Fluids and Electrolyte Management
Authors
Rasha D. Sawaya, MD, Assistant Professor of Pediatrics and Emergency Medicine, George Washington University Medical Center, Washington DC; Attending Physician, Children’s National Health Systems, Washington, DC
Bahareh Ravandi, MD, Pediatric Resident, Children’s National Health Systems, Washington, DC
Peer Reviewer
Christopher J. Haines, DO, FAAP, FACEP, Chief Medical Officer, Children’s Specialized Hospital, New Brunswick, NJ; Associate Professor of Pediatrics and Emergency Medicine, Drexel University College of Medicine; Attending Physician, St. Christopher’s Hospital for Children, Philadelphia, PA
Statement of Financial Disclosure
To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, we disclose that Dr. Dietrich (editor), Dr. Skrainka (CME question reviewer), Ms. Wurster (nurse planner), Dr. Sawaya (author), Dr. Ravandi (author), Dr. Haines (peer reviewer), Ms. Coplin (executive editor) and Ms. Mark (executive editor) report no relationships with companies related to the field of study covered by this CME activity.
DISORDERS OF FLUIDS IN CHILDREN
Normal Fluid Requirements in Children. The unique physiology of children results in relatively higher fluid requirements for children than adults. Infants and young children have a greater surface area to weight ratio, which means proportionally larger insensible losses. In addition, children may be less likely to hydrate themselves depending on their developmental level.
Maintenance fluid requirements are based on expenditure, which is proportional to surface area. When calculating maintenance fluid requirements, weight is used as a surrogate for surface area. The ratio of surface area to weight for babies is greater than for older children, which explains the need for proportionally more fluid for the first 20 kg of weight. Maintenance fluid requirements are calculated based on the Holliday-Segar formula1:
- 100 mL/kg/d for the first 10 kg (roughly 4 mL/kg/hr);
- 50 mL/kg/d for the second 10 kg (roughly 2 mL/kg/hr);
- 20 mL/kg/d for the rest of the weight of the child (roughly 1 mL/kg/hr).
The following 4:2:1 formula is used to rapidly calculate a child’s maintenance fluid requirements: For example, a 12 kg child would require: (4 x 10 kg) + (2 x 2 kg) = 44 mL/kg/hr of maintenance fluid.
Traditionally, the use of hypotonic fluids, such as dextrose 5% with 0.25% normal saline (D5 ¼ NS) for infants and dextrose 5% with 0.5% normal saline (D5 ½ NS) for older children, was recommended. This was based on calculations of electrolyte requirements and caloric expenditures. However, more recent evidence from common clinical scenarios in hospitalized children, such as respiratory illness, central nervous system disturbances, pain, and emesis, show an increase in antidiuretic hormone (ADH) levels, which leads to free water retention. This combination of elevated ADH levels and hypotonic intravenous (IV) fluids results in hyponatremia.2 Hospital-acquired hyponatremia has led to significant neurologic sequelae such as coma and death.3 Evidence from systematic reviews and meta-analyses shows that hypotonic fluids may not be the safest choice in hospitalized children: Children receiving hypotonic fluids are significantly more likely to develop hyponatremia, but there is no increased risk for developing hypernatremia from isotonic fluids.4-7 Based on this mounting evidence and the fact that a child may receive several hours of maintenance fluids in the emergency department (ED), providers should use isotonic fluids, such as 0.9% normal saline with glucose (for example D5 NS), as maintenance fluids for children, and 0.45% normal saline with glucose (for example D5 ½ NS) as maintenance fluids for neonates and infants < 12 months of age.
For example, a 3-year-old boy with poor oral intake is being admitted from the ED for treatment of pneumonia. His vital signs are normal and he weighs 22 kg. What maintenance fluids should be ordered and at what rate?
a. Fluid type: Dextrose 5% with 0.9% normal saline
b. Fluid rate: (10 kg x 4) + (10 kg x 2) + (2 kg x 1) = 40 + 20 + 2 = 62 mL/kg/hr
Special considerations: Certain clinical situations, including more insensible losses, increasing metabolic demand, and ongoing losses, contribute to a change in the basal requirements. For example, insensible losses are increased in burns, increased respiratory rate, fever, and in preterm infants. Children with short bowel syndrome whose enteral absorption is impaired and those with an array of metabolic diseases will require more than maintenance fluids. Conversely, children with heart failure and renal failure may need more careful titration of maintenance fluids.
DEHYDRATION/HYPOVOLEMIA
Definition. Dehydration is defined as loss of total body water resulting in hypovolemia. The negative balance of total body water can result from decreased intake, increased output, or movement of water out of the intravascular space.
