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• W2076451147 abstract "A 31-year-old white woman was admitted to the hospital because of diffuse cramping abdominal pain. The pain was associated with nausea, vomiting, and an inability to eat or hold down fluids. One week prior to admission, the patient had rhinitis. The day of admission coincided with the patient's onset of menstrual bleeding. Her medical history revealed 30 hospital admissions over the previous six years for acute intermittent porphyria. During previous attacks of porphyria, the physical examination had shown diffuse abdominal tenderness and a diminution or absence of bowel sounds. A neurologist had documented that the patient could not extend the fingers of both hands completely. Otherwise, the physical examination had been unremarkable. Also, the patient's routine laboratory tests generally had been normal, except that she had elevated excretion of protoporphyrins and porphyrins multiple times, both during exacerbations of the porphyria as well as during remission. Neither cimetidene nor luteinizing hormone-releasing hormone (LHRH) improved the porphyria. Her exacerbations usually were treated with glucose infusions and meperidine. Otherwise, her medical, family, and social histories were unremarkable. Physical examination disclosed that she was in acute distress from severe pain. Her blood pressure was 130/100 mm Hg; pulse rate, 110 beats/min and regular; and temperature, 36.3°C. She was awake and fully oriented. Her mental status, cranial nerves, and deep tendon reflexes all were normal. Examination of the heart and lungs was normal. Her abdomen showed tenderness to deep palpation in the right upper quadrant and over the lower quadrants. The skin was normal and showed no obvious signs of dehydration. She had no ankle edema. Laboratory studies revealed: serum sodium concentration, 140 mmol/L; serum creatinine, 147 μmol/L (1.7 mg/dL); urea, 14.8 mmol/L; total porphyrin, 0.53 mg/L (normal, <0.3 mg/L); and delta-amino-levulinic acid, 317 μmol/L (normal, <220 μmol/L). Urinary porphobilinogen was 20.3 mg/24 h (normal, <1.9 h); and delta-amino-levulinic acid, 17.5 mg/24 h (normal, <6.1 mg/24 h). On admission the patient was given 3.6 L of 10% glucose/day intravenously (IV). These infusions were supplemented with 40 mmol of NaCl/L of infusate, but her pain failed to disappear under this regimen. Her nausea continued and she vomited three to five times per day. Gastroscopy was unremarkable. On the 3rd hospital day, the serum sodium concentration was 132 mmol/L. On the 5th hospital day, the vomiting intensified. She became somnolent and confused. The serum sodium concentration was 115 mmol/L. The creatinine concentration was 133 μmol/L (1.5 mg/dL), the urea concentration was 13.9 mmol/L, and the glucose concentration was 9.6 mmol/L. On the 7th hospital day, the patient vomited multiple times. Her regimen of glucose infusions supplemented by NaCl was continued at 3.6 L/day. She was agitated and confused, and she was periodically unable to speak. On the 8th hospital day, the serum sodium concentration had fallen to 97 mmol/L. The patient had a grand mal seizure. A cerebral computed tomography scan (CCT) demonstrated symmetrically small ventricles and “blurring of sulci,” findings suggestive of cerebral edema. An infusion of 10% NaCl corrected the severe hyponatremia from 98 mmol/L to 128 mmol/L within 36 hours Figure 1. On the 13th hospital day, a second CCT was unremarkable. After the rapid correction of the hyponatremia, the patient at first continued to be somnolent, unable to communicate, and apparently confused. She had a tremor of her hands. Her attempts at speaking showed a scanning rhythm. The consulting neurologist did not find any cranial nerve disturbances, difficulty swallowing, evidence of pseudobulbar palsy, or abnormalities of the deep tendon reflexes. The intravenous infusions of 10% glucose had been discontinued. No fluid restriction was ordered; the chart documented that daily fluid consumption ranged between 1 and 2 liters. The abdominal pain, the nausea, and the vomiting disappeared between days 10 and 14. From day 14 onwards, she began to communicate