Long-term neurologic outcome in psychogenic water drinkers with severe symptomatic hyponatremia: the effect of rapid correction
Article Abstract:
Psychogenic or compulsive water drinking may lead to hyponatremia or decreased blood sodium, which may cause seizures, coma, and death. Although hyponatremia should be treated promptly, rapid elevation of low sodium levels to normal values may cause nerve complications, such as central pontine myelinolysis. This nerve disorder is characterized by the destruction of the myelin (fatty) sheath surrounding nerves, specifically in the pons, a region of the brain. Hyponatremia in psychogenic water drinkers is usually managed by administering saline, a physiological salt solution, and restricting fluids, or by restricting fluids alone. In patients who rapidly excrete water, restriction of fluids alone may rapidly increase the blood sodium levels. The safety of rapid treatment of hyponatremia in psychogenic water drinkers was assessed by reviewing the medical histories of 34 psychogenic water drinkers, recorded between 1977 and 1989. Thirteen of the patients with severe hyponatremia experienced a total of 27 seizures. These patients were treated within two hours after the seizure, by increasing the blood sodium level, which was about 111 millimoles per liter (mmol/L) in all seizure episodes, at a rate of about 1.65 mmol/liter per hour. In all but one seizure episode, hyponatremia was rapidly treated by elevating sodium levels to 120 to 130 mmol/L within 12 hours. Sodium levels were increased by about 15 mmol/L in 12 hours, 22 mmol/L in 24 hours, and 26 mmol/L in 48 hours, but levels did not exceed normal values. All patients recovered immediately after treatment and showed no signs of nerve complications after treatment or six years thereafter. The results demonstrate that, in psychogenic water drinkers, rapid treatment of hyponatremia by increasing sodium levels by 15 mmol/L in 12 hours or 26 mmol/L in 48 hours does not cause nerve complications. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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Reversal of a neurologic paraneoplastic syndrome with octreotide (Sandostatin) in a patient with glucagonoma
Article Abstract:
The case history is presented of a 69-year-old female patient who developed diabetes mellitus and, several years later, metastatic pancreatic cancer. The diabetes was controlled with diet alone for eight years, then with glibenclamide, and insulin therapy was added after nine years. The patient developed diarrhea, dementia, leg weakness, and, ultimately, globally decreased cognitive function, visual changes, and profound weakness of the lower limbs. Exploratory surgery revealed, besides the tumor, sheets of glucagon-producing cells in the liver (glucagon is a hormone that increases the concentration of glucose in the blood). Treatment with a somatostatin analogue (a drug with similar actions to somatostatin) led to marked improvement of the patient's symptoms, and she was able to read and even walk again. The patient's symptoms were consistent with the glucagonoma syndrome, caused by excess production of glucagon by a tumor. In another report, a patient with a glucagonoma and dementia, optic atrophy, loss of balance, and lower limb weakness was described. It appears that a specific neurologic paraneoplastic syndrome (a condition affecting the nervous system in patients with cancer that cannot be attributed to the tumor or the tissue in which it is located) can be associated with glucagonomas. A circulating factor (probably not glucagon itself) may have caused the neurologic symptoms; somatostatin may have inhibited the production or action of that factor. Such a factor may be involved in other paraneoplastic neurologic syndromes. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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The treatment of hyponatremia: first, do no harm
Article Abstract:
Studies show that rapid treatment of hyponatremia (low sodium level in the blood) or low blood sugar may lead to a rare nerve disorder called central pontine myelinolysis (CPM). This nerve disease is characterized by destruction of the myelin (fatty) sheaths surrounding nerves in the pons, a portion of the brain. Most patients with hyponatremia do not require rapid treatment, and sodium levels can be increased gradually by less than 12 milliEquivalents (mEq) per liter per day. Although, hyponatremia should not be treated too rapidly, it must be treated promptly. Emergency therapy should be reserved only for hyponatremia associated with seizures, coma, or for symptoms of water intoxication in patients receiving parenteral fluids, (which are administered continuously into the circulation). In these emergency cases, sodium levels must be increased rapidly to improve symptoms of hyponatremia and reduce water accumulation in the brain. When emergency treatment is required, sodium levels are increased at a rate of 1 to 2 mEq per liter per hour for two to three hours. The extent to which hyponatremia should be corrected has not been determined. Consequently, treatment of hyponatremia must always be approached with caution. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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