Pediatric surgeons frequently encounter pathologic conditions that lead to shifts in fluid balance and derangements in electrolytes. The previously mentioned guidelines for maintenance fluid need to be tailored to the clinical situation, with additional fluid given according to ongoing losses and/or fluid shifts.
Traumatic soft tissue injuries, severe burns, peritonitis, or extensive surgical procedures are all associated with a redistribution of fluid from the intravascular space to the extravascular space. These “third space losses” have been attributed to osmotic and hydrostatic forces as well as cytokine production from injured tissues. The clinical situation will dictate the amount and type of fluid necessary for adequate fluid balance. Bowel obstructions are a classic example of major fluid shifts at work. Both the intestinal lumen and associated soft tissues see an increase in fluids and this can be difficult to measure; therefore, an accurate measurement of intake and output is necessary. A related scenario frequently seen is the association of systemic sepsis, which will further increase the amount of fluid shifted into the abdomen. With severe sepsis, the entire “third space” of the body may see large shifts of fluid. Pancreatitis with severe sepsis is a frequently seen clinical scenario that illustrates the above point, and the amount of replacement necessary can be massive. The composition of “third space losses” has been extensively studied with transmembrane potentials and radioisotopes, providing a guide for the type of fluid necessary for replacement. Based on the data, a balanced salt solution with other additives as needed is an appropriate choice for fluid replacement. Some surgeons would prefer Lactated Ringer 's solution because it provides a close approximation of the fluid losses. However, some clinicians may prefer to avoid the lactate administration. The actual fluid chosen is not as important as an understanding of the clinical situation and an accurate measurement of fluid intake and output. The renal compensation in otherwise healthy children will usually take care of any minor excess or deficits.
Another source of fluid loss that complicates fluid and electrolyte replacement is external loss from body cavities or the gastrointestinal tract. An accurate measurement of the ongoing loss will provide an idea for the amount of fluid needed and the composition of electrolytes lost depending on the source (Table 5-3). When calculating the volume and type of replacement, a standard maintenance fluid calculation should be used with additional replacement based on the amount lost from the source, with a milliliter per milliliter regimen. To most accurately replace the lost electrolytes, the output fluid should be sent for analysis; however, this may become tedious and not cost-effective, so rough approximations of electrolytes allow the surgeon to begin an appropriate fluid replacement strategy.
Table 5-3Composition of Gastrointestinal Secretions |Favorite Table|Download (.pdf) Table 5-3 Composition of Gastrointestinal Secretions
|Type ||Na (mEq/L) ||K (mEq/L) ||Cl (mEq/L) ||HCO3 (mEq/L) |
|Salivary ||10 ||25 ||10 ||30 |
|Stomach ||60 ||10 ||130 || |
|Duodenum ||140 ||5 ||80 || |
|Ileum ||140 ||5 ||104 ||30 |
|Colon ||60 ||30 ||40 || |
|Pancreas ||140 ||5 ||75 ||115 |
|Bile ||145 ||5 ||100 ||35 |
One of the most common clinical scenarios encountered by pediatric surgeons requiring extensive fluid shifts and management is peritonitis, which can range from simple appendicitis in a 10-year-old to necrotizing enterocolitis in a premature neonate. The initial fluid management may require an estimation of the physiologic insult, but often a “guess ” based on experience is utilized at the beginning. To better estimate the degree of fluid requirement, Filston advocated one method of calculating a “guess” at the volume needed to replace fluid loss from intraabdominal pathology: (1) divide the abdomen into 4 quadrants (4 quadrants = 1 maintenance fluid volume); (2) estimate the effects of peritonitis (maximum of 4 quadrants of 100% of the maintenance volume) and surgical manipulation (maximum of 4 quadrants or 100% of the maintenance volume); and (3) add this volume to the maintenance fluids plus any losses measured and then given back as maintenance fluid for the calculated maintenance and the remainder as Ringer lactate solution. The above strategy can be cumbersome to use, so the most commonly utilized indicator of adequate fluid resuscitation is urine output. Sepsis may compound peritonitis and greatly increase the amount of fluid required. Insensible fluid losses are exaggerated, and obligatory isotonic volume loss occurs in both the bowel and soft tissues. These fluid losses must be replaced prior to any use of ionotropic agents to increase cardiac output or renal perfusion pressure. The typical pediatric fluid mix is too hypotonic in this situation. Therefore, a balanced salt solution, such as Ringer lactate solution, provides a better source of volume resuscitation. Care must be taken to avoid volume excess. It has been shown that hypervolemia, especially in preterm infants, has been implicated in the reopening of a previously closed ductus arteriosus when more than 170 cc/kg/24 h is given.
Another common problem encountered by pediatric surgeons is pyloric stenosis, which is a classic example of derangements in both fluids and electrolytes. The excessive vomiting seen in these infants leads to an overall loss of volume as well as a loss of chloride. A hypochloremic, hypokalemic metabolic alkalosis with associated volume depletion quickly develops. Renal compensation for the chloride loss involves retaining bicarbonate to maintain electroneutrality, with a resulting paradoxical aciduria. Normal saline should be used initially for resuscitation. After urine output is documented, potassium should be added as these infants typically have a deficit in total body potassium. After adequate volume and electrolyte replacement, a general anesthetic can be safely given for operative correction.