somewhat better. An electroencephalogram (EEG) obtained on the 16th hospital day showed generalized changes of moderate severity together with frontotemporal slowing. The patient was given intensive physical rehabilitation therapy. A neurologic consultation on day 35 disclosed that the patient was occasionally confused, although mostly awake and alert; she communicated frequently. She still exhibited occasional episodes of unfounded agitation. Neurologic consultation on the 60th hospital day revealed a reduced ability to concentrate. An EEG on the 65th hospital day showed only mild irregularities of the alpha rhythm. During the neurologic consultation on the 70th hospital day, the patient complained of difficulty memorizing and concentrating. However, she was generally judged to be stable and improved. On the 80th day of hospitalization, the patient was discharged home. The serum sodium concentration had ranged between 140 to 146 mmol/L from day 10 onwards. The discharge plasma creatinine concentration was 88 μmol/L (1.0 mg/dL); urea was 4.7 mmol/L. The urinary excretion rates of delta-amino-levulinic-acid and that of total porphyrin remained elevated. Prof. Dr. Peter Gross (Schwerpunkt Professor für Nephrologie, Medizinische Klinik III und Medizinische Poliklinik, Universitätsklinikum Carl Gustav Carus, Dresden, Germany): This patient's severe symptomatic hyponatremia was related to an attack of acute intermittent porphyria. Although porphyria, vomiting and abdominal pain all cause non-osmotic ADH release1Grandchamp B. Acute intermittent porphyria.Semin Liver Dis. 1998; 18: 17-24Crossref PubMed Scopus (62) Google Scholar, 2Gordon N. The acute porphyrias.Brain Dev. 1999; 21: 373-377Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 3Susa S. Daimon M. Morita Y. et al.Acute intermittent porphyria with central pontine myelinolysis and cortical laminar necrosis.Neuroradiology. 1999; 41: 835-839Crossref PubMed Scopus (40) Google Scholar, 4Suarez J.I. Cohen M.L. Larkin J. et al.Acute intermittent porphyria: Clinicopathologic correlation.Neurology. 1997; 48: 1678-1683Crossref PubMed Scopus (62) Google Scholar, the overriding stimulus of antidiuretic hormone (ADH) in this patient probably was plasma volume contraction. The hyponatremia was precipitated by voluminous amounts of glucose solution given to treat the porphyria. Her physicians failed to react to the worsening hyponatremia until she had diffuse cerebral edema and a grand mal seizure. The hyponatremia was corrected at a rate of 0.9 mmol/L/h. A computerized axial tomogram (CT) disclosed no evidence of (central pontine) myelinolysis. The patient had hyponatremic encephalopathy with permanent physical disability resulting from the cerebral edema. Severe hyponatremia is arbitrarily defined as a serum sodium concentration <115 mmol/L5Palm C. Gross P. V2-vasopressin receptor antagonists—mechanism of effect and clinical implications in hyponatraemia.Nephrol Dial Transplant. 1999; 14: 2559-2562Crossref PubMed Scopus (15) Google Scholar,6Gross P. Reimann D. Neidel J. et al.The treatment of severe hyponatremia.Kidney Int. 1998; 53: S6-S11Google Scholar. The designation “acute” refers to a duration of <36 to 48 hours. This condition commonly occurs after surgery7Arieff A.I. Llach F. Massry S.G. Neurological manifestations and morbidity of hyponatremia: Correlation with brain water and electrolytes.Medicine. 1976; 55: 121-129Crossref PubMed Scopus (433) Google Scholar. In that setting, previously asymptomatic patients who receive large amounts of hypotonic fluid (3 to 8 L/12 to 24 h) can develop neurologic signs of increasing severity Table 18Fraser C.L. Arieff A.I. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy.Am J Med. 1997; 102: 67-77https://doi.org/10.1016/s0002-9343(96)00274-4Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar. If the hyponatremia is progressive, obtundation, confusion, coma, generalized seizures, and respiratory arrest can occur8Fraser C.L. Arieff A.I. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy.Am J Med. 1997; 102: 67-77https://doi.org/10.1016/s0002-9343(96)00274-4Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar. Imaging studies usually demonstrate brain edema Figure 2. Autopsy studies have revealed: diffuse cerebral edema, edema of the brain stem, obliteration of sulci, and herniation of the brain stem into the foramen magnum9Arieff A.I. Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women.N Engl J Med. 1986; 314: 1529-1534Crossref PubMed Scopus (456) Google Scholar. This acute hyponatremic syndrome also can occur in psychotic patients with polydipsia, labor and delivery in the presence of high doses of oxytocin given with hypotonic fluids, child abuse involving forced water intake, patients receiving thiazides, and marathon runners8Fraser C.L. Arieff A.I. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy.Am J Med. 1997; 102: 67-77https://doi.org/10.1016/s0002-9343(96)00274-4Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, 9Arieff A.I. Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women.N Engl J Med. 1986; 314: 1529-1534Crossref PubMed Scopus (456) Google Scholar, 10Ayus J.C. Arieff A.I. Pathogenesis and prevention of hyponatremic encephalopathy.Endocrinol Metab Clin North Am. 1993; 22: 425-446PubMed Google Scholar, 11Cheng J.-C. Zikos D. Skopicki H.A. et al.Long-term neurological outcome in psychogenic water drinkers with severe symptomatic hyponatremia: The effect of rapid correction.Am J Med. 1990; 88: 561-566Abstract Full Text PDF PubMed Scopus (78) Google Scholar, 12Ashouri O.S. Severe diuretic-induced hyponatremia in the elderly. A series of eight patients.Arch Intern Med. 1986; 146: 1355-1357Crossref PubMed Scopus (68) Google Scholar, 13Keating J.P. Schears G.J. Dodge P.R. Oral water intoxication in infants.Am J Dis Children. 1991; 145: 985-990Crossref PubMed Scopus (91) Google Scholar, 14Ayus J.C. Varon J. Arieff A.I. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners.Ann Intern Med. 2000; 132: 711-714Crossref PubMed Scopus (247) Google Scholar. The consequences of acute hyponatremia are more serious in young (prepubertal) children and premenopausal women15Arieff A.I. Ayus J.C. Fraser C.L. Hyponatraemia and death or permanent brain damage in healthy children.Br Med J. 1992; 304: 1218-1222Crossref PubMed Scopus (308) Google Scholar, 16Arieff A.I. Ayus J.C. Endometrial ablation complicated by fatal hyponatremic encephalopathy.JAMA. 1993; 270: 1230-1232Crossref PubMed Scopus (151) Google Scholar, 17Ayus J.C. Wheeler J.M. Arieff A.I. Postoperative hyponatremic encephalopathy in menstruant women.Ann Intern Med. 1992; 117: 891-897Crossref PubMed Scopus (356) Google Scholar. A further aggravating factor is hypoxia; Ayus and Arieff postulated a vicious cycle between hyponatremic brain edema and hypoxia18Ayus J.C. Arieff A.I. Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure.Chest. 1995; 107: 517-521Crossref PubMed Scopus (105) Google Scholar,19Ayus J.C. Arieff A.I. Chronic hyponatremic encephalopathy in postmenopausal women. Association of therapies with morbidity and mortality.JAMA. 1999; 281: 2299-2304Crossref PubMed Scopus (171) Google Scholar. Progression to death or permanent brain damage is a common event in acute severe hyponatremia left untreated9Arieff A.I. Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women.N Engl J Med. 1986; 314: 1529-1534Crossref PubMed Scopus (456) Google Scholar,19Ayus J.C. Arieff A.I. Chronic hyponatremic encephalopathy in postmenopausal women. Association of therapies with morbidity and mortality.JAMA. 1999; 281: 2299-2304Crossref PubMed Scopus (171) Google Scholar. It is generally agreed that the acute hyponatremic syndrome should be treated rapidly. Ayus and coworkers proposed an hourly correction rate of 1.3 mmol/L, using 5% saline with furosemide while avoiding correction to normo/hypernatremia and an increase of the serum sodium concentration by more than 25 mmol/L in the first 48 hours20Ayus J.C. Krothapalli R.K. Arieff A.I. Treatment of symptomatic hyponatremia and its relation to brain damage. A prospective study.N Engl J Med. 1987; 317: 1190-1195Crossref PubMed Scopus (338) Google Scholar. According to the literature, this protocol is beneficial and does not cause brain lesions of its own21Sarnaik A.P. Meert K. Hackbarth R. Fleischmann L. Management of hyponatremic seizures in children with