Fluid and Electrolyte, Genitourinary And Gastrointestinal Alterations

Fluid and Electrolyte, Genitourinary and Gastrointestinal Alterations

Fluid and Alterations

An understanding of body fluids, electrolytes, and acid-base buffers (a substance that either releases or absorbs hydrogen ions to maintain a stable blood pH) is essential in the treatment of many childhood illnesses. Alterations in electrolytes, fluids, and acid-base metabolism can occur quickly in children and, as a result, can be life threatening. Any illness that alters a child’s intake, elimination, or need for water and electrolytes has the potential to cause imbalances. The child’s survival hinges on the ability of health care providers to accurately assess at-risk situations, diagnose the alteration, initiate the appropriate treatment plan, and implement prevention strategies.

 

ANATOMY AND PHYSIOLOGY

The complex chemical and physiological processes that sus­tain life depend on the presence of water and the body’s ability to maintain homeostasis, a dynamic equilibrium of the body that is maintained by processes of feedback and regulation. The most abundant body fluid is water. Four key physiological factors are responsible for the fluid and elec­trolyte (a charged particle found in body fluid) differences between children and adults. These include (1) percentage and distribution of body water, (2) body surface area, (3) rate of basal metabolism, and (4) status of kidney function. Infants and children have a higher proportionate body water content than adults. Water constitutes approximately 50% of the body weight of adults and adolescents, 65% of body weight in children, and 80% of the body weight of infants.

The body’s water is found in two main fluid compart­ments: within the cell (intracellular, or ICF) and outside the cell (extracellular, or ECF). Intracellular fluid is body fluid that is located inside the cells and contains large amounts of potassium, phosphate, sulfate, and proteins. Extracellular fluid includes interstitial fluid (the fluid between the cells and outside the blood and lymph vessels), intravascular fluid (within the blood vessels, e.g., plasma), and lymphatic fluid. Extracellular fluid is predominately saline because it contains large amounts of sodium, chloride, and bicarbonate (Figure 21-1).

The distribution of water between these two compart­ments is also different in infants and children as compared to adults. Forty percent of body water in the newborn is in the extracellular compartment, as compared with 20% in the adult. By the time infants are 1 year of age, 30% of their body water is extracellular. Children reach adult water distri­bution percentages by the time they are 5 years old (Fann, 1998). During illness states (vomiting, diarrhea, or hemor­rhage), fluid that is located in the extracellular compartment is lost first. Therefore, children are more at risk for fluid alterations because a higher percentage of their body weight is water and more of that water is located in the extracellular compartment (Figure 21-2).

The second factor accounting for fluid and electrolyte differences is that infants and children have a relatively greater body surface area than does an adult. Therefore, insensible water losses through the skin and lungs are higher for children, and any situation that results in an increase in loss of water and electrolytes alters the body fluid balance to a greater degree than in an adult. Additionally, infants and young children will lose water more quickly than adults because they have a higher basal metabolic rate (BMR). Due to their higher BMR, the fluid intake per kilogram of body weight per day must exceed the per kilogram fluid require­ments of an adult. Further, their bodies cannot regulate homeostatic changes as quickly as adults due to immature kidneys and buffering systems. They need more water to excrete a given amount of solute.

The distribution and movement of body fluids between the ICF and ECF compartments are affected by the amount and type of solutes present, the type of membrane to be crossed, and changes in the permeability of the capillary beds. A solute is a substance that is dissolved in a solution (e.g., a teaspoon of salt dissolved in a glass of water is an example of a solute). Solutes found in the human body include electrolytes, such as potassium, sodium, and cal­cium; nonelectrolytes, such as glucose, urea, and creatinine; and large molecules, such as plasma proteins.

Primarily, fluids move as a result of diffusion, filtration, and osmosis. Diffusion is the movement of a solute across a membrane when the pressures on either side of the mem­brane are equal. In this situation, solutes will flow from an area of higher concentration to an area of lower concentra­tion until an equilibrium is reached. Filtration is the movement of a solute based on the force exerted by the weight of the solution. The fluid containing the solute will move from an area of greater pressure to an area of lesser pressure. Osmosis is the movement of water across a semipermeable membrane from a solution that has a lower solute concentra­tion to one that has a higher solute concentration. Osmosis accounts for the movement of fluid between intracellular and extracellular spaces. The concentration of a solute in a fluid creates a type of pressure called osmotic pressure (a force within the capillary beds that tends to pull water into the capillaries). Osmotic pressure is determined by the type and thickness of the capillary membrane, and the size and concentration of circulating molecules.

 

Figure 21-1.    Body Fluid Compartments

 

 

 

 

 

Figure 21-2.   Distribution of Total Body Water by Age

 

Oncotic pressure, which is caused by the amount of plasma proteins present in the vascular system, holds fluids in the capillaries. A decrease in plasma proteins would allow fluid to escape into interstitial spaces. Capillaries are nor­mally impermeable to plasma proteins. However, in certain illnesses, such as sepsis and burns, capillary permeability increases, allowing proteins to move into interstitial spaces along with water, resulting in the formation of edema. Finally, another pressure within the body that is responsible for the movement of fluids is hydrostatic pressure. Hydrostatic pressure is the pressure of blood against the capillary walls generated by the contraction of the heart. Hydrostatic pressure within the capillary bed pushes fluid across capillary membranes into the interstitial space and is balanced by osmotic pressures. It is measured by blood pres­sure and is important in maintaining the fluid balance within the vascular system.

During various illness states (e.g., shock, burns, dehy­dration), it becomes important to maintain osmotic pressure within the body. This is often accomplished by giving intra­venous solutions at a rate sufficient to replace the loss of fluids. If the child is not able to tolerate fluids orally, the rate also needs to include fluids to cover the daily mainte­nance requirements. While administering intravenous flu­ids, it is important to decide the type of solution based on the intended need and to determine the appropriate rate. Table 21-1 provides a classification of common intravenous fluids.

ELECTROLYTE IMBALANCES

Serum electrolyte concentrations within the ICF and ECF are the same for adults and children. Although many elec­trolytes are found in the body, all serving vital functions, sodium, potassium, and chloride are the major electrolytes that influence fluid balance. Normal serum levels of these electrolytes are listed in Table 21-2. Electrolytes influence the formation and retention of water in the ICF and ECF, and can have a dramatic effect on the function of vital organs.

Sodium Imbalance

Sodium, the major extracellular electrolyte, is responsible for establishing and maintaining the osmolarity (the concentra­tion of solute within a solution measured by the number of moles per liter of water) and volume of ECF. A decrease in the serum sodium concentration (hyponatremia) produces a decrease in the intravascular osmolality (the concentration of solute within a solution measured by the number of moles per kilogram of water). In this situation, free water moves from the intravascular to the interstitial space until the osmo-lality of the compartments is equal. Low serum sodium levels (<135 mEq/L) are associated with increased gastrointestinal output such as diarrhea, vomiting, nasogastric suctioning, diuretics, excessive sweating, and renal disease. Signs and symptoms are headache, muscle weakness, abdominal cramps, lethargy, oliguria, and cerebral edema. An excessive intake of sodium or an increased water loss related to sodium loss (e.g., watery diarrhea) causes an increased serum sodium level (hypernatremia). If that level is >145 mEq/L, water will be pulled out of the cells into extracellu­lar spaces (seen as edema) and, if not compensated for, will cause an intracellular fluid deficit. An intracellular fluid deficit can be suspected if a child has flushed skin, dry mucous membranes, an elevated temperature, and intense thirst.

 

 

 

 

 

Potassium Imbalance

Potassium is the major electrolyte found in the ICF, and the difference between the intracellular and extracellular potas­sium determines the excitability of neurons and muscles. The serum potassium concentration (3.5-5.0 mEq/L) represents the minority of total body potassium. The majority of the body’s potassium is in ICF (about 140 mEq/L). Potassium is also necessary for the transmission of glucose into cells. Extracellular potassium, measured by a blood sample of plasma serum, is extremely important to monitor because any imbalance will greatly affect heart muscle contraction. An elevated serum potassium can cause cardiac irritability, which can lead to ventricular fibrillation. The cardiac irritability associated with an elevated or decreased serum potassium can be seen by an electrocardiogram (EKG) reading.

Concentration of hydrogen ions also affects the movement of potassium in and out of cells. Hydrogen ions affect the pH of body fluids. An excess serum hydrogen concentration will cause potassium to move from intracellular to intravascular spaces, while a decreased hydrogen concentration will move potassium from the bloodstream into the cells.

 

 

 

Hypokalemia (potassium of <3.5 mEq/L) can occur with a loss of gastric or intestinal fluids or when IV fluids do not adequately replace body fluid losses. Signs and symptoms include lethargy, confusion, dizziness, arrhythmias, diarrhea, a decreased blood pressure, and EKG changes (flattened T wave and ST wave depression). Hyperkalemia (potassium >5.0 mEq/L) can occur with tissue necrosis, hemolysis, renal failure, or a rapid infusion of IV potassium. Signs and symp­toms include abdominal cramps, muscle weakness, arrhyth­mias, and EKG changes (tall peaked T waves and a widened QRS complex), and will lead to cardiac arrest if not treated quickly.

 

Chloride Imbalance

Chloride is primarily an extracellular electrolyte responsible for maintaining electroneutrality in the ECF. Chloride levels usually parallel sodium levels, meaning, if sodium levels are increasing, chloride levels will increase and vice versa. Hypochloremia (chloride of <98 mEq/L) will occur with diarrhea, vomiting, gastric suctioning, sweating, and exces­sive use of diuretics. The child will have hypotonic muscles and decreased respirations, and will often be very irritable.

Hormones can also affect fluid balance in the body. Two major hormones are the antidiuretic hormone (ADH) and aldosterone. ADH is secreted by the posterior pituitary when serum osmolality increases, causing the renal tubules of the kidneys to reabsorb water. ADH is secreted during times of dehydration, since it causes an immediate increase in vascular volume and a decrease in urine output. Aldosterone is a mineralocorticoid produced by the adrenal cortex, which causes the distal renal tubules of the kidneys to reabsorb sodium and excrete potassium. Aldosterone is excreted when the body wants to retain fluids, since the increased sodium retention leads to water reabsorption. Table 21-3 provides a summary of common disturbances in water, potassium, and sodium balances.

 

ACID-BASE BALANCE AND IMBALANCE

Homeostasis in body fluids is also affected by acid-base metabolism. The balance of free acids and bases within the body is regulated by the respiratory and renal systems and must be maintained within a very limited range in order to sustain life. The acidity of body fluids is affected by the con­centration of hydrogen ions in the blood, or blood pH. Blood pH is best measured by obtaining an arterial blood gas (ABG). Normal blood pH ranges from 7.35 to 7.45. A blood pH below 6.80 or higher than 7.80 is incompatible with life.

Acidosis is indicated by a blood pH below 7.35, while alka­losis is indicated by a blood pH above 7.45.

The respiratory system controls acid-base metabolism by retaining or releasing carbon dioxide (CO2), thereby caus­ing a shift in the bicarbonate-carbonic acid buffering system. The amount of dissolved carbon dioxide in the blood (pCO2) is measured by an arterial blood gas, and ranges from 35 to 45 mm Hg. Carbonic acid (H2CO3), is a weak, unstable acid, formed when carbon dioxide combines with water (HgO), that will dissociate into bicarbonate and one hydrogen ion (HCO3 + H⁺). The free hydrogen ions will combine with oxygen to form water. Bicarbonate and water can then be released or retained by the kidneys in order to maintain the necessary balance. Bicarbonate levels are measured by an arterial blood gas and range from 22 to 26 mEq/L. The abil­ity of the kidneys to excrete hydrogen ions and bicarbonate can be inferred from the blood bicarbonate level obtained from an arterial blood gas.