Hypernatremia is defined as a serum sodium concentration greater than 145 mEq/L and it is most often seen in older pediatric patients associated with dehydration. The clinical signs of dehydration may not be as apparent when compared to isotonic dehydration secondary to osmosis and a relative preservation of the extracellular fluid space. Neurologic symptoms including irritability, weakness, or lethargy are the most common clinical manifestation of hypernatremia. When evaluating a patient with hypernatremia it is important to measure serum and urine osmolarity, as well as the sodium content and specific gravity of the urine. Initially patients should be treated with isotonic fluids and, as volume expansion occurs, hypotonic fluids may then be given. Rapid correction of sodium may lead to cerebral edema and permanent neurologic deficits; slowly correcting the sodium over 48 to 72 hours is recommended.
Hyponatremia, defined as a serum sodium concentration less than 135 mEq/L, is more frequently seen in the pediatric population. While hypernatremia is most commonly seen with dehydration, hyponatremia may be seen in hypo-, hyper-, or euvolemic states, and proper treatment depends on recognizing the corresponding fluid state. Symptoms of hyponatremia are rarely seen until the sodium decreases below 120 mEq/L. Nausea and vomiting may be seen as well as neurologic symptoms, which can range from confusion to seizures or coma. The brain is particularly sensitive to changes in serum osmolarity that are associated with hyponatremia, and rapid correction may lead to central pontine myelinolysis, secondary to fluid shifts out of neural tissue. An algorithm for the diagnosis of hyponatremia is presented in Fig. 5-1. With chronic hyponatremia, brain injury can usually be avoided by limiting correction to <18 mmol/L in 48 hours. There is some evidence to suggest that correcting acute or postsurgical hyponatremia by less than 4 mmol/L may be associated with an excess mortality. Therefore, to attempt to avoid secondary injury, correction of hyponatremia should probably take place over 48 hours and with more than 4 mmol/L/24 h but less than 18 mmol/L/48 h correction rates. Postsurgical patients or those undergoing volume resuscitation for severe trauma, sepsis, or burns frequently develop hypervolemic or euvolemic hyponatremia secondary to excessive administration of hypotonic fluids. In the presence of normal renal function, simple fluid restriction will correct most cases. Other causes of hyponatremia include congestive heart failure, cirrhosis, and the nephrotic syndrome. These are associated with an increase in total body sodium and water; fluid restriction is initiated but diuretics may need to be added. The syndrome of inappropriate antidiuretic hormone (SIADH) may also cause a low serum sodium in a euvolemic state, and urine concentrations of sodium are increased. Initial therapy for SIADH includes water and sodium restriction. Rarely, cerebral salt wasting may also cause hyponatremia in children with neurologic injury or disease. Treatment for hyponatremia is summarized in Table 5-4.
Algorithm for the assessment of hyponatremia. From Perkins RM, Levin DL. Pediatr Clin North Am 1980;27(3):567, with permission.
Table 5-4Treatment of Symptomatic Hyponatremia |Favorite Table|Download (.pdf) Table 5-4 Treatment of Symptomatic Hyponatremia
Calculate Na+ deficit needed to bring serum Na+ to 125 mEq/L (125 – observed Na+) × weight (kg) × 0.6 = mEq/L
Administer 2 mL of 3% NaCl/mEq required, as calculated above, over 5-30 min, based on acuteness of situation
Closely follow serum Na+ level and potential for fluid overload
Potassium is the primary intracellular cation and plays an important role in regulating the cellular transmembrane potential. Disorders of potassium are frequently seen in the hospitalized pediatric population, and symptoms range from cardiac dysrhythmias to muscle weakness. Hyperkalemia is defined as a serum level greater than 5.5 mEq/L in children and 6 mEq/L in newborns. When compared to adults, children better tolerate hyperkalemia. The most common cause of hyperkalemia is hemolysis of the drawn lab specimen and an analysis should be repeated to rule this out. Other causes include renal failure or iatrogenic ones secondary to parenteral nutrition or potassium-containing fluids. Hyperkalemia will be demonstrated on an electrocardiogram (ECG) as peaked T waves followed by widening of the QRS complex. When serum levels approach 9 mEq/L, ventricular fibrillation is seen but may occur with any elevated level. Table 5-5 lists an approach to symptomatic hyperkalemia.
Table 5-5Treatment of Hyperkalemia |Favorite Table|Download (.pdf) Table 5-5 Treatment of Hyperkalemia
Stop potassium administration
Give 50 mg/kg calcium gluconate IV over 5-15 min with ECG monitoring; watch for bradycardia
Give 1-2 mEq/kg NaHCO3 IV over 5 min
Give 4 mL/kg glucose insulin as bolus, then IV at 4-8 mL/kg/h (4 units regular insulin/100 mL of D25); may increase to 6 units/100 mL D25 if hyperglycemia develops
Sodium polystyrene sulfonate 1 g/kg via rectum in sorbitol
Loop diuretics may be effective with adequate renal response
Monitor K+ frequently
Hypokalemia (serum K concentration <3mEq/L) has multiple causes, which include decreased intake or increased excretion in the urine or gastrointestinal tract. Severe diarrhea or administration of loop diuretics is a frequent cause seen in hospitalized patients. Asymptomatic mild hypokalemia may not require treatment except in the patient receiving digitalis. Symptomatic patients should be first treated with oral supplementation if possible with a dose ranging from 0.5 to 1 mEq/kg. If intravenous replacement of large concentrations of potassium is necessary, continuous cardiac monitoring in an ICU setting is recommended. In addition, frequent monitoring of serum potassium levels is recommended during oral or intravenous replacement to avoid hyperkalemia. Difficulty replacing potassium should prompt a reevaluation of ongoing losses or evaluating the serum concentration of magnesium.