Part 10.1: Life-Threatening Electrolyte Abnormalities IV-123 Water deficit(in liters)Plasma Na* concentration-140 X total body water Total body water is approximately 50%0 of lean body If the patient develops neurologic compromise, weight in men and 40% of lean body weight in women. For 3% saline IV immediately to correct(raise)the serum sodium example, if a 70-kg man had a serum Na level of 160 at a rate of l mEq/L per hour until neurologic symptoms are mEq/L, the estimated free water deficit would be controlled. Some experts recommend a faster rate of correc- 160-140 tion(ie, increase concentration 2 to 4 mEq/L per hour) when (0.5×70)=5L seizures are present. After neurologic symptoms are con- trolled, provide 3% saline I to correct(raise) the serum Once the free water deficit is calculated, administer fluid to sodium at a rate of 0.5 mEq/L per hour ower serum sodium at a rate of 0.5 to I mEq/h with a To determine the amount of sodium (eg, 3% saline decrease of no more than approximately 12 mEq/L in the first required to correct the deficit, calculate the total body sodium 24 hours and the remainder over the next 48 to 72 hours deficit. The following formula may be used Na* deficit=(desired [Na*]-current [Na DX0.6* xbody Hyponatremia is defined as a serum sodium concentration wt(kg)(use 0.6 for men and 0.5 for women). <130 to 135 mEq/L. It is caused by an excess of water Once the deficit is estimated determine the volume of 3% relative to sodium. Most cases of hyponatremia are caused by saline (513 mEq/ Na") necessary to correct the deficit reduced renal excretion of water with continued water intake (divide the deficit by 513 mEq/L). Plan to increase the or by loss of sodium in the urine Impairment of renal water sodium by I mEq/L per hour over 4 hours(or until neurologic may be caused by symptoms improve); then increase the sodium by 0.5 mEq/L per hour. To calculate this amount, use the amount you wish Use of thiazide diuretics to correct the sodium in an hour(eg, 0.5 mEq/L) and multiply Renal failure by 0.6(or 0.5 in women) and then multiply by the body ECF depletion(eg, vomiting with continued water intake weight: that will calculate the amount of sodium to administer Syndrome of inappropriate antidiuretic hormone(SIADh) that hour. Check serum sodium frequently and monitor secretion neurologic status. Edematous states(eg, congestive heart failure, cirrhosis with ascites) Magnesium (Mg) Hypothyroidism Magnesium is the fourth most common mineral and the Adrenal insufficiency second most abundant intracellular cation(after potassium) in Most cases of hyponatremia are associated with low serum the human body. Because extracellular magnesium is bound osmolality(so-called hypo-osmolar hyponatremia). The one to serum albumin, magnesium levels do not reliably reflect common exception to this is in uncontrolled diabetes, in total body magnesium stores. Magnesium is necessary for the which hyperglycemia leads to a hyperosmolar state despite a movement of sodium, potassium, and calcium into and out of serum sodium that is below normal(hyperosmolar cells, and magnesium plays an important role in stabilizing hyponatremia). excitable membranes. Low potassium in combination with Hyponatremia is usually asymptomatic unless it is acute or low magnesium is a risk factor for severe arrhythmias. Thus, evere(<120 mEq/L). An abrupt fall in serum sodium magnesium balance is closely tied to sodium, calcium, and produces a free water shift from the vascular to the interstitial potassium balance. space that can cause cerebral edema. In this case the patient may present with nausea, vomiting, headache, irritability Hypermagnesemia lethargy, seizures, coma, or even death. Hypermagnesemia is defined as a serum magnesium concen- tration >2.2 mEq/L(normal: 1.3 to 2.2 mEq/L). The most Treatment of Hyponatremia mon cause of hypermagnesemia is renal fail Treatment of hyponatremia involves administration of so- pre-eclampsia in pregnant women is treated with magnesium dium and elimination of intravascular free water, If SIAdh is administration, often titrated to maintain the serum magne- present, the treatment is restriction of fluid intake to 50%to sium near the maximum normal concentration, without com- 6% of estimated maintenance fluid requirement Correction plications of hypermagnesemia. of asymptomatic hyponatremia should be gradual: typically Neurologic symptoms of hypermagnesemia are muscular increase the Na* by 0.5 mEq/L per hour to a maximum weakness, paralysis, ataxia, drowsiness, and confusion. Mod- change of about 12 mEq/L in the first 24 hours. Rapid erate hypermagnesemia can produce vasodilation; severe orrection of hyponatremia can cause coma, which may be hypermagnesemia can produce hypotension. Extremely high associated with osmotic demyelination syndrome or central serum magnesium levels may produce a depressed level of pontine myelinolysis, lethal disorders thought to be caused by consciousness, bradycardia, cardiac arrhythmias, hypover apid fluid shifts into and out of brain tissue. 10. lation, and cardiorespiratory arrest. 