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PDF Download Encephalopathies Caused by Electrolyte Disorders Martin A. Samuels, M.D.,1 and Julian Lawrence Seifter, M.D.2 ABSTRACT Some of the most common reasons for metabolic neurologic disturbances in the setting of a general hospital are frequently encountered electrolyte and related osmolality disorders. Hyperosmolality is usually related to hypernatremia and/or hyperglycemia. Identifying the cause and carefully calculating the water deficit is crucial to appropriate management. Hyponatremia may be hypertonic, isotonic, or hypotonic. When hypotonic, it may be hypervolemic, euvolemic, or hypovolemic in nature. Determining the precise nature of thehyponatremiaallowstheclinicianto focus the therapy appropriately. The rate of development of hyponatremia is crucial to safe and appropriate treatment. In acutely developing hyponatremia, hypertonic saline is required, whereas in slowly developing hyponatremia, water restriction and slow correction is required to avoid the syndrome of osmotic demyelination. Disorders of potassium metabolism are also common electrolyte disorders seen in the general hospital. Appropriate diagnosis and management of hyperkalemia and hypokalemia are also discussed. KEYWORDS: Hyperosmolarity, hypertonicity, hypernatremia, hyponatremia, hypokalemia, hyperkalemia HYPEROSMOLALITY AND Effective hyperosmolality is called hypertonicity HYPERTONICITY and indicates the effect of increased extracellular osmoles Normal serum, and therefore body fluid, osmolality is in to draw water from cells by osmosis. If hyperosmolality is the range of 275–295 mOsm/kg, but clinically signifi- due to hypernatremia, cells will initially shrink until cant deleterious effects are generally seen at levels greater adaptive mechanisms allow cell volume to recover. Sim- than 325 mOsm/kg. Osmolality may be measured di- ilarly, a diabetic with hyperglycemia will lose cell water rectly by freezing point depression or calculated as serum and develop a hypertonic syndrome. In contrast, osmolarity in mOsm/L, using the following formula, azotemia (i.e., an elevated blood urea nitrogen [BUN]) This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. which accounts for the millimolar quantities of major may cause hyperosmolality, but not hypertonicity be- serum solutes: cause the high cellular permeability of urea allows solute movement into cells so that cell water does not leave by 2Na ðmEq=LÞþglucoseðmg=dLÞ=18 osmosis. The difference between hyperglycemia (glucose þ BUNðmg=dLÞ=2:8 cannot enter cells) and azotemia is seen by the effect on 1Department of Neurology, 2Division of Nephrology, Brigham and Acute and Subacute Encephalopathies; Guest Editor, Martin A. Women’s Hospital, Harvard Medical School, Boston, Massachusetts. Samuels, M.D. Address for correspondence and reprint requests: Martin A. Semin Neurol 2011;31:135–138. Copyright # 2011 by Thieme Samuels, M.D., Chairman, Department of Neurology, Brigham and Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, Women’s Hospital, Professor of Neurology, Harvard Medical School, USA. Tel: +1(212) 584-4662. 75 Francis Street, Boston, MA 02115 (e-mail: msamuels@partners. DOI: http://dx.doi.org/10.1055/s-0031-1277983. org). ISSN 0271-8235. 135 136 SEMINARS IN NEUROLOGY/VOLUME 31, NUMBER 2 2011 the serum Na concentration. Water leaving cells in the 1. Calculate the normal total body water (NTBW) as: hyperglycemic patient lowers serum [Na], while [Na] is Body weight (in kg) Â 0.6 ¼ NTBW. not altered by a rise in BUN. Addition of extrinsic 2. Estimate the total body solute (TBS) (sodium þ osmoles such as mannitol, like glucose, causes hyper- potassium) as: NTBW Â 140 mEq/L ¼ TBS. Note osmolality, hypertonicity, loss of cell water, and hypo- that the 140 mEq/L is a normal serum [Na]. natremia. On the other hand, alcohols that quickly 3. Calculate the patient’s body water (PBW) as follows: permeate cells, like ethanol, ethylene glycol, isopropyl TBS/patients serum [Na] ¼ PBW. alcohol, and methanol act more like azotemia causing 4. Calculate the patient’s water deficit (PWD) as fol- hyperosmolality, but not hypertonicity or hyponatremia. lows: NTBW – PBW ¼ PWD. Because measured osmolality is increased with addition 5. Apart from deficit correction, estimate large ongoing of these extrinsic solutes, but Na, glucose, and urea are losses in the urine (osmotic diuresis or diabetes not, there is an osmolal gap defined as the difference insipidus) or sweat (fever) and replace. between measured and calculated osmolality. The osmo- lal gap should be < 10 mOsm/L. Replace the water losses so that the serum sodium Hypernatremia is defined as a serum sodium falls no faster than 2 mEq/L/h using water or 5% concentration of greater than 145 mEq/L. In other