Epidemiology. In 2010, 15% of pediatric ED visits leading to admission were for fluid and electrolyte disturbances.8 The most common illness leading to dehydration in children is acute gastroenteritis. Globally, diarrhea is the second leading cause of death in children < 5 years of age and kills about 760,000 children annually.9
Etiology. While the discussion of dehydration commonly centers on acute gastroenteritis, it is important for emergency physicians to have a broad differential. It is helpful to divide the causes of dehydration in three categories: 1) decreased intake, 2) increased output, and 3) movement of fluid out of the intravascular state. Table 1 lists the most common causes of dehydration in children presenting to the ED.
TABLE 1. MOST COMMON CASES OF DEHYDRATION IN CHILDREN 10 |
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Decreased Intake |
Increased Output |
Movement of Fluids |
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|
|
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SOURCE: Author adapted. |
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Pathophysiology. Water is initially lost from the extracellular space, leading to compensatory shifts of water from the intracellular to the extracellular space. Dehydration can result in a hyponatremic, isotonic, or hypernatremic state. Isotonic dehydration, the most common form of dehydration, results from a proportional loss of fluid and sodium where the sodium level remains between 135-145 mmol/L. Hyponatremic and hypernatremic dehydration will be discussed in the section on sodium homeostasis.
Clinical Features. History. As with the clinical assessment of any child, a thorough and detailed history is key. Ask details about the duration of symptoms, source of fluid loss, and fluid intake. Press the parents for specific details such as the number of wet diapers (especially compared to usual), the quantity and content of emesis (bilious or bloody), and the types of fluids used for rehydration. For example, a baby rehydrated with free water only is at risk for hyponatremia. Although the history is essential in helping determine the cause of dehydration, its findings have not been shown to help identify the degree of dehydration, which determines the rehydration plan. Parental reports of normal fluid intake, urine output, and tear production reduce the likelihood of significant dehydration. Conversely, a parental report of a sunken fontanelle or decreased tears is associated with a higher likelihood of hospital admission.11
Physical exam. First, determine the hemodynamic status of the child using the vital signs and a rapid assessment. Any concern for shock, including tachycardia, cool and pale distal extremities, prolonged capillary refill, weak peripheral pulses, and normal systolic blood pressure, should trigger rapid resuscitation. As the body’s compensatory mechanisms fail, the patient may develop a depressed mental status, decreased urine output, decreased blood pressure, tachypnea, weak central pulses, and mottling.
A full physical exam for dehydration includes clues to the cause of the illness as well as signs to help determine the degree of dehydration. This list includes evaluating the following: general appearance, skin turgor, production of tears, mucous membranes, sunken eyes, capillary refill, vital signs, and pulse.
The most practical scale used to describe the degree of dehydration is the World Health Organization (WHO) scale: no or mild dehydration (< 5% dehydration), some dehydration (5-10%), and severe dehydration (> 10%).12 The traditional method for determining the degree of dehydration is to calculate the degree of fluid deficit as a percentage of body weight, usually by subtracting the patient’s weight at presentation from his or her baseline weight.12 However, since the pre-illness weight is often not available in the ED, the fluid deficit method is not clinically practical. Therefore, clinical dehydration scores, such as the 10-point Gorelick Scale and the Clinical Dehydration Scale (CDS), which includes four data points, have been developed to help guide physicians in assessing dehydration. The CDS was developed for children between 1-36 months old with gastroenteritis and is methodologically sound and easy to use. (See Table 2.) A score of 0 indicates no dehydration, 1-4 indicates mild-to-moderate dehydration, and 5-8 indicates severe dehydration.13-15 A recent meta-analysis showed CDS has a higher positive likelihood ratio (1.87-11.79) than negative likelihood ratio (0.30-0.71).14
TABLE 2. CLINICAL DEHYDRATION SCORE16 |
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|
Score of 0 |
Score of 1 |
Score of 2 |
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|
General appearance |
Normal |
Thirsty, restless, or lethargic but irritable when touched |
Drowsy, limp, cold, sweaty ± comatose |
|
Eyes |
Normal |
Slightly sunken |
Very sunken |
|
Mucous membranes |
Moist |
Sticky |
Dry |
|
Tears |
Tears |
Decreased tears |
Absent tears |
|
SOURCE: Author adapted. |
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It is noteworthy that additional research on the CDS shows moderate inter-observer reliability, no associations with fluid deficit calculation, and modest associations with the length of stay.16-17 However, the CDS is a good predictor of length of stay in the ED.13 The most predictive individual exam findings for 5% hypovolemia are delayed capillary refill, abnormal skin turgor, and a deep respiration pattern.18
Diagnostic Studies. Overall, laboratory tests are not helpful in determining the degree of dehydration, especially in the setting of acute gastroenteritis. The Centers for Disease Control and Prevention (CDC) and the American Academy of Pediatrics (AAP) recommend against obtaining routine laboratory tests in acute gastroenteritis.19 However, in clinical practice, tests are obtained more often than is necessary. One study evaluated electrolyte panels in patients with gastroenteritis receiving IV fluids based on the evaluation by a pediatric emergency medicine attending physician. Interestingly, the physician’s prediction of a clinically significant electrolyte abnormality based on history and physical exam had poor sensitivity (58%).19 Moreover, while almost half of the patient electrolyte panels had an abnormality, only 10% were clinically significant (changed management of the patient).19 In 2010, Colletti et al wrote a review for the ACEP Pediatric Emergency Medicine Committee on the management of acute gastroenteritis.12 They reported that in cases of uncomplicated gastroenteritis, electrolytes, blood urea nitrogen (BUN), creatinine, and urine indices are not helpful in determining the degree of dehydration or the management. However, electrolytes could be helpful in cases of severe dehydration for children < 6 months old with an altered mental status, signs of hypokalemia or hyponatremia, or a diagnostic dilemma. Even bicarbonate, often ordered to correlate with the degree of dehydration and response to treatment, is poorly justified by the current evidence. Most studies of hypoglycemia were done in under-developed or developing nations where the cause of gastroenteritis is often bacterial. However, because it is a relatively cheap and non-invasive test, and hypoglycemia was not found to correlate with the severity of dehydration, Colletti et al recommend checking it liberally.12 A bedside glucose is reasonable if the decision is made to give IV fluids to a child with acute gastroenteritis.
