Aktuelle Neurologie 2001; 28(3): 103-113
DOI: 10.1055/s-2001-12520
ÜBERSICHT
Übersicht
© Georg Thieme Verlag Stuttgart · New York

Bedeutung von Störungen des Elektrolyt- und Wasserhaushaltes in der neurologischen Intensivmedizin

The Importance of Disturbed Electrolyte and Fluid Balance in Neurological Intensive-Care MedicineG.  F. Hamann
  • Neurologische Klinik, LMU Klinikum Großhadern, München
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
31. Dezember 2001 (online)

Zusammenfassung

Die Bedeutung von Störungen des Wasser- und Elektrolythaushaltes für die Neurologie und insbesondere die Intensivmedizin ergibt sich aus der Häufigkeit dieser Veränderungen und der Tatsache, dass diese Veränderungen sowohl Folge einer neurologischen Grunderkrankung sein können, als auch Ursache neurologischer Symptome. Es werden Grundlagen des Wasser- und Elektrolythaushaltes kurz rekapituliert. Besonderes Gewicht wird auf die Hyponatriämie gelegt. Mechanismen der hyponatriämischen Enzephalopathie und der zentralen Myelinolyse werden dargelegt. Die derzeitig gültigen Therapieempfehlungen der akuten Hyponatriämie führen zu einem protrahierten Natriumausgleich (< 0,5 mmol Serumnatrium/h, < 12 mmol/ 24 h und < 24 mmol/48 h). Chronische Hyponatriämien sollten noch langsamer und vorsichtiger ausgeglichen werden. Auch Hypernatriämien sind bedrohlich und können eine Myelinolyse und Enzephalopathie erzeugen, wobei v. a. der osmotische Stress (Wechsel von Hyponatriämie zu Hypernatriämie) wichtig ist. Weitere Elektrolytstörungen, wie Hypo- und Hyperkaliämie, Hypo- und Hyperkalziämie, Hypo- und Hypermagnesiämie und Hypo- und Hyperphosphatämien werden in ihren neurologischen Auswirkungen und Therapiemöglichkeiten besprochen.

The Importance of Disturbed Electrolyte and Fluid Balance in Neurological Intensive-Care Medicine

Fluid and electrolyte disturbances are frequently seen in neurological patients, and especially in neurological intensive-care patients. The importance of these changes is underlined by the possible link to a neurological disease. Neurological symptoms may also occur as a consequence of a fluid or electrolyte imbalance. The pathophysiological base of the understanding of the fluid and electrolyte system is summarised. The emphasis of this review is on the most frequent electrolyte disorder, namely, hyponatremia. The mechanisms of hyponatremic encephalopathy and central pontine myelinolysis are discussed. The actual therapeutic recommendations point to a slow normalisation of acute hyponatremia (< 0.5 mmol serum sodium/1h, < 12 mmol/24 h, < 24 mmol/48 h). Hyponatremia caused by chronical changes may need even less active treatment. Hypernatremia may also cause an encephalopathy and myelinolysis. This seems to be rather an effect of osmotic stress (especially in hypernatremia subsequent to hyponatremia). A brief overview concerning the following electrolyte disorders relevant in neurological intensive care management is given: hypo- and hyperkalemia, hypo- and hypercalciemia, hypo- and hypermagnesiemia, and hypo- and hyperphosphatemia.