To maintain a stable acid-base balance, the body will try to maintain a 20:1 ratio between bicarbonate and carbonic acid, and an equilibrium of the carbonic acid and dissolved carbon dioxide found in blood. The lungs will compensate for pH changes caused by metabolic disorders (e.g., diabetes, vomiting, diarrhea) by controlling the carbon dioxide level in the blood. Hyperventilation or deep rapid breathing (Kussmaul respirations) will occur in an attempt to blow off carbon dioxide. The kidneys will compensate for pH changes caused by respiratory problems or a buildup of metabolic acids (e.g., lactic acid, hydrochloric acid, pyruvic acid, sulfuric acid) by controlling hydrogen ion and bicarbonate levels in the blood. However, renal compensation is much slower than respiratory compensation and often requires days to restore balance. Compensation is a body process used to restore blood pH to normal by changing the partial pressure of car­bon dioxide (pCO₂) or the bicarbonic ion concentration. (Figure 21-3 illustrates acid-base balance and imbalance.)

Acid-base imbalances are common in children and fall into four categories: respiratory acidosis, respiratory alkalo-sis, metabolic acidosis, and metabolic alkalosis. The body will compensate for these disturbances by using a renal or a res­piratory buffering mechanism. These responses are moni­tored by arterial blood gas analysis. Table 21-4 lists the causes, clinical manifestations, and management of the four acid-base disturbances.

Figure 21-3.  Acid-Base Balance and Imbalance

 

Respiratory Acidosis

Respiratory acidosis can be caused by any condition that decreases a child’s respiratory effort. Slowed or shallow res­pirations will result in a buildup of carbon dioxide, which combined with water forms carbonic acid and leads to acido­sis (4 pH, t pCO2). Many clinical conditions can cause res­piratory acidosis and are listed in

Box 21-1

.

Acidosis causes central nervous system depression. As a result, the child will be lethargic, confused, and disoriented, may complain of a headache, and, if not treated, may become comatose. Efforts are directed toward correcting the underly­ing cause by improving ventilation. Without correction, the body, via the kidneys, will attempt to neutralize the increased acid by increasing the retention of bicarbonate. However, the body’s attempt at compensation does not correct the underly­ing problem, and renal compensation is always slow.

BOX 21-1 Clinical conditions associated with respiratory acidosis   Asthma Croup/epiglottitis Cystic fibrosis Atelectasis Muscular dystrophy Pneumothorax Head trauma General anesthesia Drug overdose Brain tumor Sleep apnea Mechanical under ventilation

 

Respiratory Alkalosis

Respiratory alkalosis occurs when the carbon dioxide level is too low. This most commonly occurs from conditions that cause the child to hyperventilate (e.g., anxiety, pain, menin­gitis, gram-negative septicemia, early response to salicylate poisoning, mechanical overventilation). The child will often feel numbness or tingling in toes and fingers, lightheaded-ness, and confusion, and may faint. Renal compensation for respiratory alkalosis is rarely seen clinically because the underlying condition is often corrected before the kidneys have time to respond. However, if seen, the kidneys would retain free hydrogen ions and excrete bicarbonate. The child’s urine pH would increase as a result of the increased bicarbonate excretion.

Metabolic Acidosis

Metabolic acidosis is most commonly caused by a loss of bicarbonate in the stool or an increase in ketone bodies (e.g., acetoacetic acid, acetone, beta-hydroxybutyric acid) in the blood. These conditions most frequently result from diar­rhea and diabetic ketoacidosis. Children are often confused, lethargic, and tachycardic. The body compensates by increasing the depth and rate of respirations in order to blow off carbon dioxide.

Metabolic Alkalosis

Metabolic alkalosis occurs as a result of bicarbonate reten­tion or hydrogen ion loss. It is most commonly seen in chil­dren with prolonged vomiting, but also occurs with ingestion of large quantities of bicarbonate antacids, massive blood transfusions, loss of nasogastric fluids, and hypokalemia. A child experiencing metabolic alkalosis is often weak and dizzy, and may complain of muscle cramps. The respiratory response would be to increase pCC>9 by decreasing the rate and depth of respirations (hypoventilation).

DEHYDRATION

Dehydration is a critical condition that results from an extra­cellular fluid loss. Since a large portion of a child’s body fluid is located in extracellular spaces, a child is more susceptible to dehydration states than an adult. Dehydration that is not corrected will lead to hypovolemic shock and death.

There are three types of dehydration: hypotonic, isotonic, and hypertonic. Hypotonic dehydration occurs when there is a sodium loss that is greater than the water loss, resulting in the serum sodium falling below 130 mEq/L. When this occurs, the intracellular fluid becomes more concentrated and the body responds by moving fluid from extracellular spaces to intracellular spaces. While this response helps to reestablish an osmotic equilibrium within the body, it also increases the extracellular fluid losses and, if untreated, can result in shock. Hypotonic dehydration is commonly caused by inappropriate IV therapy, gastroenteritis, nephrosis, adrenal insufficiency, or not replacing gastric secretions. The child with this type of dehydration will appear sicker than the one with isotonic dehydration.

Isotonic dehydration occurs when the loss of sodium and water are equal so that the serum sodium level remains normal. Fluid loss is from both intracellular and extracellular spaces. Since there is no osmotic variation to cause a redis­tribution of water, the major loss of fluid comes from the extracellular spaces. This is the most common form of dehy­dration in children. Isotonic dehydration reduces plasma vol­ume and can result in hypovolemic shock. Losses are usually replaced by intravenous fluids that are high in sodium to prevent a drop in the serum sodium level. It is important that the serum sodium level be maintained between 130 and 150 mEq/L. If sodium drops below 130 mEq/L, the condi­tion then becomes hypotonic dehydration.

Hypertonic dehydration occurs when the loss of water is greater than the loss of sodium. Infants who are treated for diarrhea with fluids containing high concentra­tions of electrolytes may develop this type of dehydration. In this situation, the serum sodium level will rise >150 mEq/L, and serum osmolarity will increase. The body will compen­sate by pulling water from intracellular spaces to the intravascular compartment; thus, intravascular volume is maintained, and shock is less apparent. However, it is the most dangerous type of dehydration because the fluid replacement strategy is much more difficult to determine and manage. Hypertonic dehydration can also occur if the child has severe vomiting or diabetes insipidus.

Incidence and Etiology

Although the exact incidence of dehydration is not known, many common illnesses or any hospital procedure that requires a prolonged NPO status can cause a child to become dehydrated. Infants and young children are particu­larly vulnerable to developing dehydration. Some conditions that cause dehydration are listed in

Box 21-2

.

Pathophysiology

The body compensates for extracellular fluid losses in very specific ways. A decrease in the fluid circulating in the vascu­lar system lowers cardiac output and can lead to hypotension (a decrease in blood pressure). Blood pressure sensors in the heart, kidneys, and brain react quickly to increase cardiac out­put and increase sodium and water retention. Any decrease in blood pressure triggers sensory nerves in the aortic arch to stimulate the sympathetic nervous system, causing the fight or flight response or a release of epinephrine. Epinephrine improves cardiac output by increasing heart rate, cardiac con­tractility, and venous constriction. This compensatory mecha­nism helps to circulate the remaining blood faster but does not increase the circulating volume. Compensatory mecha­nisms within the kidneys activate the renin-angiotensin sys­tem, which improves circulating fluid volume by increasing sodium retention. Additionally, blood pressure sensors in the brain respond by releasing ADH, which stimulates thirst and retention of water by the kidneys. These compensatory mech­anisms are the body’s first line of defense but are only tempo­rary. Without prompt recognition and treatment, cardiac ischemia and arrhythmias will develop.

Clinical Manifestations

The clinical manifestations of dehydration depend on the degree of dehydration; however, in general, they include weight loss, rapid-thready pulse, hypotension, decreased peripheral circulation, decreased urinary output, increased specific gravity, decreased skin turgor, dry mucous mem­branes, absence of tears, and a sunken fontanel in infants. Clinical dehydration is classified as mild (<5% weight loss), moderate (5-10% weight loss), or severe (>10% weight loss). Table 21-5 lists the clinical manifestations associated with the degree of dehydration.

 

Diagnosis

A diagnosis of dehydration is determined based on the clini­cal manifestations that are identified during the history, physical examination, and laboratory tests. The most reli­able method for diagnosing dehydration is measurement of acute weight loss. However, because a child’s true pre-illness weight is rarely known in the acute care setting, an estimate of fluid deficit is made based on clinical assessment (Gorelick, Shaw, & Murphy, 1997). Laboratory findings are dependent on the type of dehydration. In hypotonic and isotonic dehydration, hemoglobin, hematocrit, glucose, blood urea nitrogen, creatinine, and protein are elevated due to a loss of circulating plasma fluid (hemoconcentration). Usually the urine is highly concentrated with a spe­cific gravity exceeding 1.030, is dark amber in color, and has a strong odor.

 

 

*- Classic symptoms of impending shock.

Treatment

How the dehydration state is treated depends upon the degree to which the child is dehydrated. Management focuses on correcting the fluid and electrolyte imbalances, and treating the underlying cause. The section on acute gas­troenteritis discusses treatment of mild, moderate, and severe dehydration associated with diarrhea and vomiting. Initially, fluids are replaced by giving an oral rehydration solutions (ORS). Oral rehydration therapy (ORT) has been recommended as the treatment of first choice for children with mild or moderate dehydration (American Academy of Pediatrics [AAP], Subcommittee on Acute Gastroenteritis, Provisional Committee on Quality Improvement, 1996). Rehydration solutions should contain glucose, sodium, potassium, and bicarbonate. Glucose must be present in order for the intestines to absorb sodium chloride. Appropriate oral rehydration solutions such as Pedialyte, Lytren, Infalyte, and Resol are available commercially. Other popular liquids such as soft drinks, fruit juices, broth, and athletic drinks (e.g., Gatorade, Powerade) should not be used for rehydration because they have high-carbohydrate content and low-electrolyte concentrations (Hugger, Harkless, & Rentschler, 1998).

For those who cannot afford to purchase commercially available rehydration solutions, a homemade solution can be prepared. The ability of the caregivers to follow formulation instructions should be assessed prior to recommending this alternative in order to assure accurate preparation. The recipes in

Box 21-3

are examples for homemade ORS.

Whenever possible, fluids should be replaced by the oral route. However, when dehydration is severe or life-threatening, when vomiting is uncontrollable, and when the child is unable to drink for other reasons, intravenous ther­apy is initiated. The rate of fluid replacement is dependent on the child’s degree of dehydration and the presence of car­diac, pulmonary, or renal problems. The volume of fluid to be given is based on the child’s weight and clinical signs and symptoms. The type of solution used varies with the type of dehydration. Generally, isotonic dehydration (most common type in children) is treated with isotonic fluids (fluids that have the same concentrations as normal body fluid), hypo-tonic dehydration with hypertonic fluids (fluids that are more concentrated than normal body fluid), and hypertonic dehydration with hypotonic fluids (fluids that are less con­centrated than normal body fluid). (Refer to Table 21-1.) Common solutions are Ringer’s lactate (RL) and normal saline (NS), including one-fourth and one-half strength.

Nursing Management Assessment

The skin is assessed for color, warmth, and turgor. Color indi­cates the state of perfusion and will turn from pink to pale, dusky, or gray as perfusion decreases. Perfusion is also reflected in the temperature of the skin. The skin will feel cool, and the child may complain of cold fingers and toes with decreased perfusion. Assess for capillary refill time, which will be increased. Additional measures of the quality of systemic perfusion include assessment of heart rate, blood pressure, and peripheral pulses. A postural change in heart rate is a useful cue in assessing fluid status in children over 4 years of age. When the child moves from a lying to a standing position, an increase greater than 20 beats per minute indi­cates hypovolemia. Changes in postural blood pressure have not been found to be useful in children under 9 years of age (Eliason & Lewan, 1998). Extracellular fluid losses will cause the skin to become dry and loose, referred to as a loss of skin turgor. Decreased skin turgor results in a tenting of the skin when pinched and indicates a decreased fluid state.