Management of Dehydration and Hypovolemia. Most reported studies are on children with acute gastroenteritis, which is the most common cause of dehydration in children. Data on the treatment of dehydration secondary to other causes are limited or are related to the specific treatment of the underlying disease.
Immediate Stabilization. As previously described, vital signs and physical examination will reveal if a child is in hypovolemic shock. Once it is determined that a patient is in shock, the general principles of hypovolemic shock management per pediatric advanced life support (PALS) should be followed,20 including obtaining rapid vascular access, which may be in the form of peripheral intravenous (PIV) access or an intraosseous (IO) route if peripheral access is not successful. Fluid resuscitation should begin immediately after vascular access is obtained. A 20 mL/kg bolus of an isotonic crystalloid should be given over 5-10 minutes, followed by clinical evaluation and repeat boluses. Rapid delivery is key in fluid resuscitation. Most children in hypovolemic shock will require at least 60 mL/kg of fluid in the first hour of care. Patients who have compromised cardiac function may benefit from 10 mL/kg boluses. Frequent reevaluations of mental status, perfusion, and vital signs guide the provider to the next step in management.
Management of Severe Dehydration. The correction of isonatremic hypovolemia will be discussed here, and correction of hyponatremic and hypernatremic hypovolemia will be discussed in the section on disorders of sodium homeostasis. As per the CDC, a hemodynamically stable child diagnosed with severe dehydration (caused by diarrhea) should be treated preferably with 20 mL/kg of lactated Ringer's (LR) or NS fluid rapid bolus, to be repeated until perfusion and mental status have improved, followed by twice maintenance therapy of D5 ½ NS or D5 NS.21,22 Oral hydration, breast feeding, or formula should be restarted as soon as tolerated.
Management of Mild-to-Moderate Dehydration. In mild-to-moderate dehydration, oral rehydration therapy (ORT) is the management of choice as long as the child is able to tolerate oral liquids either by mouth or nasogastric tube. It is important to understand the physiology by which ORT works. Glucose and sodium have coupled transport at the brush border of intestinal epithelial cells. The glucose:sodium ratio of rehydration fluids should not exceed more than 2:1 for effective fluid repletion. Pedialyte (or equivalent) is the most effective oral rehydration solution (ORS). Although commonly used, the majority of fluids given as oral rehydration to children such as sodas, juice, or sports drinks have a glucose:sodium ratio that is too high to be effective as ORS. If a child is refusing Pedialyte, Gatorade (or an equivalent drink) can be diluted 1:1 with water and given with salt crackers instead.
How to rehydrate with ORS:
1) Administer ORS with a teaspoon, syringe, or dropper, if needed, to provide 1-2 mL/kg of fluid every 5 minutes (or 5-10 mL every 5-10 min) with a goal of 50-100 mL/kg over 3 to 4 hours. Parents should be instructed not to give it faster to be successful, especially for children with nausea and vomiting.21
2) Replace ongoing losses with ORS as per Table 3. Educate even well-hydrated patients about replacement fluids for home.