Literatur

  • 1 Hamann G F. Hormonelle, autonome Veränderungen bei lebensbedrohlichen intrakraniellen Erkrankungen - klinische und biochemische Ergebnisse zur zerebralen Stressreaktion. Homburg; Habilitationsschrift, Med. Fakultät der Universität des Saarlandes 1993
  • 2 Childers M K, Rupright J, Jones P S, Merveille O. Assessment of neuroendocrine dysfunction following traumatic brain injury.  Brain Inj. 1998;  12 517-523
  • 3 Keller E, Reeker W. Elektrolythaushalt und Ernährung. In: Schwab S, Krieger D, Müllges W, Hamann G, Hacke W (Hrsg) Neurologische Intensivmedizin. Berlin, Heidelberg, New York, Tokyo; Springer Verlag 1999: 789-811
  • 4 Riggs J E. Neurologic manifestations of fluid and electrolyte disturbances.  Neurol Clin. 1989;  7 509-523
  • 5 Fanestil D D, Moore F D. Compartmentation of body water. In: Narins RG (ed) Clinical Disorders of Fluid and Electrolyte Metabolism. 5. ed. New York; Mac Graw-Hill 1995: 3-20
  • 6 Hamann G F. Störungen des Wasser- und Elektrolythaushaltes. In: Wallesch CW, Diener HC, Felgenhauer K, Wiegand F Sonderband Aktuelle Neurologie: Neurologie 1999. Stuttgart; Thieme 1999: A7-1-A7-8
  • 7 Yasumura S, Cohn S H. et al . Measurement of extracellular space by total body neutron activation.  Am J Physiol. 1983;  244 R36-R40
  • 8 Brown R G. Disorders of water and sodium balance.  Postgrad Med. 1993;  93 227-239
  • 9 Kirchner K A, Stein J H. Sodium metabolism. In: Narins RG (ed) Clinical Disorders of Fluid and Electrolyte Metabolism. 5. ed. New York; Mac Graw-Hill 1995: 45-80
  • 10 Morrison G, Singer I. Hyperosmolal states. In: Narins RG (ed) Clinical Disorders of Fluid and Electrolyte Metabolism. 5. ed. New York; Mac Graw-Hill 1995: 617-657
  • 11 Sterns R H, Ocdol H, Schrier. et al .Hyponatremia: pathophysiology, diagnosis, and therapy. In: Narins RG (ed) Clinical Disorders of Fluid and Electrolyte Metabolism. 5. ed. New York; Mac Graw-Hill 1995: 583-615
  • 12 Brown R G. Disorders of water and sodium balance.  Postgrad Med. 1993;  93 227-239
  • 13 Young G B, DeRubeis D A. Metabolic encephalopathies. In: Young GB, Ropper AH, Bolton CF Coma and Impaired Consciousness. New York; Mac Graw-Hill 1998: 307-383
  • 14 Fraser C L, Arieff A I. Metabolic encephalopathy associated with water, electrolyte, and acid-base disorders. In: Narins RG (ed) Clinical Disorders of Fluid and Electrolyte Metabolismm. 5. ed. New York; Mac Graw-Hill 1995: 1491-1547
  • 15 Clark E C, Thomas D, Baer J, Sterns R H. Depletion of glutathione from brain cells in hyponatremia.  Kidney Int. 1996;  49 470-476
  • 16 Arieff A I, Kozniewska E, Roberts T P. et al . Age, gender, and vasopressin affect survival and brain adaptation in rats with metabolic encephalopathy.  Am J Physiol. 1995;  268 R1143-R1152
  • 17 Wechsler Z S, Aus J C, Roberts T P. et al . Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.  J Clin Invest. 1994;  93 256-264
  • 18 Vexler Z S, Roberts T P, Kucharczyk J, Arieff A I. Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia.  Acta Neurochir Suppl (Wien ). 1994;  60 246-249
  • 19 Adams R D, Victor M, Mancall E L. Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients.  Arch Neurol Psychiatry. 1959;  81 154-172
  • 20 Sterns R H, Riggs J E, Schochet-SS J. Osmotic demyelination syndrome following correction of hyponatremia.  N Engl J Med. 1986;  314 1535-1542
