The Art and Science of Infusion Nursing

Michael L. Moritz, MD

Case Studies in Fluid and Electrolyte Therapy
ABSTRACT Disorders in serum sodium, hyponatremia and hypernatremia, are frequently encountered in both inpatient and outpatient settings. Many sodium disorders are iatrogenic, caused by inappropriate intravenous fluid management. The methods of prevention and treatment of serum disorders differ based on the underlying disease states. Nine cases are presented to illustrate different aspects of fluid management, with an emphasis on the prevention and treatment of disorders in serum sodium. Key concepts that are discussed are (1) when to use an isotonic fluid versus a hypotonic fluid, (2) when to restrict or liberalize maintenance intravenous fluids, (3) how to use 3% sodium chloride for the treatment of hyponatremic encephalopathy, (4) when to use desmospressin to prevent the overcorrection of chronic hyponatremia, and (5) strategies to treat different causes of hypernatremic dehydration in children. Key words: dehydration, demyelination, diabetes insipidus, encephalopathy, fluid therapy, hyponatremia, hypernatremia, saline
Author Affiliations: Department of Pediatrics, Children’s Hospital of Pittsburgh of UPMC, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Michael L. Moritz, MD, is an associate professor of pediatrics at the University of Pittsburgh School of Medicine and the clinical director of pediatric nephrology and medical director of pediatric dialysis at the Children’s Hospital of Pittsburgh of UPMC. Dr Moritz is a leading expert in the epidemiology and treatment of disorders of sodium and water homeostasis in children. The author of this article has no conflicts of interest to disclose. Corresponding Author: Michael L. Moritz, MD, Division of Nephrology, Children’s Hospital of Pittsburgh of UPMC, One Children’s Hospital Drive, 4401 Penn Ave, Pittsburgh, PA 15224 (moritzml@upmc.edu). DOI: 10.1097/NAN.0b013e318297bd7f

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lectrolyte disorders are frequently encountered in both inpatient and outpatient settings. The most common electrolyte disorders are those involving disorders in serum sodium, hypo-, and hypernatremia.1 Disorders in serum sodium are frequently iatrogenic, from improper fluid management; therefore, fluid management requires great care. The management of disorders in serum sodium can be quite complicated because therapy can vary significantly according to the etiology of the disorders. Nurses are on the front line of care for patients at risk for, or who have developed, a disorder in serum sodium. They therefore must be able to recognize and treat a disorder in serum sodium when it is occurring. This article will discuss 9 case studies related to fluid therapy and disorders in serum sodium. Three cases will discuss each of the following: (1) the adjustment of maintenance intravenous fluids (mIVFs) in the acutely ill patient, (2) the treatment of hyponatremia, and (3) the treatment of hypernatremic dehydration. The objective of these cases is to illustrate key concepts in the prevention and management of disorders in sodium and water homeostasis.

ADJUSTMENT OF mIVFs IN THE ACUTELY ILL PATIENT
Intravenous fluid (IVF) therapy is an integral component of the care of the acutely ill patient. The objective of mIVFs in the acutely ill patient is to maintain vascular perfusion while avoiding fluid overload and volume depletion, and to maintain normal serum biochemistries while avoiding hypo- or hypernatremia.2 A one-sizefits-all approach to mIVFs cannot be used for all acutely ill patients because there will be unique physiologic issues that could require adjustments in both the composition and quantity of fluids administered. In general,