3) Breast feeding or formula should not be stopped during this therapy. The CDC does not recommend dietary restrictions during diarrheal episodes. However, avoid carbonated drinks and drinks or food with high concentrations of simple carbohydrates.21
TABLE 3. RECOMMENDATIONS FOR ADMINISTRATION OF ORS21 |
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|
No Dehydration |
Child <10 kg: Administer 60-120 mL (2-4 oz) ORS for each episode of vomiting or diarrhea Child >10 kg: Administer 120- 240 mL (4-8 oz) ORS for each episode of vomiting or diarrhea |
|
Mild-to-Moderate Dehydration |
Administer 50-100 mL of ORS/ kg of child’s weight over 3-4 hours to replace the fluid deficit, then continue as above when rehydrated |
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For example, a 2-year-old 15 kg girl presents to the ED with diarrhea. She is mildly dehydrated based on the physical exam with a non-surgical abdomen. The triage nurse asks to start oral rehydration solution in triage. a How much do you recommend? (1 mL x 15 kg) = 15 mL (1/2 oz) of Pedialyte every 5-10 min b You reassess the child in 2 hours in her room. What would be an acceptable quantity of ORS intake to discharge her home? (50 mL x 15 kg ) = 750 mL over 3-4 hours c She stools twice while waiting in the ED. What would you recommend her to do? Drink an additional (120 mL x 2 stools) = 440 mL of Pedialyte Note, in this example, the lower end of the volume calculation is used as the child is mildly dehydrated. Give more oral fluids for more moderately dehydrated children. |
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SOURCE: Author adapted. |
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Effectiveness of ORT and Its Advantages over IV Therapy. The AAP, WHO, and CDC advocate for ORT as first-line therapy for mild and moderately dehydrated children.21,23 Despite perceptions of the ineffectiveness of ORT, evidence shows that for every 25 children getting oral or nasogastric rehydration, only one will fail and require IV therapy.12 When using a lower osmolarity solution, such as a WHO ORS or Pedialyte, only one in 100 children will fail ORT.12 Another study shows similar percentages of children with improved dehydration scores after 2 hours and successful rehydration by 4 hours when comparing those receiving IV fluids and ORT.24 Side effects of ORT are minimal. While paralytic ileus was seen more often in ORT, 33 children need to receive IV therapy to prevent one case of paralytic ileus.25 Moreover, IV fluid therapy is associated with developing phlebitis in 2.5% of children.12 There is little evidence available comparing cost effectiveness of IV therapy compared to ORT.
Barriers to ORT. Despite the convincing data, ORT is still underutilized in the management of dehydration in acute gastroenteritis. In a survey of pediatric emergency fellowship directors about cases of mild and moderately dehydrated children, only 17% thought ORT would be superior to IV therapy in those situations.26 One-third of the physicians surveyed reported usually using ORT for all mildly but not for moderately dehydrated children. Cited barriers included time and the expectations of caregivers and primary care physicians. In addition, the majority of parents surveyed in pediatric EDs expected IV therapy, and half of all respondents refused to consider ORT. The most commonly cited reasons were: “it is more likely to be successful” and “I tried oral fluid at home and it didn’t work.”26 However, parents are more likely to consider ORT after the use of an antiemetic.27
Overall, the evidence is in support of ORT. Although effective strategies have been implemented to improve ORT at home,28 in the United States, additional education and outreach are needed to encourage providers and families to use ORT more frequently. Pathways encouraging provider and parental engagement in ORT early during the ED visit, even as soon as in triage, may increase its use.
Pharmacologic Therapy. Antibiotics and Antidiarrheal Agents. Antibiotics are not indicated in the treatment of acute gastroenteritis, given that the majority of cases are caused by viruses. In developing countries where bacterial causes are more common, local and WHO guidelines should be followed. In addition, there is no evidence to support the use of antidiarrheal agents.12,29
Antiemetic Use. When antiemetics, such as promethazine, were the only available agents, the use of these agents was discouraged for concerns about their side effects, mainly the extrapyramidal reactions. However, newer antiemetics, such as ondansetron, have been proven safe in multiple studies.30 Ondansetron has been shown to effectively decrease vomiting during rehydration when compared to placebo, to decrease the need for IV therapy and hospital admission, and to be cost effective.12,31-34 However, it did not decrease the length of stay or rates of return to the ED.32 There is some concern about the association of ondansetron and cardiac arrhythmias. In a systematic review, there were no reports of a single dose of ondansetron leading to arrhythmia. In cases in which ondansetron may have played a role in an arrhythmia, the patients had complicated medical histories and were taking other QT prolonging agents.30 In summary, we recommend the use of ondansetron in patients who are vomiting and unable to tolerate oral fluids, while screening by history for risks of cardiac disease and QT prolonging medications.
Ondansetron oral disintegrating tablet is recommended as first-line therapy as follows:
- 8-15 kg: 2 mg;
- 15-30 kg: 4 mg;
- > 30 kg: 8 mg (max dose).