  • 21 Illowsky B P, Laureno R. Encephalopathy and myelinolysis after rapid correction of hyponatraemia.  Brain. 1987;  110 855-867
  • 22 Laureno R. Central pontine myelinolysis following rapid correction of hyponatremia.  Ann Neurol. 1983;  13 232-242
  • 23 Laureno R, Karp B I. Myelinolysis after correction of hyponatremia.  Ann Intern Med. 1997;  126 57-62
  • 24 Ayus J C, Armstrong D L, Arieff A I. Effects of hypernatraemia in the central nervous system and its therapy in rats and rabbits.  J Physiol (Lond). 1996;  492 243-255
  • 25 Soupart A, Penninckx R, Namias B. et al . Brain myelinolysis following hypernatremia in rats.  J Neuropathol Exp Neurol. 1996;  55 106-113
  • 26 Laureno R, Mark A S. MRI in central pontine myelinolysis.  Neurology. 1995;  45 1025-1026
  • 27 Karp B I, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia.  Medicine (Baltimore). 1993;  72 359-373
  • 28 Diringer M N. Management of sodium abnormalities in patients with CNS disease.  Clin Neuropharmacol. 1992;  15 427-447
  • 29 Arieff A I, Ayus J C, Fraser C L. Hyponatremia and death or permanent brain damage in healthy children.  BMJ. 1992;  304 1218-1222
  • 30 Fraser C L, Kucharczyk J, Arieff A I. et al . Sex differences result in increased morbidity from hyponatremia in female rats.  Am J Physiol. 1989;  256 R880-R885
  • 31 Arieff A I, Ayus J C. Endometrial ablation complicated by fatal hyponatremic encephalopathy.  JAMA. 1993;  270 1230-1232
  • 32 Ayus J C, Arieff A I. Brain damage and postoperative hyponatremia: the role of gender.  Neurology. 1996;  46 323-328
  • 33 Ayus J C, Arieff A I. Chronic hyponatremic encephalopathy in postmenopausal women: association of therapies with morbidity and mortality.  JAMA. 1999;  281 2299-2304
  • 34 Silver S M, Schroeder B M, Bernstein P, Sterns R H. Brain adaptation to acute hyponatremia in young rats.  Am J Physiol. 1999;  276 R1595-R1599
  • 35 Arieff A I. Management of hyponatraemia.  BMJ. 1993;  307 305-308
  • 36 Arieff A I, Ayus J C. Pathogenesis of hyponatremic encephalopathy. Current concepts.  Chest. 1993;  103 607-610
  • 37 Soupart A, Decaux G. Therapeutic recommendations for management of severe hyponatremia: current concepts on pathogenesis and prevention of neurologic complications.  Clin Nephrol. 1996;  46 149-169
  • 38 Soupart A, Penninckx R, Stenuit A. et al . Reinduction of hyponatremia improves survival in rats with myelinolysis-related neurologic symptoms.  J Neuropathol Exp Neurol. 1996;  55 594-601
  • 39 Soupart A, Penninckx R, Stenuit A. et al . Treatment of chronic hyponatremia in rats by intravenous saline: comparison of rate versus magnitude of correction.  Kidney Int. 1992;  41 1662-1667
  • 40 Pfister H W. Zentrale pontine Myelinolyse. In: Schwab S, Krieger D, Müllges W, Hamann G, Hacke W (Hrsg) Neurologische Intensivmedizin. Berlin, Heidelberg, New York, Tokyo; Springer Verlag 1999: 661-665
  • 41 Meyer P, Jouanny P, Laurain M C. et al . Myelinolyse centropontine: a propos d'une forme paucisymptomatique.  Rev Med Interne. 1994;  15 282-286
  • 42 Hund E F, Böhrer H. et al .Disturbances of water and electrolyte balance. In: Hacke W (ed) Neurocritical Care. Heidelberg; Springer Verlag 1994: 917-927