dextrose in water (D5W). In the hypotensive or vol- tissues, hypernatremia leads to loss of intracellular water ume-depleted patient, normal saline may first be needed leading to cell shrinkage. The nervous system is unique to correct blood pressure. In renal failure patients, in that it is capable of generating (or accumulating dialysis may be required. Insulin is administered, with from the extracellular fluid) solutes referred to as idio- frequent blood sugar testing, if there is hyperglycemia. genic osmoles, such as amino acids (glutamine, taurine, Intramuscular and subcutaneous insulin may be unpre- glutamate), polyols (myo-inositol), and methylamines dictably absorbed, particularly in hypovolemic patients (glycerophosphorylcholine, and choline) to minimize because of poor tissue perfusion. Rapid-acting insulin cell shrinkage, a process that is complete in 1 to 0.1 units/kg by rapid intravenous (IV) infusion followed 2 days. When hypernatremia is unusually severe (serum by 0.05 U/kg/h by continuous IV infusion is usually sodium over 160 mEq/L) these mechanisms fail, leading sufficient to reduce the blood sugar adequately and to encephalopathy. When hypernatremia occurs, anti- safely, but the mainstay of hyperglycemia correction in diuretic hormone (ADH) is released and thirst increases the hyperosmolar type II diabetic is volume expansion leading to renal retention of ingested water, thereby leading to urinary glucose clearance. Rapid reduction of lowering serum sodium toward normal. Hypernatremia extreme elevations of glucose should be avoided. is thus due to a defect in thirst or inability to access Diabetes insipidus (DI) is recognized as hyper- water, inadequate release or effect of ADH, loss of natremia (osm > 292) with simultaneous submaximal hypotonic fluid, or addition of concentrated sodium. concentration of the urine. A subcutaneous dose of Hyperglycemia is nearly always due to diabetes vasopressin and a serum ADH level will distinguish mellitus caused by inadequate insulin production (type I) central from nephrogenic DI. Treatments include dea- or insulin resistance (type II). In neurologic patients, this mino D-arginine vasopressin (DDAVP), an ADH ana- is often precipitated by stress, infection, or the thera- log used in central diabetes insipidus. Salt restriction and peutic use of glucocorticoids. Azotemia is due to renal even thiazide diuretics may help in nephrogenic diabetes failure or inadequate renal perfusion (prerenal azotemia). insipidus. Hyperosmolar agents, such as mannitol or glycerol, are often used in neurologic patients to treat increased intracranial pressure and may result in hyperosmolality. Hyponatremia Hyperosmolality usually produces a generalized Hyponatremia is defined as a serum sodium less than This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. encephalopathy without localizing or lateralizing fea- 135 mEq/L, but may be asymptomatic at levels less tures, but an underlying focal lesion (e.g., stroke, multi- than 125 mEq/L in chronic, slowly developing cases. ple sclerosis, neoplasm) could become symptomatic Hypotonicity is always associated with hyponatremia, under the metabolic stress of a hyperosmolar state. The but hyponatremia may be isotonic (e.g., as an artifact prognosis of the hyperosmolality itself is good, but the in hyperlipidemia, or hyperproteinemia); hypertonic long-term outlook depends upon the cause. For un- (e.g., hyperglycemia; mannitol); or hypotonic (impair- known reasons, hyperosmolality alone, particularly ment of free water excretion in low cardiac output when due to hyperglycemia, may lead to continuous states or the syndrome of inappropriate antidiuretic partial seizures, even when careful studies fail to uncover hormone (SIADH), or with an enormous free water any underlying lesion. These seizures generally respond load, as in psychogenic water drinking). Osmolality is promptly to lowering of the serum glucose. estimated using the formula above (see discussion of The treatment of hyperosmolality requires calcu- hyperosmolality) and may be measured in the clinical lation of apparent water losses. laboratory. The difference between the calculated and ENCEPHALOPATHIES CAUSED BY ELECTROLYTE DISORDERS/SAMUELS, SEIFTER 137 measured osmolality (the osmolal gap) should not (syndrome of inappropriate secretion of antidiuretic exceed 10 mOsm/L. Factitioushyponatremiaisdue hormone, psychogenic water drinking, hypothyroidism, to a laboratory artifact in diluted samples when the and resetting of the osmostat). The treatment depends solids of plasma are increased (e.g., hyperlipidemia, on the type of hyponatremia. In hypertonic hyponatre- severe hyperproteinemia as in myeloma). The undi- mia, one treats the underlying
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