If the child cannot tolerate the oral dose, the IV form may be used: 0.1-0.5 mg/kg/dose (max 4 mg).35 Although the idea of prescribing ondansetron for home use for vomiting in acute gastroenteritis is tempting and useful, the data in terms of its efficacy are still limited.36
Additional Aspects. Certain pathological states and disease conditions require a different approach to fluid status. For example, patients with compromised cardiac function may require less fluid (start with a 10 mL/kg bolus), while those with gastrointestinal and renal losses may require additional fluid and electrolyte repletion. Patients with metabolic conditions have higher maintenance fluid requirements and often need a different composition of fluids than most pediatric patients. The fluid status of patients with diabetic ketoacidosis, sickle cell disease, or those with special formulas or total parenteral nutrition (TPN) require special attention as well. While the discussion of the management of these patients is beyond the scope of this article, it is important to tailor the fluid and electrolytes of each patient based on his or her unique clinical situation and to consult with a specialist early.
Disposition37
Criteria to Discharge Home:
- Well-appearing patients without any significant electrolyte derangements;
- Patients with mild to moderate dehydration tolerating ORT;
- Parents understand the instructions for further ORT as per Table 3 at home, understand pain and fever control if needed, and are able and committed to follow through;
- Available primary care physician follow-up.
Criteria to Admit to the Inpatient Pediatric Ward:
- Patients who cannot tolerate ORT even after appropriate ED care, such as with IV therapy, pain management (for stomatitis and pharyngitis, for example), and the use of an antiemetic when appropriate. These patients require more IV fluids and observation;
- Severe dehydration requiring ongoing IV fluids;
- Significant electrolyte abnormalities;
- Concerns about parental investment in treatment at home or the lack of follow-up;
- Concern about the etiology of dehydration requiring further investigation.
Criteria to Admit to the Pediatric Intensive Care Unit (PICU):
- Hemodynamic instability or altered mental status from hypovolemia that has not improved with initial ED therapy;
- Significant electrolyte derangements requiring frequent monitoring and intervention at PICU level.
DISORDERS OF SODIUM HOMEOSTASIS: HYPONATREMIA
Normal serum sodium levels are 130-145 mEq/L in infants and 135-147 mEq/L in children > 1 year of age.37 Hyponatremia (low serum sodium) is defined as a serum sodium level < 135 mEq/L. Mild hyponatremia is a sodium level of 130-135 mEq/L, moderate is 125-129 mEq/L, and severe is < 125 mEq/L. Low serum sodium is relative to the total body water amount (i.e., while serum sodium may be low, the total body sodium may be low, normal, or high, depending on the free water amount in the body). Hyponatremia can be acute (a drop over 24-48 hours) or chronic (a drop over days to weeks).
Epidemiology. Hyponatremia is not uncommon, though it is not always clinically significant. Of the children presenting to an ED who had their sodium level checked, 22% had a sodium level < 135 mEq/L.38
Etiology. In the pediatric ED, the most common cause of hyponatremia is hypovolemic hyponatremia secondary to acute gastroenteritis, although most hypovolemia caused by gastroenteritis is isotonic hypovolemia. Other less common causes of hyponatremia are found in Table 4.
TABLE 4. CAUSES OF HYPONATREMIA40 |
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|
Hypovolemic Hyponatremia |
Hypervolemic Hyponatremia |
Hyperosmolar Hyponatremia |
Pseudohyponatremia |
|
Decreased total body water Low sodium |
Increased total body water Normal, low, or high sodium |
Normal total body water Normal sodium |
Normal sodium |
|
Gastroenteritis Renal pathology (e.g., renal tube acidosis, diuretics) 3rd space loss: (e.g., burn, peritonitis) Adrenal pathology (e.g., mineralocorticoid deficiency) |
Syndrome of inappropriate antidiuretic hormone secretion (e.g., from pneumonia) Water intoxication (e.g., from incorrect formula preparation) Nephrotic syndrome, congestive heart failure Drugs (e.g., NSAIDS, cyclophosphamide) |
Hyperglycemia |
Diabetic ketoacidosis Hyperlipidemia Hyperproteinemia |
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SOURCE: Author adapted. |
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Water intoxication is a unique clinical presentation in young infants that occurs with incorrect formula preparation or by providing free water to babies.39 Increases to the free water content lead to hyponatremia. Since babies cannot verbalize their thirst or lack of it, they have no control over their body’s needs and thirst response. In addition, as mentioned earlier, the incorrect use of IV fluids for infants and children can also lead to hyponatremia.40 Another cause of hyponatremic dehydration in neonates is heat. This is seen in the hot summer months especially, since infants cannot verbalize their thirst, or if they are rehydrated with free water rather than formula or electrolyte solutions.