  • 43 Sterns R H. The syndrome of inappropriate antidiuretic hormone secretion of unknown origin.  Am J Kidney Dis. 1999;  33 161-163
  • 44 Chan T Y. Drug-induced syndrome of inappropriate antidiuretic hormone secretion. Causes, diagnosis and management.  Drugs Aging. 1997;  11 27-44
  • 45 Hirshberg B, Ben Yehuda A. The syndrome of inappropriate antidiuretic hormone secretion in the elderly.  Am J Med. 1997;  103 270-273
  • 46 Gross P, Wehrle R, Bussemaker E. Hyponatremia: pathophysiology, differential diagnosis and new aspects of treatment.  Clin Nephrol. 1996;  46 273-276
  • 47 Naito A, Ohtake Y, Hasegaw H. et al . Pharmacological profile of VP-343, a novel selective vasopressin V2 receptor antagonist, in rats.  Biol Pharm Bull. 2000;  23 182-189
  • 48 Serradeil-Le G C. Nonpeptide antagonists for vasopressin receptors. Pharmacology of SR 121463A, a new potent and highly selective V2 receptor antagonist.  Adv Exp Med Biol. 1998;  449 427-438
  • 49 Peters J P, Welt L G. et al . A salt wasting syndrome associated with cerebral disease.  Trans Assoc Am Physicians. 1950;  63 57-64
  • 50 Harrigan M R. Cerebral salt wasting syndrome: a review.  Neurosurgery. 1996;  38 152-160
  • 51 Isotani E, Suzuki R, Tomita K. et al . Alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after subarachnoid hemorrhage.  Stroke. 1994;  25 2198-2203
  • 52 Damaraju S C, Rajshekhar V, Chandy M J. Validation study of a central venous pressure-based protocol for the management of neurosurgical patients with hyponatremia and natriuresis.  Neurosurgery. 1997;  40 312-316
  • 53 Uygun M A, Ozkal E, Acar O, Erongun U. Cerebral salt wasting syndrome.  Neurosurg Rev. 1996;  19 193-196
  • 54 Zafonte R D, Mann N R. Cerebral salt wasting syndrome in brain injury patients: a potential cause of hyponatremia.  Arch Phys Med Rehabil. 1997;  78 540-542
  • 55 Berendes E, Walter M, Cullen P. et al . Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage.  Lancet. 1997;  349 245-249
  • 56 Berendes E, Scherer R, Schuricht G. et al . Massive Natriurese und Polyurie nach dreimaliger kraniozervikaler Subarachnoidalblutung: Cerebral-Salt-Wasting-Syndrome?.  Anasthesiol Intensivmed Notfallmed Schmerzther. 1992;  27 445-448
  • 57 Berendes E, Walter M, Cullen P. et al . Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage.  Lancet. 1997;  349 245-249
  • 58 Kurokawa Y, Uede T, Ishiguro M. et al . Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm.  Surg Neurol. 1996;  46 500-507
  • 59 Gowrishankar M, Lin S H, Mallie J P. et al . Acute hyponatremia in the perioperative period: insights into its pathophysiology and recommendations for management.  Clin Nephrol. 1998;  50 352-360
  • 60 Gowrishankar M, Lin S H, Mallie J P. et al . Acute hyponatremia in the perioperative period: insights into its pathophysiology and recommendations for management.  Clin Nephrol. 1998;  50 352-360
  • 61 Laureno R, Karp B I. Pontine and extrapontine myelinolysis following rapid correction of hyponatraemia.  Lancet. 1988;  1 1439-1441
  • 62 Sterns R H. Severe hyponatremia: the case for conservative management.  Crit Care Med. 1992;  20 534-539
  • 63 Fraser C L, Arieff A I. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy.  Am J Med. 1997;  102 67-77