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the maintenance need for fluids in an acutely ill hospitalized patient is approximately 1500 mL/m2/d, which correlates to 2.4 L/d in the average-sized adult.3 This quantity of fluids should be sufficient both to maintain vascular perfusion and to correct subclinical volume depletion if it is present. The following 3 cases will discuss how to adjust the rate and composition of mIVFs for patients with pneumonia but with different underlying disease states. The discussion will be restricted to the choice of sodium chloride (NaCl) composition in the IVF and will not discuss the potassium or dextrose concentration. Case #1. Pneumonia A 65-kg, 42-year-old female is traveling on business. She presents to the local emergency department (ED) with a 3-day history of fever, chills, and a productive cough with decreased oral intake. On physical examination, she appears ill, is tachypneic, and is mildly dehydrated. A chest X-ray reveals bilateral lower-lobe pneumonia. Her blood work is unremarkable. She is given a 0.9% NaCl (154 mEq/L) fluid bolus, feels improved, and urinates. She is not deemed well enough to return alone to her hotel room and is admitted for IVF therapy and intravenous (IV) antibiotics. Question: What would be the most appropriate rate and sodium composition of the mIVFs and why? Answer: An appropriate rate would be 100 mL/h with a sodium composition of 0.9% NaCl (154 mEq/L). Discussion This patient presented to the ED mildly dehydrated and was volume expanded with 0.9% NaCl. Much of the extracellular volume deficit has already been corrected, so a standard maintenance rate of IVF at 100 mL/h should be sufficient both to maintain good vascular perfusion and to correct any remaining subclinical volume depletion. If the patient is deemed to be volume depleted, it would be preferable to administer an additional fluid bolus of 0.9% NaCl rather than to increase the rate of mIVF. For a variety of reasons, the most appropriate composition of IVF would be 0.9% NaCl, which is an isotonic fluid. This patient likely has some subclinical extracellular volume depletion with some remaining extracellular volume deficit that will require replacement. An isotonic fluid, such as 0.9% NaCl, is a more effective extracellular volume expander than a more hypotonic fluid, such as 0.45% NaCl (77 mEq/L) or 0.2% NaCl (34 mEq/L), because sodium is restricted to the extracellular space. Administering 0.9% NaCl would maintain vascular perfusion better than a hypotonic fluid with a lower sodium concentration because 0.9% NaCl primarily remains in the extracellular space, whereas a more hypotonic fluid would distribute into

both intracellular and extracellular space. This patient has both hemodynamic and nonhemodynamic stimuli for antidiuretic hormone (ADH) production.4 ADH plays a critical role in renal concentration and dilution. ADH increases water permeability in the cortical collecting ducts, thus increasing urine concentration and impairing free water excretion. Pneumonia is a nonhemodynamic stimulus for ADH production. Patients with pneumonia frequently develop hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH) production. Therefore, hypotonic fluids should be avoided, and 0.9% NaCl should be administered when indicated.5,6 Key concept: The most appropriate mIVF for most acutely ill patients is 0.9% NaCl because it is an excellent volume expander and will help prevent the development of hyponatremia in the presence of ADH excess. Case #2. Congestive Heart Failure and Pneumonia An 80-kg, 72-year-old male with congestive heart failure (CHF) that is well controlled with a low-sodium diet presents to the local ED with a 3-day history of fever, chills, and a productive cough with decreased oral intake. On physical examination, he appears ill, is tachypneic, and is mildly dehydrated. A chest X-ray reveals bilateral lower lobe pneumonia. His blood work is unremarkable. He is given a 0.9% NaCl (154 mEq/L) fluid bolus, feels improved, and urinates. He is not deemed well enough for discharge and is admitted for IVF therapy and IV antibiotics. Question: What would be the most appropriate rate and sodium composition of the IVFs and why? Answer: An appropriate rate would be 60 mL/h with a sodium composition of 0.9% NaCl. Discussion CHF is an edematous state in which there is an impaired ability to excrete both salt and water. In general, IVFs are best avoided, and the patient should be managed with an oral sodium restriction. In this case, the patient is acutely ill and likely has some remaining subclinical volume depletion; therefore, he would benefit from IVF. The volume of fluids should be restricted in order to prevent fluid overload. An appropriate rate of mIVF would be 60% of standard mIVF, or 60 mL/h or 1.5 L/d.2 The patient should be monitored for the development of fluid overload, and mIVF should be discontinued as soon as possible. If signs of fluid overload develop, the mIVF should be either discontinued or restricted to a rate of 40 mL/h. The best choice of fluid for this patient would be 0.9% NaCl because there may still be some subclinical volume depletion. A more hypotonic fluid, such as 0.45% NaCl, could result in