hypertonic saline: A safe and effective strategy.Crit Care Med. 1991; 19: 758-762Crossref PubMed Scopus (121) Google Scholar, 22Arieff A.I. Management of hyponatraemia.Br Med J. 1993; 307: 305-308Crossref PubMed Scopus (107) Google Scholar, 23Ayus J.C. Olivero J.J. Frommer J.P. Rapid correction of severe hyponatremia with intravenous hypertonic saline solution.Am J Med. 1982; 72: 43-47Abstract Full Text PDF PubMed Scopus (119) Google Scholar.Table 1Signs and symptoms of hyponatremiaMildAnorexia, nausea, vomiting, weakness, muscle cramps, headache, difficulty in concentrating, impaired memorySevereConfusion, hallucinations, obtundation, urinary and fecal incontinence, respiratory insufficiency, coma, decorticate or decerebrate posturing, generalized seizures, respiratory arrest Open table in a new tab Animal models have been used to gain further insight into cerebral edema in acute hyponatremia. Abrupt hypo-osmolality (hyponatremia) of the extracellular space causes an aquaporin-4 (AQP-4)-mediated osmotic water movement into brain cells and swelling. Manley and Verkman presented data at the Third International Conference on the Molecular Biology and Physiology of Water and Solute Transport (Göteborg, 2000) indicating that mice deficient in AQP-4 manifest reduced cerebral edema upon hypo-osmotic challenge24Manley G.T. Fujimara M. Ma T. et al.Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke.Nat Med. 2000; 6: 159-163Crossref PubMed Scopus (1206) Google Scholar. Compensation for swelling ensues rapidly, comprising decreased cerebral venous pooling and loss of cerebral spinal fluid from the brain8Fraser C.L. Arieff A.I. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy.Am J Med. 1997; 102: 67-77https://doi.org/10.1016/s0002-9343(96)00274-4Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar,10Ayus J.C. Arieff A.I. Pathogenesis and prevention of hyponatremic encephalopathy.Endocrinol Metab Clin North Am. 1993; 22: 425-446PubMed Google Scholar. The finding that young age appears to be a risk factor for brain edema might be explained by the relatively smaller cerebral spinal fluid spaces in young as compared to old brains. Within 5 minutes, cell volume-regulatory ions (Na+, K+, Cl-) are released from brain cells25Lang F. Busch G.L. Völkl H. The diversity of volume regulatory mechanisms.Cell Physiol Biochem. 1998; 8: 1-45Crossref PubMed Scopus (282) Google Scholar; this efflux can last as long as four hours. Stretch of cell membranes can activate relevant ion channels directly25Lang F. Busch G.L. Völkl H. The diversity of volume regulatory mechanisms.Cell Physiol Biochem. 1998; 8: 1-45Crossref PubMed Scopus (282) Google Scholar. Work by Fraser et al26Fraser 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-R885PubMed Google Scholar, Arieff et al27Arieff A.I. Kozniewska E. Roberts T.P.L. et al.Age, gender, and vasopressin affect survival and brain adaptation in rats with metabolic encephalopathy.Am J Physiol. 1995; 268: R1143-R1152PubMed Google Scholar, and Kozniewska et al28Kozniewska E. Roberts T.P.L. Vexler Z.S. et al.Hormonal dependence of the effects of metabolic encephalopathy on cerebral perfusion and oxygen utilization in the rat.Circ Res. 1995; 76: 551-558Crossref PubMed Scopus (24) Google Scholar suggests that the hormonal status in female rats alters the ionic composition of brain cells, which in turn can impair ionic volume regulation and exacerbate brain edema, thereby decreasing brain perfusion, and increasing mortality in female rats. An additional and essential decrease of brain volume can be accomplished within the first two to four days by reducing cellular osmolytes, substances that efficiently transfer osmoles from the intracellular compartment to the extracellular25Lang F. Busch G.L. Völkl H. The diversity of volume regulatory mechanisms.Cell Physiol Biochem. 1998; 8: 1-45Crossref PubMed Scopus (282) Google Scholar. The osmolytes of brain cells include polyalcohols such as sorbitol and inositol, amino acids, and methylamines26Fraser 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-R885PubMed Google Scholar. Recent work in patients established the existence of osmolyte regulation in the human brain. In 12 hyponatremic patients, proton magnetic resonance spectroscopy demonstrated decreases of cerebral osmolytes by as much as 50%29Videen J.S. Michaelis T. Pinto P. Ross B.D. Human cerebral osmolytes during chronic hyponatremia. A proton magnetic resonance spectroscopy study.J Clin Invest. 