5Water deficit (in liters) plasma Na concentration140 140  total body water Total body water is approximately 50% of lean body weight in men and 40% of lean body weight in women. For example, if a 70-kg man had a serum Na level of 160 mEq/L, the estimated free water deficit would be 160140 140 (0.570)5 L Once the free water deficit is calculated, administer fluid to lower serum sodium at a rate of 0.5 to 1 mEq/h with a decrease of no more than approximately 12 mEq/L in the first 24 hours and the remainder over the next 48 to 72 hours. Hyponatremia Hyponatremia is defined as a serum sodium concentration 130 to 135 mEq/L. It is caused by an excess of water relative to sodium. Most cases of hyponatremia are caused by reduced renal excretion of water with continued water intake or by loss of sodium in the urine. Impairment of renal water excretion may be caused by ● Use of thiazide diuretics ● Renal failure ● ECF depletion (eg, vomiting with continued water intake) ● Syndrome of inappropriate antidiuretic hormone (SIADH) secretion ● Edematous states (eg, congestive heart failure, cirrhosis with ascites) ● Hypothyroidism ● Adrenal insufficiency Most cases of hyponatremia are associated with low serum osmolality (so-called hypo-osmolar hyponatremia). The one common exception to this is in uncontrolled diabetes, in which hyperglycemia leads to a hyperosmolar state despite a serum sodium that is below normal (hyperosmolar hyponatremia). Hyponatremia is usually asymptomatic unless it is acute or severe (120 mEq/L). An abrupt fall in serum sodium produces a free water shift from the vascular to the interstitial space that can cause cerebral edema. In this case the patient may present with nausea, vomiting, headache, irritability, lethargy, seizures, coma, or even death. Treatment of Hyponatremia Treatment of hyponatremia involves administration of so￾dium and elimination of intravascular free water. If SIADH is present, the treatment is restriction of fluid intake to 50% to 66% of estimated maintenance fluid requirement. Correction of asymptomatic hyponatremia should be gradual: typically increase the Na by 0.5 mEq/L per hour to a maximum change of about 12 mEq/L in the first 24 hours. Rapid correction of hyponatremia can cause coma, which may be associated with osmotic demyelination syndrome or central pontine myelinolysis, lethal disorders thought to be caused by rapid fluid shifts into and out of brain tissue.10 –12 If the patient develops neurologic compromise, administer 3% saline IV immediately to correct (raise) the serum sodium at a rate of 1 mEq/L per hour until neurologic symptoms are controlled. Some experts recommend a faster rate of correc￾tion (ie, increase concentration 2 to 4 mEq/L per hour) when seizures are present. After neurologic symptoms are con￾trolled, provide 3% saline IV to correct (raise) the serum sodium at a rate of 0.5 mEq/L per hour. To determine the amount of sodium (eg, 3% saline) required to correct the deficit, calculate the total body sodium deficit. The following formula may be used: Na deficit(desired [Na]current [Na])0.6*body wt (kg) (*use 0.6 for men and 0.5 for women). Once the deficit is estimated, determine the volume of 3% saline (513 mEq/L Na) necessary to correct the deficit (divide the deficit by 513 mEq/L). Plan to increase the sodium by 1 mEq/L per hour over 4 hours (or until neurologic symptoms improve); then increase the sodium by 0.5 mEq/L per hour. To calculate this amount, use the amount you wish to correct the sodium in an hour (eg, 0.5 mEq/L) and multiply by 0.6 (or 0.5 in women) and then multiply by the body weight; that will calculate the amount of sodium to administer that hour. Check serum sodium frequently and monitor neurologic status. Magnesium (Mg

) Magnesium is the fourth most common mineral and the second most abundant intracellular cation (after potassium) in the human body. Because extracellular magnesium is bound to serum albumin, magnesium levels do not reliably reflect total body magnesium stores. Magnesium is necessary for the movement of sodium, potassium, and calcium into and out of cells, and magnesium plays an important role in stabilizing excitable membranes. Low potassium in combination with low magnesium is a risk factor for severe arrhythmias. Thus, magnesium balance is closely tied to sodium, calcium, and potassium balance. Hypermagnesemia Hypermagnesemia is defined as a serum magnesium concen￾tration
2.2 mEq/L (normal: 1.3 to 2.2 mEq/L). The most common cause of hypermagnesemia is renal failure. Note that pre-eclampsia in pregnant women is treated with magnesium administration, often titrated to maintain the serum magne￾sium near the maximum normal concentration, without com￾plications of hypermagnesemia. Neurologic symptoms of hypermagnesemia are muscular weakness, paralysis, ataxia, drowsiness, and confusion. Mod￾erate hypermagnesemia can produce vasodilation; severe hypermagnesemia can produce hypotension. Extremely high serum magnesium levels may produce a depressed level of consciousness, bradycardia, cardiac arrhythmias, hypoventi￾lation, and cardiorespiratory arrest.15 Part 10.1: Life-Threatening Electrolyte Abnormalities IV-123