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hyponatremia. Hyponatremia is a common finding in patients with CHF and is an independent risk factor for mortality. Therefore, the serum sodium should be monitored, and prophylactic measures should be taken to prevent hyponatremia from occurring.7 Key concept: Patients with edematous states such as CHF should have their mIVF restricted to 40% to 60% of the standard rate in order to prevent fluid overload. Case #3. Sickle Cell Disease and Pneumonia A 21-year-old, 70-kg African American male college student presents to the local ED with a 3-day history of fever, chills, and a productive cough with decreased oral intake, and he is experiencing acute pain. On physical examination, he appears ill, is tachypneic, and is mildly dehydrated. A chest X-ray reveals bilateral lower lobe pneumonia. His blood chemistries are unremarkable. He is given a 0.9% NaCl (154 mEq/L) fluid bolus and feels improved. He is admitted for IVF therapy, IV antibiotics, and pain control. Question: What would be the most appropriate rate and sodium composition of the IVFs and why? Answer: An appropriate rate would be 150 mL/h with a sodium composition of 0.45% NaCl. Discussion A variety of physiological issues must be taken into consideration in the fluid management of a patient with sickle cell disease. Acutely ill patients with sickle cell disease must be particularly well hydrated because volume depletion can promote red cell sickling. In addition, a renal concentrating defect is a universal finding in patients with sickle cell disease; therefore, patients with sickle cell disease will have higher fluid requirements due to increased obligatory urinary losses.8 This patient may also have subclinical volume depletion, so additional fluids may be required to correct the remaining volume deficit. For all of these reasons, the safest approach would be to increase the quantity of mIVF to approximately 50% above the standard maintenance rate, which in this case would be about 150 mL/h. The best choice of IVF would be 0.45% NaCl. Patients with sickle cell disease are isosthenuric, meaning that they can neither concentrate nor dilute their urine. The urine osmolality of patients with sickle cell disease is approximately the same as plasma osmolality, which is about 300 mOsm/kg. The urinary sodium composition of patients with sickle cell disease is approximately that of 0.45% NaCl; the remainder of the solute loss is primarily urea. The administration of 0.9% NaCl to a patient with a renal concentrating defect could result in hypernatremia. Hypernatremia could be particularly harmful for a patient with sickle cell disease because hypertonicity can promote red cell sickling. On the other hand,

research has shown that hypotonicity can actually prevent red cell sickling; therefore, patients with sickle cell disease should have their serum osmolality kept at the lower limits of normal.9 Patients with sickle cell disease are not immune to the development of hyponatremia, so significantly hypotonic fluids, such as 0.2% NaCl, should be avoided because they could result in hyponatremia with hyponatremic encephalopathy. Key concept: Patients with significant renal concentrating defects will require hypotonic mIVF at an increased rate.

THE MANAGEMENT OF HYPONATREMIA
Hyponatremia, defined as serum sodium < 135 mEq/L, is the most common electrolyte abnormality and occurs in as many as 30% of hospitalized patients. The most serious complication of hyponatremia is hyponatremic encephalopathy, which can result in death or permanent neurologic impairment if not recognized and treated promptly.10 A less common yet potentially serious complication of hyponatremia is cerebral demyelination, which results from the overcorrection of severe and chronic hyponatremia.11 When cerebral demyelination occurs, it can be either symptomatic or asymptomatic. The classic neurologic features are mutism, dysarthria, spastic quadriplegia, ataxia, and pseudobulbar palsy with a locked-in stare. Not all patients are at equal risk for the development of hyponatremic encephalopathy or cerebral demyelination, so one must be able to identify high-risk patients for either complication. It is now recognized that even mild hyponatremia can have neurologic manifestations12 and increases the risk of all-cause mortality in hospitalized patients.13 The next 3 cases will illustrate groups at high risk for the development of hyponatremic encephalopathy and of cerebral demyelination. Case #4: Acute Symptomatic Hyponatremia A 28-year-old female undergoes an appendectomy. Postoperatively she is placed on 0.45% NaCl at 120 mL/h. Twelve hours later she develops a headache, nausea, and vomiting and is treated with narcotics. Twenty-four hours later she is confused and combative and is taken for an emergent head computed tomography (CT). En route to the CT, she suffers generalized tonic-clonic seizures. Rapid bedside testing reveals a serum sodium level of 122 mEq/L. Question: How should this be managed? Answer: The patient should receive two to three 100-mL boluses of 3% NaCl (513 mEq/L) in rapid sequence until the patient stops seizing in order to acutely increase the serum sodium by 4 to 6 mEq/L.