1995; 95: 788-793Crossref PubMed Scopus (175) Google Scholar. In short, an acute lowering of the serum osmolality will cause brain edema until early and late cell volume adaptations have been completed30Verbalis J.G. Adaptation to acute and chronic hyponatremia: Implications for symptomatology, diagnosis, and therapy.Semin Nephrol. 1998; 18: 3-19PubMed Google Scholar. Because of the rigid skull, cerebral edema can lead to increased intracranial pressure, decreased brain perfusion, and threatened respiratory insufficiency, and can result in herniation of the brain stem into the foramen magnum31Vexler Z.S. Ayus J.C. Roberts T.P.L. et al.Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.J Clin Invest. 1994; 93: 256-264Crossref PubMed Scopus (82) Google Scholar, permanent brain damage, or death20Ayus J.C. Krothapalli R.K. Arieff A.I. Treatment of symptomatic hyponatremia and its relation to brain damage. A prospective study.N Engl J Med. 1987; 317: 1190-1195Crossref PubMed Scopus (338) Google Scholar. Rapid correction of an acute hyponatremia is appropriate to avoid hyponatremic brain damage. Rapid correction will restore brain cell volume to normal32Ayus J.C. Krothapalli K. Armstrong D.L. Norton J. Symptomatic hyponatremia in rats: Effect of treatment on mortality and brain lesions.Am J Physiol. 1989; 257: F18-F22PubMed Google Scholar. In contrast, when chronic hyponatremia is corrected, intracellular ions and osmolytes must re-accumulate to return cell volume to normal. Occasionally, severe hyponatremia is present in a patient for months or even years33Gross P. Wichmann A. Walb D. et al.Inappropriate secretion of antidiuretic hormone, polydipsia and hypothalamic calcifications.Klin Wochenschr. 1989; 67: 730-733Crossref PubMed Scopus (1) Google Scholar. Those patients are usually oligosymptomatic or asymptomatic. It is not clear that such patients should be treated. Much more commonly, patients will have had chronic, severe hyponatremia for only a few days, and it will have been associated with drowsiness, nausea, poor memory, or even disorientation34Sterns R.H. Riggs J.E. Schochet S.S. Osmotic demyelination syndrome following correction of hyponatremia.N Engl J Med. 1986; 314: 1535-1542Crossref PubMed Scopus (579) Google Scholar Table 1. The setting generally is thiazide-induced hypokalemic hyponatremia; the syndrome of inappropriate antidiuretic hormone secretion (SIADH); liver cirrhosis, alcoholism, and malnourishment; advanced, diuretic-treated cardiac failure; or protracted vomiting or diarrhea35Sterns R.H. Severe symptomatic hyponatremia: Treatment and outcome. A study of 64 cases.Ann Intern Med. 1987; 107: 656-664Crossref PubMed Scopus (246) Google Scholar. Physicians usually elect to treat patients with such chronic severe hyponatremia. For instance, it can be important to know whether a patient's mental changes can be improved by correcting hyponatremia. The physician might be concerned about a worsening of hyponatremia; or the need might exist for large-volume infusions (hyperalimentation). Still, the treatment of chronic severe hyponatremia is controversial because of the alleged possibility of inducing cerebral myelinolysis. In a retrospective study two decades ago, Norenberg and colleagues described autopsy results from 12 patients who had undergone “rapid” correction (20 mmol/L over 1 to 3 days, occasionally reaching hypernatremia)36Norenberg M.D. Leslie K.O. Robertson A.S. Association between rise in serum sodium and central pontine myelinolysis.Ann Neurol. 1982; 11: 128-135Crossref PubMed Scopus (257) Google Scholar. The correction was followed in 3 to 10 days by central pontine myelinolysis (CPM). Most of the 12 patients also had underlying chronic alcoholism, liver disease (hepatitis, cirrhosis), or both, and these are independent risk factors for CPM. Additional risk factors for myelinolysis include malnutrition, thiazide therapy, hypokalemia, and hyponatremia <105 mmol/L37Tomlinson B.E. Pierides A.M. Bradley W.G. Central pontine myelinolysis.Q J Med. 1976; 179: 373-386Google Scholar, 38Laubenberger J. Schneider B. Ansorge O. et al.Central pontine myelinolysis: clinical presentation and radiologic findings.Eur Radiol. 