Mucous membranes are assessed for the presence of dry, sticky mucus and the absence of tears. Tears should be present if the child is crying. The loss of tears indicates fluid loss of at least 5% of the child’s body weight. In a child less than 18 months of age, it is also important to check the ante­rior fontanel. The fontanel should be even with the contour of the skull. When the child is dehydrated, the fontanel is often depressed or sunken in appearance. Weight is a critical indicator of the child’s fluid status and should be compared with a pre-illness weight, if available, or the weight from the previous day.

Intake and output should also be assessed. An assess­ment of output should include measurements of urine, stools, emesis, wound drainage, and an estimate of insensible fluid loss. The child’s urine should be observed for amount, color, and odor. Note the presence of blood or mucus in the stools. Watery stools should also be measured or estimated, and documented as output. If the child has any draining wounds, the dressings should be weighed to estimate fluid loss. Finally, excessive perspiration may require estimating fluid loss by weighing clothing or linens. The use of radiant warmers or warming lights can also increase insensible fluid losses in small infants and should be monitored. Several behavioral changes may also be present in children with dehydration. These include decreased activity levels, loss of interest in their environment, restlessness, irritability, lethargy, and a high-pitched, weak cry. The last assessment should include a review of serum electrolyte results.

Nursing Diagnoses

Nursing diagnoses appropriate for a child with dehydration may include:

•     Deficient fluid volume related to excessive fluid vol­ume loss or inadequate fluid intake.

•     Risk for injury (fall) related to orthostatic (postural) hypotension.

•     Deficient knowledge (caregiver) related to lack of exposure to information about preventing/detecting dehydration.

Outcome Identification

•      The child will receive sufficient fluids to replace losses.

•   The child will exhibit signs of adequate hydration.

•   The child will not fall or sustain other injuries while hypotensive or lethargic.

•      Caregivers will demonstrate understanding of conditions that can lead to dehydration and of the early signs and symptoms.

Planning/Implementation

Nursing interventions include administration of IV fluids, assessment of daily weight, vital signs, and maintenance of accurate intake and output records. Injury due to falls can be prevented by making sure that the side rails of the bed are raised, assessing level of consciousness, and monitoring the serum sodium level. An elevation in serum sodium will cause the brain cells to dehydrate and result in a loss of con­sciousness if not corrected quickly. An informed nurse will be able to recognize the signs and symptoms of dehydration as they develop and to initiate an appropriate plan of care immediately.

Evaluation

Evaluation is accomplished by assessing for a decrease or absence of the defining characteristics of dehydration or electrolyte imbalance. This is accomplished by continued reassessments. To evaluate the effectiveness of the nursing interventions, explore the answers to the following ques­tions: Is the child able to take in adequate fluids and food? Is the child gaining weight? Are the child’s electrolytes within normal limits? Is the child alert and interactive? Does the family understand how to manage the child’s care at home?

Family Teaching

Dehydration can be managed at home if the caregivers are well informed and prepared. They need to know the signs of dehydration. They should watch for lethargy or changes in their child’s normal behavior. Recommend rehydration flu­ids, and discuss how to administer them. Caregivers should also be alert to changes in their child’s urine output. How often has the child voided? How much with each void? Is the urine dark or concentrated? Help them to be able to make accurate decisions as to when to contact a health care provider (no improvement after 4 hours of rehydration fluid, inability to retain fluids, decreasing urine output, and change in mental alertness).

ACUTE GASTROENTERITIS

Acute gastroenteritis, an inflammation of the mucous mem­branes of the stomach and intestines, is defined as diarrheal disease of rapid onset with or without accompanying mani­festations such as nausea, vomiting, fever, and abdominal pain. Most cases of gastroenteritis are self-limited; however, more severe or prolonged illnesses can result in dehydration with significant morbidity and mortality.

 

Incidence and Etiology

Acute gastroenteritis accounts for as many as 4.5 million deaths each year worldwide (Gerchufsky, 1995). In the United States, this illness is responsible for 200,000 hospital-izations and 500 deaths in children younger than 5 years of age (AAP, 1996). Children who attend day-care centers, schools, institutions, and other facilities are especially sus­ceptible to episodes of gastroenteritis.

The etiology is due to a variety of organisms such as viruses, bacteria, and parasites. Table 21-6 lists the causes of acute gastroenteritis. In the United States, the majority of cases are of viral origin, specifically Rotavirus and Norwalk virus (Eliason & Lewan, 1998). Rotavirus infection occurs in cooler months, beginning in November in the Southwest and peaking in February or March in the East. It is transmit­ted via the fecal-oral route, primarily affecting children 6 months to 2 years of age. By age 2 years, most children are immune to severe dehydrating rotaviral diarrhea (Meyers, 1995). Norwalk viruses primarily affect older children and are a major cause of epidemic gastroenteritis worldwide, especially in developing countries. Several pathogens (Shigella, Salmonella, Campylobacter) are responsible for bacterial infection. Shigella is spread by person-to-person contact or by ingestion of contaminated food. Salmonella is transmitted through contact with infected animals, such as pet turtles, hamsters, dogs and cats, and from contaminated food products, such as poultry eggs, and milk. Giardia and Cryptosporidium are the most common intestinal parasites that produce disease. Giardia is transmitted through inges­tion of cysts either from contact with an infected individual or from food or water contaminated with infected feces. It is endemic in some areas, with a very high occurrence rate in day-care centers.

Pathophysiology

The pathophysiological process of viral infection is poorly understood; however, it is hypothesized that the virus destroys or damages the epithelial cells lining the intestines. Viral illness is self-limiting, and recovery involves regeneration of these cells. There are three processes that produce bacterial gastroenteritis (

Box 21-4

).

 

Clinical Manifestations

The clinical manifestations depend on the causative organ­ism; however, in general, signs and symptoms include diar­rhea, nausea, vomiting, abdominal pain, weight loss, fever, dehydration, and electrolyte imbalances.

Diagnosis

Diagnosis is based on the history, physical exam, and labora­tory studies focused on evaluating the child’s hydration status and identifying the causative agent. The history should include the following data:

•         Recent exposure to infectious agents

•         Travel history, especially if outside the Unites States

•         Exposure to contaminated food and water supplies

•         Exposure to turtles

•         Attendance at a day-care center

The child’s hydration status is evaluated, including a history of fluid intake, such as types, amounts, and how tolerated. The stooling pattern, frequency, and volume, as well as uri­nation frequency, amount, and color is also investigated. Current weight compared to pre-illness weight is useful in determining fluid loss.

 

 

 

Generally, if no systemic manifestations are present (fever, lethargy, malaise) and if dehydration is absent, diag­nostic laboratory tests are not indicated. Stool cultures should be performed for children with a fever lasting more than 24 hours, blood or mucus in the stool, a family or household member with similar symptoms, or a positive stool white blood cell stain (Galen, 1997). The finding of white blood cells should prompt further investigation to rule out invasive bacterial disease. Rotavirus can be diag­nosed by testing the stool using a commercially available kit or electron microscopy. In cases where a parasitic infection is suspected, the stool is examined for ova and parasites.

If dehydration is present, additional tests may be per­formed to evaluate hydration status such as CBC, urinalysis, blood urea nitrogen (BUN), and electrolyte studies. If the child is dehydrated, the hemoglobin, hematocrit, and BUN will be elevated. The presence of ketones in the urine reflects increased fat metabolism due to caloric deprivation. Metabolic acidosis is common with severe dehydration and diarrhea.

Treatment

Treatment for acute gastroenteritis focuses on fluid replace­ment and correction of electrolyte disturbances, and is dependent on the degree of dehydration (Table 21-7). Initially management should begin at home since early inter­ventions can reduce complications such as dehydration and poor nutrition. The most important aspect underlying home treatment is the need to administer increased volumes of appropriate fluids as well as to maintain adequate caloric intake.

Children with no dehydration and mild diarrhea may be treated with 10 ml/kg of ORS to replace fluid lost with each stool. However, since most children who are not dehydrated dislike ORS, they can be offered age-appropriate foods and additional fluids. Breast milk, cow’s milk, and full-strength formula can continue to be consumed (Hugger, et al., 1998).

If the child is mildly dehydrated, 50 ml/kg of ORS should be given over 4 to 6 hours. Losses from diarrhea stools and emesis are replaced with an additional 10 ml/kg. Once the dehydration is corrected, the child can resume solid foods. Although there is controversy about which foods are best for refeeding, complex carbohydrates, lean meats, fruits, and vegetables are well tolerated (AAP, 1996).

 

Used with permission from Hugger, J., Harkless, G., & Rentschler, D. (1998). Oral rehydration therapy for children with acute diarrhea. The Nurse Practitioner, 23(12), 52-64.

 

The child with moderate dehydration should be given 100 ml/kg of ORS over 4 to 6 hours, with replacement of losses from diarrhea and vomitus over this same period. When dehydration is corrected, feeding can be resumed as discussed previously. Severe dehydration requires intra­venous therapy using isotonic solutions. The fluid is adminis­tered in boluses of 15 to 30 ml/kg every 20 minutes until hypovolemia is corrected (Eliason & Lewan, 1998). Electrolyte levels must be determined, and frequent reeval-uation of the child’s condition is essential. ORT can be insti­tuted when the child’s condition stabilizes. When rehydration is completed, the child can be fed according to the AAP guidelines (complex carbohydrates, lean meats, fruits, and vegetables).

Vomiting occurs frequently in children with gastroen­teritis; however, most of them with this manifestation and dehydration can be treated with ORT. The guiding principle is to administer small volumes (5 ml) frequently (every 1 to 2 minutes). As vomiting diminishes, larger amounts of ORS can be given at longer intervals.

For most cases of bacterial or viral gastroenteritis, the use of antiemetics, absorbent agents, and gut motility medications is not recommended. The vomiting and diarrhea accompany­ing this illness are the body’s method of eliminating the infect­ing organism, and these drugs can decrease the speed at which this is accomplished. When Salmonella or Shigetta are the causative organisms, the gastroenteritis is usually self-limiting, and antibiotic therapy is unnecessary. However, antibiotics are recommended for infants under 3 months of age who are at risk for Salmonella bacteremia. There are no effective antiviral medications. Parasitic infections are treated with medications such as quinacrine hydrochloride (Atabrine), furazolidone (Furoxone), or metronidazole (Flagyl).

 

 

Family Teaching

Teach the child and other family members that careful hand-washing must be practiced, especially after diapering, after using the toilet, and before feeding or eating.

Caregivers should be instructed to change diapers fre­quently to prevent irritation to the skin. Wash perineal area with mild soap and water after each diarrheal stool. Apply protective ointments to buttocks. Avoid the use of commer­cial baby wipes.

Teach them the method for monitoring intake and out­put: record amount of fluids taken; frequency, consistency, and color of stools; frequency and characteristics of vomitus; number of wet diapers per day; weighing wet diapers; and number of voids per day.

Explain signs and symptoms of dehydration, and rein­force the importance of administering ORS and maintaining hydration even in the presence of vomiting. Explain proper food handling techniques (cleaning of cutting boards and food preparation surfaces with hot water and soap; washing  hands before and after food preparation; not allowing fresh foods to be contaminated by contact with meat, poultry, or seafood juices).

Tell the caregivers to contact health care provider when (a) the child seems confused or disoriented; (b) vomiting continues for more than 12 hours; (c) blood appears in the diarrhea or diarrhea increases in frequency (bowel move­ment every hour for more than 8 hours; more than 10 watery bowel movements in one day); (d) there is continuous abdominal pain or intermittent pain that is severe enough to make the child cry or to awaken from sleep; (e) temperature over 100°F for more than 72 hours; (f) child does not urinate for more than 6 hours; (g) crying produces no tears; or (h) infants anterior fontanel appears sunken.