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Discussion This case illustrates many important points about the pathogenesis of hyponatremic encephalopathy. Postoperative patients are at particularly high risk for the development of hyponatremia because they have numerous stimuli for ADH production, including pain, stress, nausea, vomiting, narcotics, and third spacing.14 Elevated ADH production alone, though, is not sufficient to develop hyponatremia. For hyponatremia to develop, there must be a source of free water. In this case, the patient received a significant amount of free water from excessive administration of hypotonic fluids, 0.45% NaCl. The most important step that can be taken to prevent postoperative hyponatremia is avoidance of hypotonic IVF and administration of isotonic fluids, 0.9% NaCl, when IVF is indicated.5,15,16 This patient developed classic symptoms of hyponatremic encephalopathy. The universal early symptoms of hyponatremic encephalopathy are headache, nausea, and vomiting. These early symptoms were overlooked in this patient. More advanced symptoms, such as confusion, combativeness, and finally seizures, then progressed. This patient’s sodium was not particularly low at 122 mEq/L. There are 2 reasons for this: (1) this is an acute hyponatremia with a rapid fall in serum sodium, so the brain has less time to adapt to the hyponatremia, and (2) menstruant females are at increased risk for developing hyponatremic encephalopathy because estrogen impairs brain adaptation to hyponatremia.14,17 Females are approximately 30 times more likely to die or suffer permanent neurologic impairment from hyponatremic encephalopathy than males, and menstruant females are approximately 25 times more likely than postmenopausal females.14 The definitive treatment for hyponatremic encephalopathy is the rapid administration of 3% NaCl (513 mEq/L) in order to quickly increase the serum sodium and decrease brain edema.18 The medical practitioner should administer 3% NaCl in 2 to 3 sequential boluses of 100 mL (2 mL/kg in children) in order to raise the serum sodium quickly by approximately 4 to 6 mEq/L. A small yet rapid rise in serum sodium is effective in reducing brain swelling yet will not result in neurologic injury from overcorrection. Key Concepts: 1. Postoperative patients and menstruant females are at particularly high risk for developing hyponatremic encephalopathy. 2. The treatment of hyponatremic encephalopathy is the administration of 3% NaCl (513 mEq/L) to acutely increase the serum sodium by approximately 5 mEq/L. Case #5. Thiazide-Induced Hyponatremia An 80-year-old, 42-kg widowed female presents to the ED after falling in her home. She appears lethargic and a bit confused but otherwise looks well. She is found to
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have a hip fracture. Biochemistries reveal a serum sodium of 105 mEq/L and potassium level of 3.2 mEq/L. Her past medical history reveals that she was started on a thiazide diuretic a few months ago for the treatment of hypertension. She is also on a selective serotonin reuptake inhibitor (SSRI) for depression following the loss of her husband and regularly takes nonsteroidal anti-inflammatory drugs (NSAIDs) for osteoarthritis. She has a poor appetite and eats little. Nephrology is consulted, and they recommend giving a 100-mL 3% NaCl fluid bolus, placing her on a fluid restriction, and stopping the thiazide diuretic. Blood work is repeated 4 hours later, and the serum sodium is now 115 mEq/L. The urine output is 500 mL/h, with a urine osmolality of 60 mOsm/kg. Question: What is the appropriate treatment now? Answer: Desmopressin should be administered to prevent overcorrection of hyponatremia. Discussion Severe hyponatremia is a well-described, yet poorly understood, complication from thiazide diuretics.19 Thiazide diuretics work by inhibiting the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule, and as such they do not antagonize the action of ADH and do not impair water reabsorption. Some patients have an idiosyncratic reaction to thiazides and develop severe hyponatremia. This patient was also on SSRIs and NSAIDs, both of which have an SIADH-like effect and can produce hyponatremia. Another risk factor for the patient was her poor appetite. Elderly females frequently consume a lowsolute diet, referred to as the “tea and toast” diet, which increases the risk of developing hyponatremia due to decreased renal solute load.20 Despite the development of profound hyponatremia, this patient was minimally symptomatic. The reasons for this are twofold: (1) this a chronic hyponatremia that likely occurred over weeks, and therefore the brain had time to adapt, and (2) the elderly are at less risk for hyponatremic encephalopathy as the brain atrophies with age, leaving more room in the cranium for brain expansion.10 This patient’s fall and subsequent fracture were likely a consequence of her hyponatremia. It is now known that mild chronic hyponatremia can produce subtle neurologic impairment and an unsteady gait, leading to falls and fractures in the elderly.12,21,22 In addition, chronic hyponatremia appears to stimulate bone demineralization and contribute to osteoporosis.23,24 A 100-mL bolus of 3% NaCl was given to acutely raise the serum sodium by a few milliequivalents in this patient because she was mildly symptomatic. This volume expansion was sufficient to suppress ADH, resulting in a free water diuresis and overcorrection of hyponatremia. This patient is at high risk for developing cerebral demyelination from overcorrection of hyponatremia for many reasons. She has many of the risk factors for developing cerebral demyelination
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including chronic (> 48 hours) and severe hyponatremia (115 mEq/L), thiazide diuretic use, hypokalemia, malnutrition, and the potential for overcorrection in the serum sodium by > 25 mEq/L in 48 hours. Preventing overcorrection of severe hyponatremia when a free water diuresis is occurring can be difficult.4 In this situation, the safest and most effective approach is to administer desmopressin.4 Desmopressin is a synthetic replacement for human arginine vasopressin, which increases renal water reabsorption. The administration of desmopressin will stop the free water diuresis, and the remainder of the serum sodium can be corrected slowly with fluid restriction. If desmopressin is used, care must be taken that the serum sodium is not inadvertently lowered. Desmopressin is available for IV, subcutaneous, oral, and intranasal administration. Key Concepts: 1. Patients with severe (< 115 mEq/L) and chronic (> 48 hours) hyponatremia are at risk for developing cerebral demyelination from overcorrection (> 25 mEq/L/48 h) of hyponatremia. 2. Desmopressin can be used to prevent an overcorrection of severe hyponatremia when a free water diuresis is occurring. Case #6. Hyponatremia in Central Nervous System Disease A 21-year-old male is admitted to the medical intensive care unit for what appears to be viral encephalitis. His serum sodium level upon admission is 142 mEq/L. He is placed on 0.9% NaCl at 100 mL/h. Eighteen hours later, his serum sodium is 134 mEq/L, urine sodium is 255 mEq/L, and urine osmolality is 900 mOsm/kg. Question: How should the IVFs be managed now? Answer: Health care personnel should start a 3% NaCl infusion and decrease the rate of the 0.9% NaCl infusion. Discussion Patients with central nervous system (CNS) disease are at particularly high risk for neurologic deterioration from hyponatremia.4 One feature of encephalitis is vasogenic cerebral edema, meaning that there is increased interstitial fluid in the brain. Hyponatremia would induce a component of cytotoxic cerebral edema, meaning that there would be an increase in brain cell water content from water moving into the brain. A patient with encephalitis may not be able to regulate brain cell volume as an otherwise healthy person can, and even a minor fall in serum sodium can contribute to neurologic deterioration.25,26 This patient experienced an acute fall in serum sodium even with 0.9% NaCl. Administration of 0.9%