1996; 6: 177-183Crossref PubMed Scopus (45) Google Scholar, 39Estol C.J. Faris A.A. Martinez A.J. Ahdab-Barmada M. Central pontine myelinolysis after liver transplantation.Neurology. 1989; 39: 493-498Crossref PubMed Google Scholar. Clinical consequences of CPM in these 12 patients included a sudden disturbance in mental status, flaccid quadriparesis, abnormal conjugate eye movements, and pseudobulbar palsy36Norenberg M.D. Leslie K.O. Robertson A.S. Association between rise in serum sodium and central pontine myelinolysis.Ann Neurol. 1982; 11: 128-135Crossref PubMed Scopus (257) Google Scholar. When Norenberg et al compared the 12 index patients with 9 others in whom the hyponatremia had been corrected more slowly Figure 3, and in whom attainment of normo/hypernatremia had been avoided, they found that none of the 9 had CPM, as shown either by computerized tomography or autopsy. The authors concluded that CPM can be caused by a too rapid or excessive rise in serum sodium from a hyponatremic baseline. The Norenberg study is open to criticism, however, because the 12 index patients had a much lower baseline hyponatremia than did the 9 so-called controls (106 mmol/L vs. 118 mmol/L). Several additional reports have since appeared indicating that myelinolysis occurring after rapid correction of chronic hyponatremia can be pontine or extrapontine34Sterns R.H. Riggs J.E. Schochet S.S. Osmotic demyelination syndrome following correction of hyponatremia.N Engl J Med. 1986; 314: 1535-1542Crossref PubMed Scopus (579) Google Scholar, 35Sterns R.H. Severe symptomatic hyponatremia: Treatment and outcome. A study of 64 cases.Ann Intern Med. 1987; 107: 656-664Crossref PubMed Scopus (246) Google Scholar, 38Laubenberger J. Schneider B. Ansorge O. et al.Central pontine myelinolysis: clinical presentation and radiologic findings.Eur Radiol. 1996; 6: 177-183Crossref PubMed Scopus (45) Google Scholar, 40Sterns R.H. Cappucio J.D. Silver S.M. Cohen E.P. Neurologic sequelae after treatment of severe hyponatremia: A multicenter perspective.J Am Soc Nephrol. 1994; 4: 1522-1530PubMed Google Scholar, 41Brunner J.E. Redmont J.M. Haggar A.M. et al.Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: A prospective magnetic resonance imaging study.Ann Neurol. 1990; 27: 61-66Crossref PubMed Scopus (152) Google Scholar, 42Harris C.P. Townsend J.J. Baringer J.R. Symptomatic hyponatraemia: Can myelinolysis be prevented by treatment?.J Neurol Neurosurg Psychiatry. 1993; 56: 626-632Crossref PubMed Scopus (22) Google Scholar. In one publication, 8 patients with chronic, severe, and symptomatic hyponatremia had been treated at a correction rate of 0.5 to 1.2 mmol/L/h (“rapid correction”); all developed a syndrome compatible with CPM34Sterns R.H. Riggs J.E. Schochet S.S. Osmotic demyelination syndrome following correction of hyponatremia.N Engl J Med. 1986; 314: 1535-1542Crossref PubMed Scopus (579) Google Scholar. Of 55 comparable patients undergoing correction at less than 0.5 mmol/L/h, however, none had any neurologic sequelae34Sterns R.H. Riggs J.E. Schochet S.S. Osmotic demyelination syndrome following correction of hyponatremia.N Engl J Med. 1986; 314: 1535-1542Crossref PubMed Scopus (579) Google Scholar. However, the study was retrospective. Furthermore, 7 of the 8 patients with CPM had thiazide-induced hyponatremia with hypokalemia. Therefore, hypokalemia could have been a precipitating co-factor of CPM. Other potential problems with the interpretation of this study were that 2 of the 8 patients with CPM were alcoholics; the hyponatremia in the 8 patients with CPM apparently was more severe than that in the 55 uncomplicated patients; and proof of demyelination [CT, magnetic resonance tomography (MRT), autopsy] was missing in 4 of 8 patients with clinically diagnosed CPM. In another study, Sterns et al surveyed the total experience with extreme hyponatremia (<105 mmol/L) of 4100 U.S. nephrologists40Sterns R.H. Cappucio J.D. Silver S.M. Cohen E.P. Neurologic sequelae after treatment of severe hyponatremia: A multicenter perspective.J Am Soc Nephrol. 