 

EDEMA

 

Edema is an excess accumulation of interstitial fluid that usually results from a disturbance in the fluid exchange between capillaries and interstitial spaces.

Incidence and Etiology

Edema is associated with many illnesses. Heart failure, renal failure, and acute pulmonary edema cause an increase in blood hydrostatic pressure that results in the formation of edema. A loss of blood protein or albumin (often seen with liver disease, nephrotic syndrome, or malnutrition) will cause a shift of fluid into interstitial spaces due to a decrease in blood osmotic pressure. Burns, allergic reactions, and inflammation alter the integrity of the capillary membrane, resulting in the movement of fluid and blood proteins into interstitial spaces. Hypothyroidism and tumors that obstruct the lymphatic system cause an increase in interstitial osmotic pressure that will pull fluid into the interstitial space, result­ing in the formation of edema.

Pathophysioiogy

Edema develops as a result of changes iormal capillary dynamics. Normal capillary dynamics are maintained by bal­ancing hydrostatic and osmotic pressures both within the capillaries and within the surrounding interstitial spaces. Hydrostatic pressures tend to push fluid out of a compart­ment, and osmotic pressures pull fluid into a compartment. Edema may be caused by four mechanisms: increased blood hydrostatic pressure, decreased blood osmotic pressure, increased interstitial fluid osmotic pressure, and impaired lymphatic drainage.

Increased Blood Hydrostatic Pressure

Blood hydrostatic pressure is the pressure of blood against the capillary walls that tends to push fluid out of the capillaries into the interstitial spaces. When this pressure is increased (as in increased capillary flow), excess fluid may enter the interstitial area, and edema is the result. Venous congestion may also increase the blood hydrostatic pressure by back pressure, as seen in heart failure.

Decreased Blood Osmotic Pressure

Severe and widespread edema may occur when the serum albumin is decreased. Albumiormally contributes to the inward pull of blood osmotic pressure. With decreased num­bers of albumin particles, this inward pull diminishes and fluid leaks out into the interstitial area. A decrease in serum albumin may be caused by either albumin loss or diminished albumin synthesis. The most common condition associated with massive albumin loss is nephrotic syndrome. Decreased albumin syn­thesis accompanies severe protein-calorie malnutrition.

Increased Interstitial Fluid Osmotic Pressure

Normally the interstitial fluid osmotic pressure is small com­pared to the blood osmotic pressure because of the absence of large amounts of protein in the interstitial Quid If protein leaks into this fluid, increased interstitial fluid osmotic pres­sure results, and edema develops. The major cause of this process is increased capillary permeability due to major burns and locally with inflammation (sprained ankle) and hypersensitivity reactions (bee sting).

Impaired Lymphatic Drainage

The lymph vessels normally drain small amounts of fluid and protein from the interstitial spaces and return them to the capillaries. However, if the lymph drainage is impaired through obstruction by a tumor or surgery, fluid and proteins accumulate in the interstitial area, causing edema.

Clinical Manifestations

Edema results in swelling, either localized or general. In most cases, edema in children is manifested initially perior-bitally or dependently. If the child is ambulatory, dependent edema will be evident in the ankles. Children on bed rest will have edema in the sacral area. Pitting edema is always a clear sign of an extracellular fluid excess. It is assessed by pushing a finger gently into the edematous tissue and observing for an indentation on the skin. The degree of edema is rated on a four-point scale:

+0 = No persisting indentation

+ 1 = ¼ ” indentation (mild)

+2 = ¼ – ½ ” indentation (moderate)

+3 = ½  – 1″ indentation (severe)

+4 = greater than 1″ indentation (very severe)

 

Edematous areas may also appear shiny and full. Additional signs may include a sudden weight gain, an elevation in blood pressure, a bounding pulse, neck vein distention, and dyspnea.

Diagnosis

A diagnosis of edema is determined based on the clinical manifestations that are identified during the history and physical examination. It is important to determine the underlying cause so that appropriate treatment is initiated.

Treatment

Treatment for edema is focused on correcting the underlying condition and often includes the use of diuretics and restric­tion of sodium and fluid intake. Diuretics are given to pro­mote fluid excretion through the kidneys. Since most diuretics cause potassium losses, it is extremely important to monitor serum potassium levels and provide potassium sup­plements as necessary. Edema that is due to an inflammatory response, such as an injury or allergic reaction, can be treated by applying cold compresses to reduce blood hydro­static pressure by decreasing capillary blood flow.

Nursing Management

Nursing management begins with a thorough history and phys­ical assessment. Note the location and extent of the edema. The caregiver may note that the child complains of tight shoes by the end of the day; eyes may appear puffy due to periorbital edema; or the child may complain that his fingers are swollen or feel like sausages. The child may also voice concerns about looking fat. Assess for alterations in body image. Ask if the edema is causing any pain or restriction of movements.

The nurse must maintain accurate measurements of intake and output as well as body weight, which should be measured on the same scale at the same time each day. When diuretics are used, blood electrolytes should be monitored for a potassium depletion. If daily measurements of an edematous limb or abdomen are performed, it should be taken at the exact same location with the same measuring tape. Double check any measurement that shows a dramatic increase or decrease. Edematous limbs should also be checked for circu­lation integrity by assessing peripheral pulses. Elevating the limb on a pillow will also help the reabsorption of extracellular fluids. Vital signs are important to monitor especially blood pressure and respiratory rate. An increasing blood pressure reflects an increased loss of fluids into extracellular spaces; an increased respiratory rate, along with the presence of rales, often reflects pulmonary edema. Consider elevating the head of the bed if pulmonary edema is suspected.

Family Teaching

Prevention of skin breakdown is paramount. Teach care-givers the importance of good skin care for their child. Edematous tissue is very fragile and, if not kept dry and free from friction, it can easily break down. Special care must be taken to keep the diaper area clean and dry. An infant or child on bed rest should be turned every 2 hours to prevent pressure sores. If the child is on a potassium-depleting diuretic, encourage caregivers to include potassium-rich foods and fluids in the diet such as bananas, apricots, cantaloupe, dates, tomato juice, orange juice, peaches, potatoes, raisins, and figs. Older children may need to be reassured that the edema will be temporary.

BURNS

Significant research-based advances over the past 50 years in fluid therapy, wound care management, respiratory, metabolic, and nutritional support have improved the survival rate for children with burns (Greenfield & Jordan, 1996; Periti & Donati, 1995), The deliver)’ of ideal burn care requires a team of health care providers working together, and carefully assessing and timing the treatments necessary for survival. The team must establish a communication system that includes the child’s family so that they can be fully informed of the current care and prepared for future treatments. Although these advances are noteworthy, burns still result from accidents that, for the most part, could have been pre­vented. Health care providers need to be concerned not only with burn management but also with burn prevention (Forjuoh, 1998).

Incidence and Etiology

Estimates show that 1.25 million people in the United States are burned yearly, 5,500 people die from fire-related burns, 51,000 people are admitted to hospitals for burn care, and 80-90% of the burn injuries are potentially preventable (Brigham & McLoughlin, 1996). Approximately one-third to one-half of the yearly hospitalizations for burns occur in chil­dren younger than 18 years of age (Hansbrough & Hansbrough, 1999). At least half of these accidents involve children under 15 years of age, with 1,000 deaths a year in this age group. Deaths from fires and burns are second only to those from motor vehicle accidents in these children (American Academy of Pediatrics, Committee on Injury and Poison Prevention, 2000).

There are four major types of burns: thermal (most common in children), electrical, chemical, and radiation. (1) Thermal burns occur from flames, flash, scalds, or contact with hot objects. Flame injuries are caused by ignition of combustible materials and contact with the fire; household or residential fires are responsible for most flame burns. Flash injuries are caused by explosions, especially of combustible fuels such as gasoline, kerosene, and charcoal lighter. Scald burns occur when hot liquids spill on a child or from hot tap water. Contact burns result from exposure to a hot object   such as an oven, hot irons, and radiators. (2) As children become more mobile and curious, they are exposed to addi­tional household burn hazards such as electricity. Chewing on electrical wires or inserting objects into electric sockets can cause electrical burns. (3) Chemical burns are caused when children ingest or are exposed to caustic agents such as household cleaning products. (4) Radiation burns commonly result from overexposure to the ultraviolet rays of the sun.

The majority of burn injuries in children are related to scalds (85%), which are most common in those under 4 years of age (Hansbrough & Hansbrough, 1999). Flame burns pre­dominate in older children and adolescents and account for 13%. The remainder include electrical and chemical.

Since 16% of burns are due to child abuse, it is extremely important to make a determination of cause (Herrin & Antoon, 1996). Was the burn accidental or intentional? Physical findings that are inconsistent with the reported his­tory or incompatible with the child’s motor ability, an unclear history of the injury, a delay in seeking treatment, and con­flicting stories about how the burn occurred should alert the health care provider to the possibility of an inflicted injury. Additionally, certain types of wounds are noted in child abuse cases: immersion burns (i.e., stocking and glove burns with a clearly demarcated line at the ankle or wrist), doughnut-shaped burns on the buttocks, burns from a cigarette or an iron. This information should be documented thoroughly (Hultman, et al., 1998). If abuse is suspected, a referral should be made to hospital and community resources. Figure 21-4 illustrates an immersion burn of a child’s hand.

 

Figure 21 -4   Immersion Burns of a Child’s Hand. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

Pathophysiology

The impact of a burn can range from a minor local injury to a multisystem involvement when a major burn is sustained. All organs and body systems are affected. Table 21-8 lists the alterations of the cardiovascular, renal, respiratory, gastroin­testinal, and central nervous systems as well as the changes in metabolism.

Clinical Manifestations

The severity of the burn is determined by the depth of the tissue destroyed and the total body surface area involved. In the past, burns were classified as first, second, third, and fourth degree. However, currently burns are categorized based on the depth of tissue destruction into superficial, par­tial, and full thickness wounds. First degree burns are cate­gorized as superficial thickness, second degree as partial thickness, and third and fourth degree burns as full thick­ness. Both classification methods are used in many clinical settings. Figure 21-5 illustrates the tissues involved with dif­ferent depths of injury.

Superficial (first degree) burns involve only the epidermis, are very painful and red, and heal spontaneously in approximately 5 to 10 days without scarring. Systemic effects are uncommon. An example of a superficial burn is a minor sun­burn (Figure 21-6). In a partial thickness burn (second degree), the epidermis and upper layers of the dermis are destroyed. The skin is moist, bright red, extremely painful, and sensitive to cold air. It is common to see blisters form that will blanch with pressure. These wounds will usually heal within 14 to 21 days and may result in some scarring if the burn involves the deep dermal layers of the skin (Figure 21-7). Third degree burns (full thickness) involve the epidermis, dermis, and extend into the subcutaneous tissues. These burns usually will form eschar, thick leather-like dead skin (Figure 21-8). Fourth degree burns, also known as full thickness, extend into the ten­dons, muscles, and bones and are usually caused by electrical burns. Full thickness burns are characterized by a whitish, leathery, dry appearance that has a decreased sensation to pain. These burns will result in scarring and contractures and will require skin grafting, skin flaps, or possible amputation to fully heal (Greenfield & Jordan, 1996).