NaCl may not always be effective in preventing hyponatremia, especially in patients with CNS disease. This patient could have either a severe case of SIADH or cerebral salt wasting (CSW).27 SIADH and CSW are similar conditions that can be nearly indistinguishable. In SIADH, fluid retention and subclinical volume expansion from excess ADH release is the primary event that leads to natriuresis as a compensatory mechanism. In CSW, an inappropriate natriuresis with volume depletion is the prime event, with ADH release and fluid retention being the compensatory mechanism. In either condition, a 3% NaCl infusion will have to be started in addition to the 0.9% NaCl in order to raise the serum sodium and preserve intravascular volume. The serum sodium should be raised to the high normal range (142145 mEq/L) to prevent cerebral edema. In all likelihood, a combination of 50 mL/h of 3% NaCl and 50 mL/h of 0.9% NaCl would have to be given to both raise and maintain the serum sodium. The 3% NaCl and 0.9% NaCl infusions must be titrated to maintain serum sodium. This patient should not be treated with fluid restriction because this could lead to volume depletion if the patient has CSW. Key concept: Patients with CNS disease are at particularly high risk for developing neurologic deterioration from hyponatremia, and the addition of a 3% NaCl infusion may be needed to maintain a normal serum sodium level.

MANAGEMENT OF HYPERNATREMIC DEHYDRATION
Hypernatremia, defined as serum sodium > 145 mEq/L, usually occurs in patients who have an impaired ability to consume fluids. Patients at high risk for developing hypernatremia are infants and small children, the elderly, and patients with profound neurological impairment.28 Patients who develop hypernatremia will usually have a source of excessive free water losses, either from diarrhea, a renal concentrating defect, or increased insensible losses. Free water losses alone are not a sufficient reason to develop hypernatremia, though, because hypernatremia should not develop in someone who has unrestricted access to fluids. Hypernatremia is a powerful stimulus for thirst. In any patient who develops hypernatremia, the causes for both decreased fluid intake and free water losses should be investigated.1,29 The treatment of hypernatremia is twofold: (1) to expand the extracellular volume to restore perfusion and (2) to provide sufficient free water to correct serum sodium. Extracellular volume expansion is the first priority, and correction of hypernatremia should only be undertaken once good perfusion has been established. The amount of volume expansion and free water requirements largely depend on the etiology of the