  • 64 Gowrishankar M, Chen C B, Cheema D S, Halperin M L. Prevention of acute hyponatremia by mannitol: an unanticipated mechanism.  Clin Nephrol. 1998;  50 295-300
  • 65 Sterns R H. Hypernatremia in the intensive care unit: instant quality-just add water.  Crit Care Med. 1999;  27 1041-1042
  • 66 Krieger S, Petros S. et al .Enzephalopathien bei erworbenen metabolischen Erkrankungen. In: Schwab S, Krieger D, Müllges W, Hamann G, Hacke W (Hrsg) Neurologische Intensivmedizin. Berlin, Heidelberg, New York, Tokyo; Springer Verlag 1999: 609-646
  • 67 Manoukian M A, Foote J A, Crapo L M. Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes.  Arch Intern Med. 1999;  159 601-606
  • 68 Freedman B I, Burkart J M. Endocrine crises. Hypokalemia.  Crit Care Clin. 1991;  7 143-153
  • 69 Williams M E. Endocrine crises. Hyperkalemia.  Crit Care Clin. 1991;  7 155-174
  • 70 Abe S, Tojo K, Ichida K. et al . A rare case of idiopathic hypoparathyroidism with varied neurological manifestations.  Intern Med. 1996;  35 129-134
  • 71 Davis K D, Attie M F. Management of severe hypercalcemia.  Crit Care Clin. 1991;  7 175-190
  • 72 Ferdinandus J, Pederson J A, Whang R. Hypermagnesemia as a cause of refractory hypotension, respiratory depression, and coma.  Arch Intern Med. 1981;  141 669-670
  • 73 Rizzo M A, Fisher M, Lock J P. Hypermagnesemic pseudocoma.  Arch Intern Med. 1993;  153 1130-1132
  • 74 Kingston M E, Al Siba'i M B, Skooge W C. Clinical manifestations of hypomagnesemia.  Crit Care Med. 1986;  14 950-954
  • 75 Brucato A, Bonati M, Gaspari F. et al . Tetany and rhabdomyolysis due to surreptitious furosemide-importance of magnesium supplementation.  J Toxicol Clin Toxicol. 1993;  31 341-344
  • 76 Al Tweigeri T, Magliocco A M, DeCoteau J F. Cortical blindness as a manifestation of hypomagnesemia secondary to cisplatin therapy: case report and review of literature.  Gynecol Oncol. 1999;  72 120-122
  • 77 Oechsner M, Pfeiffer G, Timmermann K. et al . Akute reversible Enzephalopathie mit Hirnödem und seriellen Anfällen bei Pseudohypoparathyroidismus.  Nervenarzt. 1996;  67 875-879
  • 78 Bugg N C, Jones J A. Hypophosphataemia. Pathophysiology, effects and management on the intensive care unit.  Anaesthesia. 1998;  53 895-902
  • 79 Zurkirchen M A, Misteli M, Conen D. Reversible neurologische Komplikationen bei chronischem Alkoholismus und Hypophosphatämie.  Schweiz Med Wochenschr. 1994;  124 1807-1812
  • 80 Cariem A K, Lemmer E R, Adams M G. et al . Severe hypophosphataemia in anorexia nervosa.  Postgrad Med J. 1994;  70 825-827
  • 81 Weber U, Huppe T, Niehaus L. CT and MRI in severe hypophosphataemia with central nervous system involvement.  Neuroradiology. 2000;  42 112-114
  • 82 Carroll J L, Kanter R K. Hypophosphatemia and Reye's syndrome.  Crit Care Med. 1985;  13 480-482
  • 83 Gadisseux P, Sica D A, Ward J D, Becker D P. Severe hypophosphataemia after head injury.  Neurosurgery. 1985;  17 35-40
  • 84 Riou B, Kalfon P, Arock M. et al . Cardiovascular consequences of severe hypophosphataemia in brain-dead patients.  Br J Anaesth. 1995;  74 424-429

Prof. Dr. med. Gerhard F. Hamann

Neurologische Klinik
Ludwig-Maximilians-Universität
Klinikum Großhadern

Marchioninistraße 15

81377 München

eMail: hamann@brain.nefo.med.uni-muenchen.de