 

 

 

1: Superficial Thickness Burn (First degree)

2: Partial Thickness Burn (Second degree)

3: Full Thickness Burn (Third degree)

4: Full Thickness Burn (Fourth degree)

Figure 21-5.   Depths of Burns and Corresponding Tissues Involved. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

Figure 21-6.   Child with a Superficial-Thickness (First Degree) Burn. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

 

Figure 21-7.   Child with a Partial-Thickness (Second Degree) Burn with a Blister. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

The extent of the burn injury is usually expressed as the percentage of the total body surface area (TBSA) affected. In children, the most accurate method of determining the area burned is by mapping the injured areas on a Lund and Browder-like body chart, taking into account the propor­tional changes that occur during growth. Figure 21-9 is an example of a chart for estimating the extent of burns on a child. If such a chart is not available, the palm of the child’s hand, representing 1% of body surface area, can be used to estimate the extent of the burn. Calculation of the percent of body surface area burned is important in determining fluid resuscitatioeeds.

 

Figure 21-8   Child with a Full-Thickness (Third Degree) Burn. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

Once the extent and depth of the burn is determined, the burn can be classified as minor, moderate, or major (Table 21-9). Additional variables to consider should include the type of burn, the presence of associated injuries, the age of the child, and the presence of any chronic health condi­tions and/or social problems. Minor burns can generally be treated on an outpatient basis, while moderate and severe burns require hospitalization. Community hospitals are usu­ally equipped to manage moderate burns. However, a child with major burns or involving the hands, feet, face, eyes, ears, and genitalia should be stabilized and then transferred to a pediatric burn unit, PICU, or pediatric burn care center.

Diagnosis

A diagnosis of burns is determined based on the clinical manifestations that are identified during the history and physical examination.

Treatment

The emphasis of treatment for major burns includes the fol­lowing: respiratory management, fluid resuscitation, pain management, wound care, prevention of impaired mobility, nutritional support, and psychological support.

Respiratory Management

Initial treatment consists of assessing for patency of the air­way and establishing and/or maintaining it. Pulmonary com­plications remain the leading cause of death in thermal burns. Anticipate respiratory involvement if the burn occurred in an enclosed space or if the child was found unconscious. Oxygen should be administered if hypoxia is present. It is important to assess the child’s ability to expand the chest. Full thickness burns that fully extend around the child’s trunk may interfere with breathing. An escharotomy, an incision made into constricting eschar to restore periph­eral blood circulation, may be required to release the chest constriction. Arterial blood gases will also provide evidence of smoke inhalation and the adequacy of gas exchange. A child who has upper body burns, facial burns, or smoke inhalation is at risk for airway obstruction from edema (Figure 21-10). Intubation may be performed if the child exhibits face and neck edema, soot in the nose or mouth, or singed nose hairs.

Fluid Resuscitation

All burn injuries alter capillary permeability and, if severe enough, will require fluid replacement. Fluid resuscitation is a major focus of seriously burned children during the initial treatment period in order to prevent hypovolemic shock. The goal is to infuse intravenous fluids (usually Lactated Ringers solution) at a sufficient rate and volume to compensate for increased capillary permeability and the loss of intravascular fluids. A large-bore central venous catheter is used in order to administer massive fluid loads. A variety of formulas are available as guidelines for fluid volume and rate of adminis­tration; however, each is based on the relationship between body weight and total body surface area burned. The Parkland formula is one that is frequently used (

Box 21-5

).

The fluid formula requirements are generally 2-4 ml/kg of body weight times the TBS A. Formulas are only guides to resuscitation, and actual fluid administration rates are based on the child’s response. Adequacy of the resuscitation is reflected in urine output of 1-2 ml/kg/hr, stable vital signs, and alert and oriented mental status. A Foley catheter is inserted to facilitate urine output measurement. If the urine output falls below this amount, the child is not receiving adequate fluids and may develop renal tubular obstruction if not corrected quickly.

After initial fluid resuscitation, capillary permeability is regained. At this time, the child’s urine output will increase dramatically because interstitial fluids are pulled back into the bloodstream. Intravenous fluids should be decreased to maintenance levels to prevent fluid overload and pulmonary edema. The type and amount of fluid used will be based on the results of blood electrolyte tests.

Figure 21-9   Estimation of the Extent of Burns in Children. Courtesy of The Shriners Burn Hospital; Cincinnati, Ohio.

Pain Management

 

The pain following a burn is both acute and chronic. Thermal destruction of tissue results in one of the most severe and prolonged types of pain known. Pain from the injury is compounded by performing procedures on the wound, especially dressing changes. It is considerably reduced when the child is at rest. Other factors such as fear and anxiety contribute to the child’s perception of pain. For children with major burns, intravenous narcotics such as morphine sulfate are indicated. Initially, these drugs are administered intravenously because the fluid shift limits absorption from the subcutaneous and intramuscular areas, and the pain will not be relieved. Acetaminophen with codeine is usually given to children with minor burns. Children should always be assessed for pain using appropri­ate assessment tools for the child’s age. Nurses have a tendency to undermedicate children due to an unrealistic  fear of respiratory depression (Ashburn, 1995; Patterson, 1995). Pain medications should be given prior to all painful procedures. Children often do better if they have some control over their pain. Therefore, patient-controlled analgesia is now commonly used with children and has been found to be effective in decreasing pain (Ashburn, 1995). Children also respond well to behavioral interventions such as imagery, relaxation therapies, and hypnosis.

 

 

 

 

Figure 21-10 A Girl Who was Wearing Flame Retardant Pajamas with Burns from a House Fire. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

BOX 21-5 Parkland formula for fluid resuscitation 4 ml Lactated Ringer’s solution x kg of body weight x % total body surface area burned 1.    One-half of total is given in the first 8 hours post-burn. 2.    One-fourth of total is given in the second 8 hours postburn. 3.    One-fourth of total is given in the third 8 hours postburn.   Note: Time is calculated from the time of the injury, not the time of admission to the hospital.

 

 

 

 

 

 

 

 

Wound: Care

Initial wound care is started after the child has been stabi­lized, Care should be taken to use aseptic techniques when cleaning the burned areas and to medicate the child prior to the procedure. The wounds are gently cleaned and debrided. Debridement is the removal of dead tissue from the burn site and is associated with severe pain. This proce­dure is performed by soaking the wound for about 10 min­utes to soften the tissue. The wound is then washed from the inner to outer edges using a firm, circular motion. Any loose or dead tissue is removed by gently lifting it up with forceps and cutting it away. After the wound and surrounding areas are cleaned, an antimicrobial cream, such as silver sulfadi-azine (Silvadene), is applied to minimize bacterial prolifera­tion and prevent infection. Some type of dressing is then applied. Table 21-10 lists several topical agents used in treat­ing burn wounds. Figure 21-11 shows a child having Silvadene applied to a burn wound.

Hydrotherapy is used to soften dead tissue to help in the debridement process and to improve circulation to the wound. The experience is very painful and scary for all burn clients (Greenfield & Jordan, 1996). Children should be medicated prior to hydrotherapy and dressing changes. It is helpful if caregivers can be present to comfort and distract the child. Figure 21-12 shows a child in a whirlpool bath.

Burn dressings are changed once or twice a day. Sheridan, Petras, Lydon, and Slavo (1998) studied the fre­quency of burn dressing changes in 50 children with an aver­age burn size of 11% TBS A and found that once daily dressing changes were just as effective as twice daily. Results showed a significant savings of nursing staff time and a decreased need for pain medication with no change in infec­tious morbidity. Since dressing changes are very frightening, painful, and costly, the researchers recommend changing burn protocols appropriately

 

 

Figure 21-11.   A Child Having Silvadene Applied to a Scald Burn of the Chest. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

Once the wounds have been debrided and are beginning to heal, various temporary skin grafts can be used to facilitate the healing process. These include homografts (cadaver skin), heterografts (pig skin), and synthetic skin coverings. (Greenfield & Jordan, 1996; McCain & Sutherland, 1998). Homografts can remain in place until donor site tissues are available. Typically, homografts will begin to slough off around 14 days. Pigskin dressings are replaced daily or every other day. They are often used in children with scald burns of the hands and face because they allow free movement and reduce risk of contracture formation. Temporary grafts accel­erate wound healing by creating an environment that pro­motes epithelial growth in the form of granulation tissue. Adequate granulation tissue must be present before the child can be permanently grafted. Figure 21-13 demonstrates a child’s hand with red granulation tissue.

Extensive full thickness burns will require a permanent skin graft, an autograft, to fully heal. The skin for an auto-graft is taken from an unburned area of the child’s own skin. Once an autograft is placed on the wound, the area must be immobilized. This is often difficult in children requiring the use of splints or casts (Staley & Serghiou, 1998). Another permanent skin graft is a cultured epithelial autograft, which is only used in children with burns covering >80% TBS A. They are sheets of skin grown in the lab from a small skin biopsy of the child. Long-term follow-up studies to determine effectiveness are still pending. However, the ability to grow cultured epithelium offers the possibility of an unlimited source of skin for children with extensive burns.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 21-12   A Child with Burns on the Legs in a Whirlpool. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

Figure 21-13  A Child’s Hands with Red Granulation Tissue. Courtesy of Dr. Robert Arensman, Chief Pediatric Surgery. Children’s Memorial Medical Center, Chicago.

 

After the grafts heal, pressure dressings are applied to prevent the formation of contractures and to minimize scar­ring. These dressing may be elastic wraps, pressure splints, or pressurized garments that provide continuous and uni­form pressure over the burned areas. The elasticized gar­ments are usually worn for several months, and therefore, need to be altered as the child grows.

Prevention of Impaired Mobility

Children are at risk for impaired mobility and the develop­ment of contractures due to prolonged bed rest, muscular atrophy and shortening, and stiffening of burned tissues. It is essential to implement appropriate positioning strategies to prevent deformities and an exercise program to maintain muscle strength and joint mobility. When joints are not being exercised, they should be maintained in maximal extension using splints if needed. Particular attention should be paid to the hands and neck since these are the most prone to rapid contractures. Early exercise is encouraged and compliance can be improved with judicious use of anal­gesics. Range of motion exercises are performed actively at least three times a day. Active range of motion of muscles is possible in infants and toddlers by using familiar toys; how­ever, most of the joints will require passive range of motion exercises. Caregivers can support and encourage older chil­dren to participate in active range of motion.

 

Nutritional Support

Children have limited glycogen stores to meet the increased energy demands of a burn injury. The burned child will require two to three times the normal amount of calories in order to heal. Children with severe injuries will require some form of caloric supplementation. The diet should be high in protein (23% of total calories) to maintain weight and muscle function (Demling & DeSanti, 1998; Mayes, Gottschlich, & Warden, 1997). Nutrition protocols also call for the addition of a multivitamin with increased amounts of vitamins A and C to help replace the losses from the changes in metabolism and losses from the open burn wounds (Mayes, et al., 1997). Children should be offered a variety of foods and be allowed to choose meals when they feel better. They will often eat more if they have their meals with other children or family members. Most children with major burns are unable to meet their nutritional requirements orally; therefore, it is necessary to use enteral feedings. Changes in stools (increased stooling, diarrhea) may indicate that the child is not tolerating the feedings.

Psychological Support

Anxiety for the child and caregivers can be overwhelming. Play therapy is used to help the child deal with the frustrations of burn therapy. It encourages the child to move and actively participate in activities with other children. As recover)’ con­tinues, counseling with various support services may be imple­mented to foster the child’s self-esteem. Caregivers also need to be supported and encouraged to participate in the care of their child, which is often very reassuring for both of them (Barnum, Snyder, Rapoff, Mani, & Thompson, 1998; Kendall Grove, Ehde, Patterson, & Johnson, 1998; Meyers-Paal, et al., 2000; Thompson, Boyle, Tell, Wambach, & Cramer, 1999).

Research on the long-term adjustment of children and families has found that they adjust well to school and their communities with the support of teachers, social workers, and community outreach groups such as burn camps (Kendall-Grove, et al., 1998; Thompson, et al., 1999). Caregivers recover on a slower basis and are often faced with divorce and many financial concerns.