Pathophysiology. Sodium is the main ion in the extracellular space. The total body concentration of sodium determines the amount of extracellular fluid, since water will shift between intracellular and extracellular spaces to reach equilibrium. The kidneys regulate sodium levels by diluting urine and excreting free water. The kidneys’ ability to excrete free water is the regulatory mechanism to maintain normal serum sodium levels in conjunction with the hypothalamic osmoreceptors, thirst mechanism, ADH, and renin-angiotensin-aldosterone system. Hyponatremia can lead to cerebral edema as water moves down the osmotic gradient into the brain cells. In the setting of chronic hyponatremia, brain cells will extrude solutes to the extracellular space to decrease movement of water into the cells; some are excitatory amino acids that may cause seizures.41 The adult brain may be more adaptable to hyponatremia than those of children, who are more vulnerable to hyponatremic encephalopathy with the potential for permanent brain damage.38
Clinical Features. History. Signs and symptoms of hyponatremia are varied and vague. They depend on the rate of drop and level of sodium. A precipitous drop in sodium is more likely to cause symptoms than chronic hyponatremia. These vary from gastrointestinal symptoms to weakness and muscle cramps. The most significant symptoms, which are related to cerebral edema, include headache, altered mental status, lethargy, and seizures.40 It is generally believed that these clinical features are seen when the sodium level is < 125 mEq/L.41 The history leading to the presentation will provide clues to the etiology of hyponatremia. Ask about the past medical history for underlying disease and medication use. Questions about the types of oral fluids given to the child and details about the ratio of water to powder in the formula preparation can reveal reasons for hyponatremia. Typically, formula should include one tablespoon of powder with two ounces of water. Breast milk or ready-made formula should not be diluted. These formulations provide for maintenance fluid requirements for children. Finally, since hyponatremia is often seen in the setting of hyponatremic dehydration, search for clues to severe dehydration and gastroenteritis.
Physical Exam. Vital signs, such as the heart rate and the blood pressure, are helpful in determining the intravascular fluid status of a patient. The physical exam should include a mental status exam, including a Glasgow Coma Scale, and a neurological examination for signs of cerebral edema, including lethargy, seizure activity, and papilledema. The exam should also note signs of dehydration (as described in the previous section) or fluid overload, such as edema, a gallop, lung crackles, hepatomegaly, or jugular venous distension, which are important factors in determining the etiology of hyponatremia.
Diagnostic Studies. As discussed previously, most cases of gastroenteritis with hypovolemia and probable mild hyponatremia do not require labs. However, in cases of unclear diagnosis or severe dehydration, laboratory tests can be helpful. Serum osmolarity will help divide the differential diagnosis into normal osmolarity hyponatremia, hypoosmolar hyponatremia, and hyperosmolar hyponatremia. Hypoosmolar hyponatremia can be differentiated further based on volume status and urine studies. (See Table 5.) Other electrolyte abnormalities may give clues to the underlying diagnoses. For example, hyponatremia in the setting of hyperkalemia may be indicative of congenital adrenal hypoplasia. Renal and liver function tests may be indicated when the etiology of hyponatremia is unclear. Figure 1 offers a diagnostic approach to hyponatremia.
TABLE 5. HYPONATREMIA AND VOLUME STATUS44 |
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Hypovolemia |
Euvolemia |
Hypervolemia |
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SOURCE: Author adapted. |
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FIGURE 1. APPROACH TO HYPONATREMIA |
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Management. Management of an asymptomatic patient. An asymptomatic patient does not need urgent correction of the sodium. If the hyponatremia is related to hypovolemia, such as with gastrointestinal losses, replacement with isotonic saline (0.9% NS) is the treatment of choice. In a neurologically stable patient, the serum sodium level should not increase by more than 12 mEq/L/day. Diagnosing the cause of the hyponatremia will guide the clinician in the treatment, assisted early on by a specialist as needed. For example, syndrome of inappropriate ADH secretion requires fluid restriction, and renal tubular acidosis requires specific treatment.
Management of a symptomatic patient. Hypertonic saline 3% is the mainstay of therapy for acute symptomatic hyponatremia. Fluid restriction alone or isotonic saline will not appropriately correct the sodium in a hyponatremic patient with symptoms concerning for cerebral edema. Anticonvulsants typically will not stop seizures from hyponatremia. There are slight variations in the recommendations for how sodium should be corrected, with the main goal being an initial target level for the serum sodium of 125-130 mEq/L. Table 6 shows the steps recommended for treating symptomatic hyponatremia.40 The first step should increase serum sodium by about 1 mEq/L for every 1 mL/kg of NaCl 3%. Therefore, it is predicted that this method will raise the serum sodium by 2 mEq/L, which has the potential to reduce brain edema. If the patient’s sodium level rises but does not improve symptomatically, an alternative etiology for encephalopathy is likely. (See Table 6.)