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hypernatremia and whether there are ongoing free water losses. The following 3 cases will illustrate how the management of hypernatremia can vary significantly on the basis of the underlying etiology. Case #7. Diarrheal Dehydration A 6-month-old, 7-kg male presents to the ED with a 3-day history of fever, vomiting, and diarrhea. The child is assessed to be 10% dehydrated on exam. Biochemistries reveal a serum sodium level of 156 mEq/L, total carbon dioxide of 12 mEq/L, blood urea nitrogen of 40 mg/dL, and creatinine of 0.8 mg/dL. Question: How should the fluids be managed? Answer: This child should receive 0.9% NaCl fluid boluses totaling 50 mL/kg in order to restore extracellular volume, followed by 0.45% NaCl at a rate of approximately 150% of standard maintenance volume to correct the remaining deficit and serum sodium. Discussion This case is a fairly typical presentation of a child with hypernatremic diarrheal dehydration. The hypernatremia developed primarily because the child was unable to take oral fluids. On exam the child appears 10% dehydrated, which means that the extracellular volume is reduced by 10% of the body weight. Therefore, this child’s volume deficit is approximately 100 mL/kg of body weight. The primary objective is to restore the extracellular volume. Therefore, this child should receive 0.9% NaCl fluid boluses totaling approximately 50 mL/kg, which would replace about half of the volume deficit acutely and restore vascular volume. Continuous fluids could then be started to correct both the remaining volume deficit and free water deficit. Standard maintenance fluids of a child of this size would be 100 mL/kg/d. The child’s remaining volume deficit is 50 mL/kg; therefore, an IVF rate equaling 150% of standard maintenance, or 44 mL/h or 1000 mL/d, should be sufficient to restore the volume deficit and maintain good hydration. The composition of fluids should be 0.45% NaCl. This would have sufficient sodium to replace the volume deficit and free water to correct the hypernatremia. This child does not have a very high serum sodium level, so a large amount of free water is not needed to correct the serum sodium, and an excessively hypotonic fluid should not be used. As a general rule of thumb, the free water deficit can be estimated by assuming that 4 mL/ kg of free water is required to decrease the serum sodium by 1 mEq/L. A reasonable rate of correction for this child’s serum sodium would be 10 mEq/L in the first 24 hours. The amount of free water needed to decrease serum sodium by 10 mEq/L in 24 hours would therefore be 280 mL (4 mL/kg × 7 kg × 10 mEq/L). This child would be getting 1000 mL/d of 0.45% NaCl, which would contain

500 mL of free water, an amount sufficient to correct the serum sodium. The actual rate of correction in serum sodium will likely differ significantly for these calculations, which are all based on crude estimates, and the renal response to fluid therapy as well as ongoing gastrointestinal fluid losses are not accounted for. These calculations provide a basis for initiating therapy, but further adjustments to the rate and composition of fluids will be necessary. Once this child is doing better, IVF should be tapered off and feeds should be resumed. Key concept: Volume expansion with 0.9% NaCl should precede correction of the free water deficit. Case #8: Hypernatremia in the Neurologically Impaired Patient A 7-year-old, 25-kg female with mental retardation and cerebral palsy who is fed via a gastrostomy tube presents to the ED with a 5-day history of fever, cough, and irritability. She is diagnosed with pneumonia but has otherwise been tolerating feeds and is not experiencing vomiting or diarrhea. Lab work reveals a serum sodium level of 184 mEq/L, blood urea nitrogen of 60 mg/dL, and creatinine of 1.4 mg/dL. A urine osmolality is 1200 mOsm/kg. On further investigation, she is found to have previous outpatient serum sodium levels in the range of 145 to 150 mEq/L. Question: How should this patient be managed? Answer: The patient should receive a fluid bolus of 20 to 40 mL/kg of 0.9% NaCl in order to establish good perfusion. The patient could then resume tube feeding and could be administered additional water through the gastrostomy tube at 50 mL/h. Discussion Patients with severe neurologic impairment are at high risk for developing hypernatremia because they do not have access to water. These patients are frequently chronically dehydrated because their nutrition is restricted in order to keep them from becoming obese. As a consequence of this, they may not get enough water to maintain good hydration. The patient has a history of mild hypernatremia, signifying that she has been chronically hypernatremic and underhydrated. With this acute illness, her insensible losses have increased, and she has become progressively more hypernatremic. The dehydration can be subclinical because fluid loss is primarily free water and has occurred over an extended period of time. As in the previous case, the primary objective is to restore vascular perfusion, so the patient should be given a fluid bolus of 0.9% NaCl. Because the fluid loss is primarily free water, fewer fluid boluses will be needed to volume expand the patient. IVFs may not be necessary because the child is tolerating the gastrostomy feeds. Oral feeds are the preferred method of correcting hypernatremia