Family Teaching

The home care needs of the family should be addressed long before the child is ready for discharge. Discharge teaching often includes nutrition and diet requirements, daily dress­ing changes and skin care, application of elasticized gar­ments (Jobst jacket or pants), application of splints, and daily range of motion exercises. Discharge teaching books are often helpful for families to refer to as they learn. However, these books must take into consideration the educational, ethnic, and language backgrounds of the caregivers (Jenkins, Blank, Miller, Turner, & Stanwick, 1996). Caregivers need support and encouragement to perform these treatments appropriately. Remember, most of these daily routines will be painful for the child. If not done well, the child’s wounds will not heal appropriately. Caregivers, who may feel guilt because of the child’s burns, often have trouble doing painful procedures without support. Home care should emphasize returning the child to as many independent tasks as possible. Home tutors may be necessary to help the child keep up with school. Support is ofteeeded to help the child and school personnel prepare for the child’s return to the class­room. Encourage all involved to explore their feelings and be supportive of the child’s return to the community.

Burn Injury Prevention

All burns are preventable by establishing a few safety pre­cautions. Since house fires are responsible for the majority of burn-related deaths in children under five years of age, families should be encouraged to have working smoke detectors in their home and establish a prearranged escape route. Scalds are the most commoonfatal burn, so remembering to turn pot handles inward on the stove and keep young children away from bowls and cups of hot liquid will help prevent burns. Setting the hot water heater ther­mostat no higher than 120°F will help to prevent scald burns from bath water. Erecting barriers around space heaters and keeping children away from stoves will also help. Electrical burns can be prevented by inserting plastic plugs into light sockets and keeping electrical cords out of sight and reach so that children cannot chew on them. Chemical burns from cleaning solutions can be prevented by storing all cleaning solutions in locked cabinets and by watching children carefully when cleaning solutions are being used. Radiation burns from ultraviolet light are easily prevented by using sunscreens and wearing protective clothing (Forjuoh, 1998). Burn prevention strategies should be discussed openly with caregivers during all health care encounters with the family.

Key Concepts

·            Forty percent of an infant’s body water is located in extracellular spaces. ECF is the first to be lost during illnesses, putting infants at a greater risk for dehydration.

·            Body fluids move as a result of the type of membrane to be crossed, changes in the permeability of capillaries, and the amount and type of solutes present.

·            The respiratory system compensates for changes in blood pH caused by metabolic conditions by retaining or releasing carbon dioxide.

·            The kidneys compensate for changes in blood pH caused by respiratory problems or a buildup of meta bolic acids by controlling hydrogen ion and bicarbon­ate levels in the blood.

·   Renal compensation is much slower than respiratory compensation.

·   Urine output should be maintained at 1-2 ml/kg of body weight per hour.

·   Assessing the specific gravity of the urine is a quick way to assess the hydration status of a child. The higher the specific gravity, the more dehydrated the child.

·  Nursing management for the child with acute gastroenteritis includes assessing fluid and electrolyte status, administering ORS or IV therapy for severe dehydration, providing an appropriate diet, and giving skin care.

·   Burns alter the integrity of the capillary membrane, resulting in the easy movement of fluid and blood proteins into interstitial spaces.

·   Immediately following a major burn, body fluids shift  from intravascular to interstitial spaces due to increased capillary permeability and cause hypovolemic shock if not corrected quickly.

·            Pain management should be integrated into the plan of care based on frequent assessments using an age appropriate pain scale. Children should not have to experience severe pain after a burn injury. Medicate based on child’s need, not the comfort level of the health professional.

·            Family involvement is essential for the child to cope with body image and selfesteem issues that arise as a result of a burn.

Review Questions

1.   Differentiate between the concepts of diffusion, filtration, and osmosis.

2.   What are the normal serum concentrations for sodium, potassium, and chloride?

3.   Describe what would happen within the body if there was an excess or a depletion of sodium or potassium?

4.   Describe the effects that antidiuretic hormone and aldosterone have on the body. Under what conditions would the body release these hormones?

5.   Describe how the body compensates for metabolic acidosis.

6.   What signs and symptoms would you expect to see if a child was experiencing respiratory acidosis? What clinical situations might cause respiratory acidosis?

7.      What clinical situations might cause metabolic alkalosis?

8.   How does the body compensate for acid-base imbalances?

9.      Outline the treatment and nursing management for a child with dehydration.

10.  What would you include in a discharge teaching plan for caregivers of a child recovering from dehydration?

11. Discuss the treatment of the child with acute gastroen­teritis who has diarrhea and vomiting, and moderate dehydration.

12. What nursing interventions will achieve the goal of maintaining skin integrity in an edematous child?

13. Outline the treatment and nursing management for a child during the first 24 hours postburn.

14. Describe how you will determine if the child is receiv­ing adequate IV fluids.

15. What is the most appropriate way to administer pain medication to a burned child? Give the rationale behind your answer.

16. What nursing interventions would you include in a plan of care for a child experiencing a burn dressing change? What role would the caregivers play? How would you facilitate their involvement?

17. Differentiate between the various types of skin grafts

 

 

 

 

GENITOURINARY ALTERATIONS

The genitourinary system is responsible for the maintenance of  homeostasis of the body (water and electrolytes) and for the excre­tion of waste products. Homeostasis is essential for creating an optimal environment for many other functions of the body. In the male client the urinary system also has a reproductive role and, hence, is critical in a child’s development past the phase of toilet training. Because of these essential functions, any alteration in the kidneys and other urinary system organs can pose a major threat to the child’s health. Such alterations include infections, structural disorders, and disease processes.

Problems involving the genitourinary system can range from the sim­ple, such as urinary tract infections and enuresis, to the complex, such as renal failure and exstrophy of the bladder.

 

ANATOMY AND PHYSIOLOGY

The genitourinary system is composed of the kidneys, ureters, bladder, and urethra (Figure 22-1). The kidneys are situated posteriorly on the abdominal wall behind the intestines. The medulla and nephrons of the neonatal kidney are functional at birth; however, the peripheral tubules are small and immature. These will slowly mature, so that by adolescence, the kidneys are of mature size and weight. The bladder presents itself in young children close to the anterior abdominal wall, and with growth, lowers into the pelvis. For these reasons it is easy to palpate a full bladder on infants and young children.

Anatomically, the kidneys are a pair of symmetrically shaped organs located in the posterior abdominal cavity adjacent to the lumbar spinal column. The right kidney is slightly lower than the left. The kidneys are partially protected by the ribs and are further protected by a tough outer capsule embedded in adipose tissue and supported by the renal fascia. The kidneys produce urine and transport it via the ureters into the bladder where it is stored until it exits the body via the urethra. The weight of the kidney is less in the child than the adult. However, in the infant and young child the kidney makes up a larger proportion of the child’s total body weight. The kidneys are less protected in the child compared with an adult because of unossified ribs, less fat padding, and the larger size proportional to the abdomen. Therefore, they are more susceptible to trauma from com­pression force to the abdomen.

To control homeostasis, the kidneys have both excretory and nonexcretory functions. The kidneys clear the body of wastes such as urea, creatinine, uric acid, phosphates, sul-fates, nitrates, and phenols, along with excreting fluids and electrolytes. It is this fine-tuning that maintains the volume and osmolarity of extracellular and intracellular fluids. Thekidneys also play a role in the excretion of some drugs and hormones. Nonexcretory functions include the secretion of renin, carbohydrate metabolism, and regulation of vitamin D. Embryologically, the fetal kidney begins to develop before many women realize they are pregnant. Prior to birth, the main function of the kidney is to maintain ade­quate amniotic fluid levels. In utero, the placenta carries out the functions of blood cleansing and homeostasis for the fetus. By the 7th week of gestation, nephrogenesis, or development and growth of the kidney, begins and continues to 32-36 weeks. Urine production begins in the third month, and by the fifth month the collecting tubules and renal pyra­mids have formed. At birth the kidney suddenly assumes the role of the placenta, and its response to this change is largely influenced by the gestational age at delivery. Renal blood flow increases dramatically at birth.

 

 

Figure 22-1.    Anatomy of the Genitourinary System with Inset of a Nephron

 

Urine production is readily established. Ninety-nine percent of newborns void within the first 48 hours post delivery. Serum creatinine levels, which are maternally influenced at birth, decrease by 50% during the first week of life. At birth the amount of fluid that is filtered by the glomeruli (glomerular filtration rate) (GFR) is lower than in adults. The GFR reaches adult levels by 2 years of age. The ability to concentrate urine is not well developed in the newborn for several months and even more restricted in the premature infant (specific gravity of 1.001 to 1.015). The neonate’s excretory units are underdeveloped and cause disruption in reabsorption of amino acids and bicarbonate, thus causing the infant to be in a state of mild acidosis (plasma pH of 7.11 to 7.36).

URINARY TRACT INFECTION

Urinary tract infection (UTI) is an infection of one or more structures of the urinary tract and can be classified as lower urinary tract (cystitis, urethritis) or upper urinary tract (pyelonephritis). The most common site is the bladder (cys­titis) with infection confined to the urethra called urethritis and to the kidneys (pyelonephritis). Pyelonephritis is usu­ally considered more severe and is accompanied by an increase in the severity of symptoms. Identification of the site of infection is important in determining the treatment.

 

Incidence and Etiology

UTI is the most common disorder of the genitourinary tract. The incidence of UTI in newborns is approximately 1%, with a greater frequency in males. However, after the first year of life, the incidence is more common in girls than boys, with 3% developing UTI during childhood compared with 1% in boys (Rushton, 1997). UTI is more common in Caucasian girls compared with African-Americans. Boys who are uncir-cumcised are more likely to have UTI than those who are circumcised (Shaw, Gorelick, McGowan, Yakscoe, & Schwartz, 1998).

The most common bacteria that infects the urinary tract is Escherichia coli, likely because of its presence in the gas­trointestinal tract and perianal skin. Less commonly seen colonization occurs from Klebsiella pneumonia, Entero-bacter, Proteus species, and Pseudomonas. The latter four are usually associated with more complicated UTI often seen in children with chronic conditions that alter the urinary tract, such as neurogenic bladder in individuals with spina bifida. Virus and fungi, particularly Candida species, may also cause UTI.

Pathophysiology

In infancy, bacteria frequently enter the urinary tract through the blood and cause infection. After infancy, almost all UTI occur when bacteria enter the urinary tract by ascending through the urethra. Females are especially at risk for infection because of the structure of the lower urinary tract, the short urethra. Males are less susceptible to UTI because of a longer urethra and secretions from the prostate that have antibacterial properties. Structural anomalies and abnormal function of the urinary tract have an important role in the pathogenesis of UTI. Such anomalies include vesicoureteral reflux and neurogenic bladder, which is com­mon in children with spina bifida. Other factors that predispose a child to infection include urinary stasis, congenital anomalies of the urinary tract, an obstruc­tion in the urinary tract, and urinary catheters. Urinary stasis increases the risk of UTI. Normally, emptying the bladder frequently completely washes out any organisms. Stasis may be caused by reflux, dysfunction of the voiding mechanism, and infrequent voiding.

Clinical Manifestations

The presenting signs and symptoms of UTI are often vague, especially in young children. Symptoms in the older child generally include malodorous urine, dysuria, (difficult or painful urination), urinary frequency, fever, vomiting, diar­rhea, irritability, poor feeding, or loss of appetite. Table 22-1 lists the clinical manifestations of UTI in children of various ages. Typically, cystitis is distinguished from pyelonephritis, a syndrome involving fever often greater than 101°F, chills, and back pain. Children with pyelonephritis will also appear to be quite ill.