TABLE 6. TREATMENT OF SYMPTOMATIC HYPONATREMIA40 |
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SOURCE: Author adapted |
Although traditionally physicians have been warned against rapid correction of sodium leading to cerebral demyelination, a hesitancy to correct sodium quickly in symptomatic patients may in fact lead to worse outcomes. Studies have found higher mortality rates in delayed or slowly corrected hyponatremia.42 It is important to note that cerebral demyelination occurs in patients with hyponatremia for > 48 hours who have underlying risk factors. There are no reports of cerebral demyelination or other neurologic complications in correcting sodium in children with acutely developing hyponatremia.40 The fear of overcorrection may lead to under-treatment of hyponatremia. In fact, the recent deaths from hyponatremia occurred in children who had a lack or delay of appropriate treatment.43-45
Additional Aspects. Pseudohyponatremia is a laboratory measurement of decreased serum sodium associated with severe hyperproteinemia or hypocholesterolemia. In these scenarios, blood plasma is expanded, which leads to falsely low sodium measurements. Hyperglycemia creates increased osmolality and water shifts into the extracellular space. Serum sodium decreases by 1.6 mEq/L for every 100 mg/dL increase in glucose from normal (100 mg/dL). There are special clinical scenarios that may cause hyponatremia. Patients who are TPN-dependent or use special formulas may become hyponatremic due to incorrect preparation or administration of these sources of nutrition.
Disposition40
Criteria to Discharge Home:
- Asymptomatic mild hyponatremia (Na > 129 mEq/L).
- The underlying disease meets discharge criteria.
- Good follow-up with the primary care provider or a specialist if needed.
Criteria to Admit to the Inpatient Pediatric Ward:
- Asymptomatic moderate hyponatremia (Na 120-125 mEq/L).
- Mildly symptomatic hyponatremia (Na >125 mEq/L) with a normal mental status.
Criteria to Admit to the PICU:
- Hemodynamic instability or altered mental status.
- Symptomatic hyponatremia.
- Severe hyponatremia (Na < 120 mEq/L).
- Underlying etiology requiring PICU, e.g., diabetic ketoacidosis.
HYPERNATREMIA
Definition. Hypernatremia is defined as serum sodium levels > 145 mEq/L. Hypernatremia can occur with loss of free water, increase in sodium, or a relatively greater loss of free water compared to the loss of sodium. Dehydration describes a clinical scenario with an isolated water deficit. Hypovolemia describes the loss of both water and salt.
Epidemiology. In children, hypernatremia is not as common as hyponatremia. One study found 0.04% prevalence (1 in 2288) of hypernatremia in hospitalized children, with a 10 times higher rate (0.4%) in neonates < 2 weeks of age.46
Etiology. Similar to understanding hyponatremia, it is important to think about both the amount of total body water and sodium relative to one another to understand hypernatremia. Hypernatremia can occur with increased total body sodium or a relative increase in relation to the increase in free water. This latter form of hypernatremia most commonly occurs accidently such as in incorrect formula preparation or gastrostomy tube feeding or higher sodium concentration in TPN. Normal total body sodium coupled with an increase in free water loss will lead to hypernatremia. This occurs with insensible losses, lack of access to water either from the environment or in children and infants who cannot self-feed, in children with diabetes insipidus, or a brain pathology leading to an impaired thirst mechanism. Conversely, a relatively lower deficit in total body sodium relative to the loss of free water is another cause of hypernatremia. Such clinical scenarios include gastrointestinal losses from diarrhea and renal losses from osmotic diuresis. Infants and children with developmental delays are vulnerable to hypernatremia since they do not have access to water. Neonates specifically may present with hypernatremia dehydration in the first days of life secondary to difficulty breast feeding, either from a poor latch or delayed milk letdown from the mother.
Pathophysiology. The body regulates sodium levels by several mechanisms described previously, mainly with the thirst mechanism to increase free water intake and ADH to control retention or excretion of free water. Hypernatremia causes water to move down its concentration gradient from the intracellular space to the extracellular space. The shift in water causes shrinkage of brain cells and volume and subsequent neurologic signs and symptoms. Similar to hyponatremia, neurological sequelae are more likely in acute changes of sodium than in chronic hypernatremia where the brain cells have protective mechanisms of creating osmoles to retain fluid within the cell. Production of intracellular osmoles, such as the amino acids glutamine, glutamate, and taurine, are seen after about 3 days of hypernatremia. Finally, the shrinking brain volume can rupture brain vessels leading to cerebral and subarachnoid hemorrhage.
Clinical Features. History. A detailed history can reveal the duration of the symptoms of hypernatremia as well as lead to the potential causes of this presentation. Ask about the child’s feeding: quantity, type and preparation of the formula, or if breast feeding, get details about the latch, suck, duration of each feed, amount of milk, and urine output in terms of number of wet diapers. The amount of breast milk production can easily be determined in the ED if the mother pumps; most EDs have a breast pump available. Inquire about recent changes in TPN or gastrostomy feeds and about the presence and duration of vomiting, diarrhea, and fever, if present, especially in children who do not have access to water. Symptoms of hypernatremia include muscle weakness, changes in mental status, and seizures.