1994; 4: 1522-1530PubMed Google Scholar. Of the 56 patients reported, 14 had neurologic sequelae, potentially from myelinolysis. This report indicates that severe hyponatremia is rare but that myelinolysis can occur in as many as 25% of such patients. Most38Laubenberger J. Schneider B. Ansorge O. et al.Central pontine myelinolysis: clinical presentation and radiologic findings.Eur Radiol. 1996; 6: 177-183Crossref PubMed Scopus (45) Google Scholar, 40Sterns R.H. Cappucio J.D. Silver S.M. Cohen E.P. Neurologic sequelae after treatment of severe hyponatremia: A multicenter perspective.J Am Soc Nephrol. 1994; 4: 1522-1530PubMed Google Scholar, 41Brunner J.E. Redmont J.M. Haggar A.M. et al.Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: A prospective magnetic resonance imaging study.Ann Neurol. 1990; 27: 61-66Crossref PubMed Scopus (152) Google Scholar, 42Harris C.P. Townsend J.J. Baringer J.R. Symptomatic hyponatraemia: Can myelinolysis be prevented by treatment?.J Neurol Neurosurg Psychiatry. 1993; 56: 626-632Crossref PubMed Scopus (22) Google Scholar but not all recent publications (abstract; Arieff, Ayus, J Am Soc Nephrol 10:19A, 1999) have indicated that cerebral demyelination is a complication of overly rapid correction of chronic hyponatremia. Like cerebral edema, demyelination also has been probed in animal experiments. Verbalis and Martinez studied a noninvasive rat model of hyponatremia (111 to 114 mmol/L; duration, 2 to 3 weeks) that is based on administering DDAVP, a pure V2-vasopressin agonist (AVP in humans is a V1/V2 agonist)43Verbalis J.G. Martinez A.J. Determinants of brain myelinolysis following correction of chronic hyponatremia in rats.in: Jard S. Jamison R. Vasopressin. vol 208. Colloque INSERM/John Libbey Eurotext Ltd, Paris and London1991: 539-547Google Scholar. Correction of the hyponatremia from 118 mmol/L to 138 mmol/L within 48 hours by water restriction alone did not cause myelinolysis. Correction from 111 mmol/L to 143 mmol/L within 8 hours by infusions of hypertonic saline (or by using a vasopressin antagonist) was followed by focal or diffuse demyelination in 90% of the rats. When the normonatremia was reversed rapidly to a serum sodium level of 111 mmol/L, only 45% of rats developed demyelination. Similar findings also have been observed by other laboratories44Lien Y.-H. Role of organic osmolytes in myelinolysis.J Clin Invest. 1995; 95: 1579-1586Crossref PubMed Scopus (87) Google Scholar. The potential pathways by which such rapid correction of chronic hyponatremia cause myelinolysis have been studied. Attention has been given to organic osmolytes and their role in “osmotic reloading” of brain cells. Thurston et al studied chronic (4-day) hyponatremia (91 mmol/L) in young mice45Thurston J.H. Hauhart R.E. Nelson J.S. Adaptive decreases in amino acids (taurine in particular), creatinine, and electrolytes prevent cerebral edema in chronically hyponatremic mice: rapid correction (experimental model of central pontine myelinolysis) causes dehydration and shrinkage of brain.Metab Brain Dis. 1987; 2: 223-241Crossref PubMed Scopus (69) Google Scholar. When the hyponatremia was corrected to 134 mmol/L by hypertonic saline within 9 hours, the mice manifested dehydration and shrinkage of the brain, normal brain levels of sodium and potassium, but amino acid content below normal. Lien et al demonstrated that in the course of rapid correction of chronic hyponatremia, re-accumulation of sodium and chloride caused elevations of these ions above the normal range in brain cells (“overshoot”)46Lien Y.-H. Shapiro F.I. Chan L. Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia.J Clin Invest. 1991; 88: 303-309Crossref PubMed Scopus (230) Google Schol" @default.
• W2076451147 created "2016-06-24" @default.
• W2076451147 creator A5026662681 @default.
• W2076451147 date "2001-12-01" @default.
• W2076451147 modified "2023-09-25" @default.
• W2076451147 title "Treatment of severe hyponatremia" @default.
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