Diagnosis

A urinalysis (UA) and urine culture with sensitivity (urine C&S) will be performed to diagnose UTI. The means by which a urine sample is obtained has great impact on the interpretation of results. Urine specimens obtained by col­lection bag methods ion-toilet trained children have been widely utilized for initial evaluation of UTI. This method of collection is not suitable for culture because of its high degree of contamination (Johnson, 1999). However in prac­tice, many health care practitioners will opt for this method of collection because it is the least traumatic. If repeated infections develop, it is prudent to perform either sterile catheterization or suprapubic aspiration of urine to evaluate true infection status. Infants and children less than 3 years of age with fever of unknown origin should be screened for uri­nary tract infections with a urinalysis and urine culture (Johnson, 1999).

The Pediatric Nursing Skills CD-ROM explains the urine specimen collection procedure. An adequate speci­men, usually 5-10 cc of urine (may differ among institu­tions) must be obtained prior to any antimicrobial therapy to avoid affecting the bacterial count and to ensure an accu­rate diagnosis. The presence of bacteria (bacteriuria) and white blood cells (pyuria) in the urine confirm the diagno­sis of a UTI. Laboratory confirmation of a positive urine culture indicates the presence of greater than 100,000 colony forming units (CFU)/ml of a urinary tract pathogen. The child with pyelonephritis usually presents with an ele­vated white blood cell count (WBC), an elevated erythro-cyte sedimentation rate (ESR), and an increased C-reactive protein (CRP) (Reynolds & Hoberman, 1995).

The health care provider may recommend renal scan­ning with dimercaptosuccinic acid or glucoheptonate to identify anatomic abnormalities that may be the cause of UTI. This study identifies both renal scarring and acute pyelonephritis but does not differentiate between the two. However, it is helpful in identifying children who require long-term follow-up and is more sensitive than the tradi­tional intravenous pyelogram (IVP), which is still utilized to rule out urinary tract obstructions. Other testing that may be ordered include a renal ultrasound and a voiding cys-tourethrogram (VCUG). A renal ultrasound may identify certain abnormalities, such as hydronephrosis, an abnor­mal swelling in the kidney, while the VCUG is utilized to identify urethral and bladder abnormalities, in particular vesicoureteral reflux.

Treatment

Treatment for UTI includes (1) eradicating the infection, (2) preventing reinfections by identifying contributing fac­tors, (3) correcting underlying causes of infection, and (4) preserving renal function. Treatment depends upon a variety of factors, including the child’s age, other existing medical conditions, and his or her ability to maintain hydration. Oral antibiotic therapy is used to treat UTI. Antibiotics such as trimethoprim in combination with sulfamethoxazole (Bactrim, Septra), amoxicillin (Amoxil), a cephalosporin, or nitrofurantoin (Furadantin) are given for seven to ten days. Follow-up urine culture should be performed 48 to 72 hours after initiating treatment. For infants or young children 2 months to 2 years of age who are assessed as toxic, dehy­drated, or unable to retain oral fluids, initial antibiotic ther­apy should be given intravenously and hospitalization should be considered (American Academy of Pediatrics Committee on Quality Improvement and Subcommittee on Urinary Tract Infection, 1999). Untreated UTI can lead to a variety of complications including renal scarring. Of those clients who develop scarring, some may develop kidney stones, hypertension, end stage renal disease, and possible complications of pregnancy. It is therefore imperative that urinary tract infections be evaluated and treated carefully. With appropriate management, many of these severe complica­tions can be prevented.

Nursing Management Assessment

Initial assessment includes interviewing the caregivers and child (if appropriate) regarding changes in urine elimination, in particular, patterns of elimination. Frequency, hesitancy, dysuria, urgency, and bed-wetting in a child who has already established nighttime control are symptoms of UTI. A careful history can assist the health care practitioner in determining the diagnosis of UTI and its possible causes. The nurse also assesses the knowledge level of the caregiver and child.

Hydration is required to maintain renal blood flow and flush out bacteria and debris; therefore, assessment for dehydration is performed. To assess for dehydration the nurse should observe for signs of tachycardia, poor skin tur-gor, dry mucous membranes, sunken fontanels, hemocon-centration, and decreased peripheral perfusion. Weight checks and urine specific gravity analysis should also be per­formed. Lastly, assessing the child’s level of comfort is important in determining need for analgesics and/or teach­ing distraction techniques. Without pain management, a caregiver cannot concentrate on learning new concepts if the child remains uncomfortable.

Nursing Diagnoses

Nursing diagnoses for the child experiencing UTI include:

1.      Risk for injury related to complications of infection (chronic renal disease and kidney damage).

2.   Risk for deficient fluid volume related to decreased fluid intake and fever.

3.   Acute pain related to UTI.

4.   Deficient knowledge (caregiver) related to lack of information of disease process, diagnostic procedures, management, and prevention of UTI.

Outcome Identification

1.  The child will be free of complications and recurrent UTI.

2.  The child will maintain adequate fluid intake.

3.  The child’s pain will be diminished or absent.

4.  The caregivers will verbalize an understanding of dis­ease process, diagnostic procedures, management, and prevention of recurrent UTI.

Planning/Implementation

Nursing care focuses on antibiotic therapy, maintaining good hydration, managing fever with antipyretics, providing comfort measures and distraction, and educating the child and caregivers. Antibiotics and antipyretics are administered as ordered. The nurse needs to educate the caregivers regarding alternative techniques to reduce fever, for example, using tepid baths (making certain that water temperature is not so cool that the child may be chilled and start to shiver, which will elevate body temperature); pro­moting surface cooling by undressing the child; and encouraging oral fluids. The nurse should administer anal­gesics as ordered and provide and teach alternative comfort measures. If bladder spasms are present, the child may respond to warm moist heat to the abdomen provided it does not increase body temperature. The nurse should offer and assist with distraction techniques. Nurses play a key role in assuring adequate hydration for the child. Accurate documentation of intake and output is essential as the child’s ability to concentrate urine may be impaired during the initial phase of renal inflammation (Reynolds & Hoberman, 1995).

Evaluation

Because of the inflammatory response of the bladder, fever may persist in a child for up to 2 to 3 days after antibiotics are begun. However, urine obtained between 24 and 48 hours after initiation of antibiotics should be negative for bacteria because of the high concentration of medication cleared via the bladder. The child should show a decrease in the degree of pyuria and leukocytes in the urine from the initial specimen, although some WBCs may persist for sev­eral days depending on the underlying pathology. If fever persists, evaluation of the initial urine culture and sensitivity is needed to assure that appropriate antibiotic therapy is being instituted. Ongoing evaluation of the child’s response to fever management, hydration, response to pain, and over­all understanding of the plan of care is essential to providing complete care.

Family Teaching

If this is the first episode of UTI, the nurse will need to instruct the family in a wide range of concepts, including anatomy and physiology of the urinary tract, disease process, diagnostic testing, management, prevention of UTI, and follow-up care. The nurse needs to stress the importance of follow-up appointments, radiologic studies, urinalysis, and cultures. Caregivers need to understand the importance of antimicro­bial therapy and possible use of prophylactic antibiotics. Furthermore, families must be instructed that although the child may no longer feel ill, the individual must complete a full course of antibiotics and comply with follow-up testing to prevent long-term complications, such as recurrent infec­tion, renal scarring, and subsequent kidney damage and deterioration. Education should also include the need for the child to frequently and completely void and to increase quantities of fluids, especially water. Prevention techniques include instructing caregivers on perineal hygiene and, for girls, wiping from front to back and avoiding the use of bub­ble baths and perfumed soaps, which tend to be irritating to the urethra. Cotton underwear, because of its breathability should be worn instead of nylon.

ENURESIS

Enuresis is defined as involuntary voiding of urine beyond the expected age at which voluntary control should be achieved, usually five years of age (Maizels, Rosenbaum, & Keating, 1999). Enuresis differs from incontinence in that incontinence results from a structural abnormality, usually an anatomic malformation (Maizels, et al., 1999). Enuresis can be primary or secondary, diurnal or nocturnal, or both. A child who has never achieved a period of dryness for at least three months is referred to as a primary enuretic. Secondary enuresis occurs when a child has been dry for at least three to six months and then resumes wetting. Diurnal enuresis is wetting that occurs only during the daytime and nocturnal enuresis is wetting that occurs only at night.

Enuresis can have a great impact on a child’s life. Children with enuresis may avoid participating in activities with their peers. Social activities such as a sleepover or a camping trip can cause a great deal of stress for these chil­dren. Children with daytime wetting often face more problems. Staying dry during the school day can be a chal­lenge and concealing wet clothing can be the largest obsta­cle of all. These children may also have problems with odor control.

Incidence

Because the age at which urinary continence is achieved covers a wide range of normal, the incidence is difficult to determine. However, it is estimated at 15-20% in 5-year-olds and 5% in 10-year-olds. Most children have nocturnal enure­sis, and most are primary enuretics. Primary nocturnal enure­sis is more common in boys, whereas primary diurnal enuresis is more common in girls (Riley, 1997). In contrast to enuresis, incontinence is caused by a malformation of the urinary tract and is the least common cause of wetting, affecting about 1-3% of children.

Etiology and Pathophysiology

Enuresis is a symptom, not a disease, and many hypotheses have been proposed to describe its causes (Karlowicz, 1995). Etiologic factors are classified as organic (having a physical basis) and non-organic or functional (exogenous or with no physical disorder or disease). Organic factors should be ruled out before non-organic ones are considered.

 

Organic causes include:

 

1.    Neurologic developmental delay in which the child is unable to inhibit bladder contraction

2.    Urinary tract infections; a child with a urinary tract infection may involuntarily lose urine, however, this is caused by the physiological response of the irritable bladder (Karlowicz, 1995)

3.    Structural disorders of the urinary tract such as obstructive lesions and small bladder capacity; the child may not be able to hold the large volume of urine produced and therefore may experience urgency and the involuntary loss of urine

4.    Disorders that affect the concentrating ability of the kidneys such as chronic renal failure

5.       Diseases associated with an excessive production of urine (polyuria), as in diabetes mellitus and diabetes insipidus

6.      Chronic constipation

 

Non-organic or functional causes include:

 

·        Sleep arousal pattern problems, that is, sleeping soundly so the child does not awaken in the night to void

·        Sleep disorders such as enlarged tonsils and sleep apnea

·        Psychological stress and family disruptions such as divorce, death, or birth of a new sibling

·        Inappropriate toilet training, that is, early chronologic or developmental age, overly demanding or punitive caregivers

Clinical Manifestations

Most children achieve urinary and bowel control between two and a half and three and a half years of age. The typical sequence for the development of bladder and bowel control is (1) nocturnal bowel control, (2) daytime bowel control,(3) daytime control of voiding, (4) nighttime control of void­ing (Rushton, 1995). It is unclear why some children are not able to accomplish bladder control while other children of the same age have attained control. Any child who continues to experience nighttime wetting after the age of five warrants an evaluation for enuresis. Possible presenting clinical mani­festations of a child with enuresis are presented in

Box 22-1

.

Diagnosis

Physical examination and a careful family history are the hall­marks of determining a diagnosis of enuresis or incontinence. A thorough physical examination to distinguish between organic and nonorganic (functional) enuresis should be per­formed initially. The examination should include assessing the abdomen and genitals for any abnormalities. A neurologic exam of the peripheral reflexes, perianal sensation, anal sphincter tone, and inspection of the lower back to rule out any spinal defects should also be included.

 

 

 

Results of the history, voiding diaiy (keeping track of frequency and amount of void), and physical examination may determine which diagnostic tests are required for fur­ther evaluation. Some of the more frequently required tests include urinalysis, urine culture, renal ultrasound, and VCUG for children with a history of urinary tract infections. Urine flow rates determine voiding characteristics. One can determine if structural problems are present by measuring the amount of urine voided and the time it takes the child to void, as well as the force of his or her urine stream.