Physical Exam. In the case of hypernatremic dehydration, the physical exam may indicate signs of dehydration with or without shock as described previously. Look for signs of hypernatremia such as lethargy, muscle weakness, irritability, seizures, focal neurological deficits, and even coma.
Diagnostic Studies. The diagnostic tests for hypernatremia are the same as those described earlier for hyponatremia and dehydration. These include serum electrolytes, with BUN and creatinine, as well as serum osmolarity, urine osmolarity, and sodium done at the same time. These will help differentiate the etiology of hypernatremia.
Management. Start by stabilizing the patient and resuscitating as needed per PALS algorithms.20
As a general rule, acute hypernatremia can be safely corrected rapidly as there is no risk for cerebral edema since the compensatory ions have not yet accumulated. Chronic hypernatremia requires a slow correction. Sodium should be lowered by about 0.5 mEq/L/hr (10-12 mEq/L in 24 hours) to reach a goal of 145 mEq/L. Rapid rehydration is the biggest risk factor for cerebral edema.43 As with hyponatremia, diagnosing the underlying cause and tailoring the treatment accordingly in consultation with a specialist is best. For example, diabetes insipidus requires free water replacement, and insensible fluid losses requires glucose and free water replacements (e.g., dextrose 5% water).
Hypernatremic dehydration is the most common cause of hypernatremia in children. If a patient is in shock, it is appropriate to resuscitate the patient with isotonic saline, such as 0.9% normal saline, as per PALS guidelines.20,47 While this may seem counterintuitive, many children presenting with hypernatremia may actually have a low total body sodium. In addition, isotonic solutions will still be hypotonic compared to the patient’s level of hypernatremia.
In a hemodynamically stable patient, or once intravascular volume has been replaced, a slower correction can take place with 0.45% normal saline (or orally if the patient can tolerate it) by calculating the water loss, adding it to the maintenance requirements, and replacing it over 48 hours. Two-thirds of the water deficit should be replaced in the first 24 hours with the remaining third during the following 12 hours. Generally, the equation below is recommended to calculate the volume of water loss:
Equation for calculating volume of water loss
Water deficit (in L) = [current Na level in mEq/L - 1] X 0.6 X weight (in kg)
145 mEq/L
However, as a rule of thumb, using 0.45% (1/2) normal saline at 1.5 times maintenance ensures appropriate rehydration as well as the desired drop in sodium. The serum sodium level should be checked frequently (every 2 to 4 hours) when using this method.48 A rapid drop of sodium in the first hours increases the risk of seizures.49
Note that if sodium is corrected too rapidly and the patient develops cerebral edema, 3% NaCl should be used to raise the serum sodium as described in the treatment of hyponatremia.
Additional Aspects. Hypoalbuminemia may falsely elevate sodium levels on laboratory tests. Point-of-care testing is not affected by this laboratory artifact. Seizures and exercise may transiently cause hypernatremia due to the shift of free water into cells. However, this effect resolves within 10 to 15 minutes.
Disposition53
Criteria to Discharge Home:
- Asymptomatic mild hypernatremia (Na 145-150 mEq/L).
- The underlying disease is known and meets discharge criteria.
- Good follow-up with specialist and primary care provider is available.
Criteria to Admit to the Inpatient Pediatric Ward:
- Asymptomatic mild hypernatremia with an unknown cause.
- Asymptomatic moderate hypernatremia (Na 150-155 mEq/L).
- Initially symptomatic hypernatremia that has responded to initial ED therapy.
- Unknown underlying etiology of the hypernatremia, putting the child at risk of further hypernatremia.
Criteria to Admit to the PICU:
- Hemodynamic instability or altered mental status.
- Symptomatic hypernatremia.
- Severe hyponatremia (Na > 155 mEq/L).
- Underlying etiology requiring PICU care.
- Frequent laboratory testing and close monitoring that cannot be done on an inpatient ward.
SUMMARY
Disorders of fluids and electrolytes are quite common in children presenting to the ED, with acute gastroenteritis being the most common etiology. Assessing the degree of dehydration will help the physician determine the best management, including oral rehydration therapy, and avoid over-treatment with IV fluids. Partnering with and educating the parents will help advocate for oral rehydration.
Urgent treatment of acute symptomatic hyper/hyponatremia is key, while chronic changes require slower treatment and asymptomatic abnormalities may allow time to diagnose the etiology behind the disorder.
This review guides clinicians in decisions for pediatric maintenance fluid therapy, rehydration therapies, and sodium homeostasis.
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MONOGRAPH: A clinical guide for pediatric maintenance fluid therapy, rehydration therapies, and sodium homeostasis.
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