron 1995; 70:143-50. 47. Moritz ML, Ayus JC. The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Nephrol Dial Transplant 2003; 18: 2486-91. Sveinsson ÓÁ, Pálsson R Central and extrapontine myelinolysis following correction of extreme hyponatremia. Case report and review of the literature We report a case of a 43-year-old woman who developed osmotic demyelination syndrome following correction of extreme hyponatremia that was considered to be of chronic nature. The serum sodium level was 91 mmol/L on admission to hospital. It was decided to correct the serum sodium slowly with the goal that the rate of correction would be no more than 12 mmol/l per 24 hours. This was achieved during the first two days of treatment but during the third day the rise in serum sodium was 13 mmol/l. On the 11 th day of admission the patient had developed manifestations of pseudobulbar palsy and spastic quadriparesis. Magnetic resonance imaging study confirmed central and extrapontine myelonolysis. The patient received supportive therapy and eventually made full recovery. Current concepts in the pathophysiology of osmotic demyelination syndrome and the treatment of hyponatremia are reviewed. We recommend that the rate of correction of chronic hyponatremia should not exceed 8 mmol/l per 24 hours. Keywords Central pontine myelinolysis, cerebral adaptation, hyponatremia, osmotic demyelination syndrome. Correspondence Runólfur Pálsson, runolfur&landspitali.is > cc < D œ i «5 _l o z LU Barst: 6. mars 2008, - samþykkt til birtingar 1. september 2008 LÆKNAblaðið 2008/94 671
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