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and are associated with the fewest complications. This child primarily needs increased fluid via the gastrostomy tube. The child’s feeding schedule should be reviewed and optimized, and additional free water should be administered via the gastrostomy tube at a rate of 50 mL/h, with the goal of lowering the serum sodium level by about 0.5 mEq/h. This child is at risk for developing seizures during the correction of hypernatremia because the serum sodium is extremely elevated and has been chronic in duration. The rate of serum sodium correction should be reduced once the serum sodium is < 155 mEq/L, and the child should be maintained mildly hypernatremic for a period of time before achieving a normal serum sodium, in order to prevent overcorrection of the serum sodium with the risk of cerebral edema.15 If seizures develop, the serum sodium could be raised a few milliequivalents by administering 3% NaCl. Key Concepts: 1. Patients with profound neurologic impairment are at risk for severe outpatient hypernatremia due to chronic underfeeding. 2. Hypernatremia is best treated with enteral feeds when tolerated. Case #9: Central Diabetes Insipidus A 7-year-old, 25-kg female with mental retardation and cerebral palsy who is fed via a gastrostomy tube presents to the ED with a 2-day history of fever, cough, and irritability. She is diagnosed with pneumonia but has otherwise been tolerating feeds and is not experiencing vomiting or diarrhea. Lab work reveals a serum sodium of 184 mEq/L, blood urea nitrogen of 60 mg/dL, and creatinine of 1.4 mg/dL. A urine osmolality is 200 mOsm/kg. Question: How should this patient be managed? Answer: This patient should be evaluated for central diabetes insipidus, and desmopressin should be started. Discussion This patient has a presentation that is similar to the child with hypernatremic dehydration in Case #8, but in this case the urine osmolality is dilute rather than concentrated, and the onset of hypernatremia took 2 days rather than 5 days. Hypernatremia is a potent stimulus for ADH production, so any patient with hypernatremia should have a near-maximally concentrated urine. This patient appears to have a renal concentrating defect. The etiology of the renal concentrating defect is not certain, but in all likelihood it is related to a partial central diabetes insipidus related to her underlying CNS disease. A significant increase in urine osmolality following the administration of desmopressin is confirmatory of central diabetes insipidus. The serum sodium

could then be corrected via the oral route once desmopressin is started. This patient’s serum sodium would have been higher and she would have appeared more ill if she had complete central diabetes insipidus with a urine osmolality ≤ 100 mOsm/kg. Key concept: A less than maximally concentrated urine in the context of hypernatremia is suggestive of diabetes insipidus.

SUMMARY
An understanding of fluid and electrolyte therapy is essential in caring for the acutely ill patient. Disorders in serum sodium, hypo- and hypernatremia, are common in both inpatient and outpatient settings, and the management differs significantly depending on the etiology. Hospitalized patients are at high risk for developing hyponatremia due to numerous stimuli for ADH production, and generally speaking, the administration of an isotonic fluid, such as 0.9% NaCl, is the most appropriate IVF to prevent the development of hyponatremia. A more hypotonic fluid, such as 0.45% NaCl, should be reserved for patients with either hypernatremia or ongoing free water losses. Patients who develop hospital-acquired hyponatremia are at risk for developing hyponatremic encephalopathy. Patients at highest risk for developing hyponatremic encephalopathy are postoperative patients, menstruant females, and patients with underlying CNS disease. Symptomatic hyponatremia should be treated with 3% NaCl with a goal of increasing the serum sodium by 5 mEq/L acutely. Hypernatremic dehydration is most often seen in children or the elderly and is usually associated with significant volume depletion. The goal of therapy is to initially restore extracellular volume by administering 0.9% NaCl. Hypotonic fluids can then be administered either intravenously or orally to lower the serum sodium once circulatory volume has been restored.
REFERENCES
1. Moritz ML, Ayus JC. Disorders of water metabolism in children: hyponatremia and hypernatremia. Pediatr Rev. 2002;23(11):371380. 2. Moritz ML, Ayus JC. Intravenous fluid management for the acutely ill child. Curr Opin Pediatr. 2011;23(2):186-193. 3. Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics. 1957;19:823-832. 4. Moritz ML, Ayus JC. New aspects in the pathogenesis, prevention, and treatment of hyponatremic encephalopathy in children. Pediatr Nephrol. 2010;25(7):1225-1238. 5. Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia: a case for using isotonic saline. Pediatrics. 2003;111(2):227-230. 6. Moritz ML, Ayus JC. Hospital-acquired hyponatremia: why are there still deaths? Pediatrics. 2004;113(5):1395-1396. 7. Gheorghiade M, Abraham WT, Albert NM, et al. Relationship between admission serum sodium concentration and clinical

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8. 9.

10.

11.

12.

13.

14.

15. 16.

17.

outcomes in patients hospitalized for heart failure: an analysis from the OPTIMIZE-HF registry. Eur Heart J. 2007;28:980-988. Ataga KI, Orringer EP. Renal abnormalities in sickle cell disease. Am J Hematol. 2000;63(4):205-211. Rosa RM, Bierer BE, Thomas R, et al. A study of induced hyponatremia in the prevention and treatment of sickle-cell crisis. N Engl J Med. 1980;303(20):1138-1143. Moritz ML, Ayus JC. The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Nephrol Dial Transplant. 2003;18(12):2486-2491. Ayus JC, Krothapalli RK, Arieff AI. Treatment of symptomatic hyponatremia and its relation to brain damage. A prospective study. N Engl J Med. 1987;317(19):1190-1195. Renneboog B, Musch W, Vandemergel X, Manto MU, Decaux G. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Am J Med. 2006;119(1):e1-e8. Wald R, Jaber BL, Price LL, Upadhyay A, Madias NE. Impact of hospital-associated hyponatremia on selected outcomes. Arch Intern Med. 2010;170(3):294-302. Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med. 1992; 117(11):891-897. Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children. Pediatr Nephrol. 2005;20(12):1687-1700. Moritz ML, Ayus JC. Hospital-acquired hyponatremia—why are hypotonic parenteral fluids still being used? Nat Clin Pract Nephrol. 2007;3(7):374-382. Arieff AI, Kozniewska E, Roberts TP, Vexler ZS, Ayus JC, Kucharczyk J. Age, gender, and vasopressin affect survival and brain adaptation in rats with metabolic encephalopathy. Am J Physiol. 1995;268(5pt2):R1143-R1152.

18. Moritz ML, Ayus JC. 100 cc 3% sodium chloride bolus: a novel treatment for hyponatremic encephalopathy. Metab Brain Dis. 2010;25(1):91-96. 19. Glover M, Clayton J. Thiazide-induced hyponatraemia: epidemiology and clues to pathogenesis. Cardiovasc Ther. 2012;30(5): e219-226. 20. Berl T. Impact of solute intake on urine flow and water excretion. J Am Soc Nephrol. 2008;19(6):1076-1078. 21. Ayus JC, Moritz ML. Bone disease as a new complication of hyponatremia: moving beyond brain injury. Clin J Am Soc Nephrol. 2010;5(2):167-168. 22. Gankam Kengne F, Andres C, Sattar L, Melot C, Decaux G. Mild hyponatremia and risk of fracture in the ambulatory elderly. QJM. 2008;101(7):583-588. 23. Kinsella S, Moran S, Sullivan MO, Molloy MG, Eustace JA. Hyponatremia independent of osteoporosis is associated with fracture occurrence. Clin J Am Soc Nephrol. 2010;5(2): 275-280. 24. Verbalis JG, Barsony J, Sugimura Y, et al. Hyponatremia-induced osteoporosis. J Bone Miner Res. 2010;25(3):554-563. 25. McJunkin JE, de los Reyes EC, Irazuzta JE, et al. La Crosse encephalitis in children. N Engl J Med. 2001;344(11):801-807. 26. Moritz ML, Ayus JC. La Crosse encephalitis in children. N Engl J Med. 2001;345(2):148-149. 27. Moritz ML. Syndrome of inappropriate antidiuresis and cerebral salt wasting syndrome: are they different and does it matter? Pediatr Nephrol. 2012;27(5):689-693. 28. Moritz ML, Ayus JC. The changing pattern of hypernatremia in hospitalized children. Pediatrics. 1999;104(3pt1):435-439. 29. Moritz ML, Ayus JC. Dysnatremias in the critical care setting. Contrib Nephrol. 2004;144:132-157.

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