 

Treatment

 

The following treatments can be used separately or in com­bination to treat children with wetting problems: medica­tion, bed-wetting alarms, motivational therapies, elimination diets, and bowel programs for children who are constipated. If the child is experiencing incontinence, the structural cause will need to be determined and treated. Successful treatment requires both the child and caregivers to commit to active involvement in an enuresis program. The most commonly used medications to treat enuresis are oxy-butynin chloride (Ditropan), desmopressin (DDAVP), and imipramine hydrochloride (Tofranil) (Table 22-2). Medications are often used in conjunction with other treat­ments for the most effective outcomes. Medications for enuresis should not be considered a cure but as part of the treatment and solely symptom relief. Children with the best long-term outcomes for staying dry most often used a combi­nation of treatments in conjunction with medications.

 

Figure 22-2. Bed-wetting alarm

 

                                       22-3A                                                                                   22-3B                       

 

Figure 22-3A.  Proper Attachment of Bed-Wetting Alarm (male)

Figure 22-3B.  Proper Attachment of Bed-Wetting Alarm (female)

 

Bed-wetting alarms are in the widely used treatment for enuresis. Some models are meant to be placed under the bottom sheet of the child’s bed (Figure 22-2). Most alarms consist of a moisture sensor that is attached to the child’s underwear or pajamas (Figures 22-3A and 22-3B). The alarm starts to buzz as the first few drops of urine are detected. The sound of the alarm arouses the child, and the urinary flow is interrupted. The child is instructed to turn off the alarm and go to the bathroom to complete voiding. The alarm teaches the child to recognize bladder fullness and awaken before bed-wetting occurs. When the bed-wetting alarm is used as the only method of treatment, there is a 70% success rate. Although 30% of these children may relapse, overall they respond quickly to a short treatment program where the alarm is reinstated for a brief period of time (Maizels, et al, 1999; Mosier, 1998).

 

Motivational therapies may include using star charts to record the child’s progress during the treatment program (Figure 22-4). Rewarding the child for dry nights is effective because over time the behavior may be changed when the child feels proud of his or her accomplishments. The child should be included when designing a reward program. By rewarding a child with special treats (stickers, collectable cards, etc.) or privileges that they value, it increases the chances that the rewarded behavior will occur again. Rewards are most effective if they are given to the child immediately after the desired behavior. Reward programs should be used with caution. If a child consistently fails to receive rewards, it can decrease self-esteem and motivation to continue the program.

 

Figure 22-4   Behavior Modification Star Chart is often used to reward desired behavior in children with enuresis.

 

Certain foods may be irritants to the bladder and increase a child’s wetting problems. Eliminating foods or beverages that are known irritants may decrease the number of wetting episodes a child has. Foods to eliminate include carbonated beverages, dairy products, beverages with artifi­cial coloring, citric fruit, heavily sugared foods, and bever­ages with caffeine. Five to 10% of children who wet benefit from the elimination diet (Maizels, et al, 1999).

Many children with wetting problems also experience constipation. The cause of constipation may be one or a combination of several factors such as insufficient fluid intake, low fiber diet, history of painful bowel movements and holding back of stool, changes in daily routine, lack of physical activity, and no routine for daily bowel movements. Stools may be infrequent, hard or large, and may be painful to pass. These children may not completely empty the colon of stool and further perpetuate the cycle of constipation. Treatment for enuresis may not be successful if constipation management is not addressed at the same time. Children may show improvement with wetting once they are on a suc­cessful bowel program. To assess for constipation a rectal exam, X ray, or ultrasound of the abdomen can determine if the child has a large mass of stool.

Nursing Management

Assessment

In assessing a child who presents with wetting problems, the history will provide important information for formulating a plan of care. Questions to cover during the assessment of the enuretic child are listed in

Box 22-2

.

 

Nursing Diagnoses

1.  Impaired urinary elimination related to lack of bladder control.

2.  Impaired skin integrity related to contact with urine.

3.  Disturbed sleep pattern related to bed-wetting and the use of bed-wetting alarms.

4.  Low self-esteem related to urinary incontinence or bed-wetting.

5.  Impaired social interactions related to urinary inconti­nence.

Outcome Identification

3.           The child will achieve bladder control.

4.       The child will be free of skin irritation in the perineal area.

5.     The child will have minimal disturbance during sleep.

6.       The child will use expressions that indicate positive self-esteem.

7.       The child will actively participate in age-appropriate social interactions.

Planning/Implementation

Nursing care of the enuretic child most often includes ongo­ing family education and support during a long treatment phase. The nurse can provide the child and family with information about the causes of enuresis and the variety of treatment options. The family should be involved in the deci­sion about the treatment plan. As appropriate to the treat­ment, the child and family need instruction on the use of bed-wetting alarms, medications, behavior modification, and elimination diets. The family should be encouraged to emphasize the child’s strengths and praise attempts at control to increase confidence and self-esteem. The nurse needs to assist the child and family to verbalize feelings of frustration.

Evaluation

Evaluation is based upon the family’s report of the child’s progress with the program. Families are instructed to follow up with the nurse by telephone one week after starting the program, or sooner if problems develop. Monthly appoint­ments may be necessary until the child achieves 14 consecu­tive dry nights.

Family Teaching

Nurses can provide children and caregivers with information on hygiene and treatment/prevention of skin breakdown caused by exposure of skin to urine. They will need educa­tion about the use of bed-wetting alarms. Explain to the caregivers that the child’s sleep will be disrupted during the program, and that it may be beneficial to the child to have an earlier bedtime. Nurses can also educate children and care­givers on the use, schedule, and adverse reactions of medica­tions prescribed as part of the enuresis program. Families and childreeed support and encouragement during the treatment for enuresis. Nurses should provide children with positive feedback for complying with the prescribed pro­grams. The nurse needs to discuss with the child feelings of embarrassment or guilt as a result of the enuresis. The nurse should encourage keeping an extra set of clothes at school until enuresis is resolved.

STRUCTURAL DEFECTS

Structural defects include vesicoureteral reflux, hypospadias, cryptorchidism, inguinal hernia, and hydrocele.

VesicoureteraS Reflux

Vesicoureteral reflux (VUR) is defined as the backflow of urine from the bladder up the ureter to the kidney. VUR results when the ureterovesical/vesicoureteral junction

(site where the ureter enters the bladder) fails to maintain a unidirectional flow of urine from the ureter to the bladder. Normally, urine is produced in the kidneys and travels down the ureters into the bladder for storage. In the normal blad­der, the junction of the ureter into the bladder forms a one­way valve mechanism or flap valve that allows urine to flow into the bladder while preventing regurgitation back into the ureters and/or kidneys.

Incidence and Etiology

VUR is the most common anatomic disorder affecting the genitourinary tract (Kaefer, et al., 2000). The exact incidence is unknown because routine screening of children without a history of urinary tract infection is not practiced. However, VUR has been consistently found in approximately one-third of children who have at least one UTI (Craig, Irwig, Knight, & Roy, 2000). Often it is diagnosed when the child is between the ages of two and three years. However, in some cases it may be diagnosed in older children or infants depending upon the underlying pathology. For example, children with spina bifida are usually screened for reflux as infants.

It is important to note that reflux has a genetic compo­nent. Familial reflux is common. Reflux is present in approxi­mately one-third of siblings who have an affected brother or sister. Of those, 75% do not present with any urinaiy tract symptoms. Recent studies have also revealed a high incidence of transmission of reflux from parent to child. The incidence of vesicoureteral reflux is also significantly lower in African-American children versus Caucasian when screening is done following a urinary tract infection. Distribution of reflux by gender reveals a possible higher frequency in females than males, although this data is influenced by other factors such as circumcision and age at diagnosis (Belman, 1995).

Pathophysiology

Anatomically, the ureter extends from its respective kidney downward to the top of the bladder trigone (a small trian­gular area at the base of the bladder where the ureters nor­mally join the bladder). It then passes obliquely through the bladder wall for a distance that enables the ureter to act as a sphincter despite not having an anatomic sphincter. The ureter at this point functions as a one-way valve to prevent reflux. When this length is not sufficient, backward flow of urine, hence vesicoureteral reflux, will ensue. With growth, the ureter tunneling through the bladder wall may elongate, and this increase in tunnel length will help promote the res­olution of reflux.

Clinicai Manifestations

The clinical manifestations of VUR usually are not directly apparent. However, persistent and repeated urinary tract infections are the most common indicator of reflux.   Therefore, the child with repeated UTI should be evaluated. Other manifestations of reflux less commonly seen are enuresis, flank pain, and abdominal pain. However, these symptoms can be vague in children too young to describe and localize their symptoms and may be easily confused with other diagnoses.

Diagnosis

The diagnosis of VUR is made by radiographic evidence of back How of urine on a cystogram (radiograph of bladder, urethra, and ureters), or voiding cystourethrogram

(VCUG) (radiograph of bladder, urethra, and ureters during voiding). Reflux is graded to determine its severity on a scale of I to V. The degree to which contrast material from the bladder travels up the ureters to the kidneys is graded I to V, with I being the least severe and V the most severe.

Treatment

The medical treatment for vesicoureteral reflux is deter­mined by the severity of the reflux and the fact that some degrees of reflux resolve spontaneously as the child grows. The less severe the reflux (grades I and II), the greater the likelihood of resolution. The goals of medical management for children with reflux include prevention of UTIs, preven­tion of kidney damage, and prevention of the subsequent complications of reflux and renal scarring. Currently, treat­ment options include long-term use of antibiotics to prevent UTI, and on occasion the use of anticholinergics. Anticholinergics such as oxybutynin chloride (Ditropan) are used to decrease bladder pressure.

Other treatment options include surveillance of the child over time to observe for signs of deterioration such as increase in incidence and severity of UTIs. Deterioration in a child would necessitate an advance in treatment, such as a change in prophylactic antibiotics and an increase in anti-cholinergic medication. Lastly, surgery to correct reflux is indicated when medical treatment options have failed. Indications of failure include breakthrough UTIs, particu­larly pyelonephritis, despite strict compliance to medical management and pharmacotherapy, or increased renal damage, which threatens the survival of the kidney (Tanagho, 1995).

Surgical management may be performed endoscopi-cally or with traditional surgical techniques involving an abdominal incision. When kidney function is impaired and the ureters are massively dilated, a urinary diversion may be recommended to improve renal function and allow the dilated ureters to reestablish tone. This is usu­ally a temporary measure to allow time to consider further reconstruction or reestablishment of the ureters into the bladder (Tanagho, 1995). Surgery involves reimplantation of the ureter into a position on the trigone that allows for sufficient submucosal length to prevent the reflux from recurring.

 

Nursing Management

Because the non-surgical management for a child with VUR focuses on UTI prevention and management, an important aspect of nursing care focuses on education of the child and caregivers. The child and caregivers should be aware that the treatment may continue for years and compliance with the medication regimen is important. They must also maintain close contact with their health care provider and inform the individual when the goals are not being achieved (i.e., recur­rent UTI), hence, necessitating more aggressive management. If surgery is necessary, the nurse provides the child and caregivers information about the surgical procedure and pre-operative and postoperative care. Immediate postoperative care for a child after reimplantation of one or both ureters can be challenging. While managing the acute pain the child may be experiencing it is important to strictly monitor intake and output. The well-organized nurse will label all drainage devices and stents and note where they originate (i.e., ureter, bladder, or peritoneum). The nurse should assess the integrity of all tubes and drainage bags; breaks in tubing can increase risk for infection by introducing bacteria into the drainage system. Noting any kinks or disruptions will assure accurate I & O.

Hypospadias

Hypospadias is a common congenital malformation in which the urethral meatus is on the ventral surface (underside) of the penis (Figure 22-5). The position of the uretheral open­ing may vary, occurring at any point along the ventral surface of the penis or on the scrotum or perineum.

Incidence and Etiology

Hypospadias occurs in 8.2 per 1,000 live births (Zaontz & Packer, 1997). Rates are highest among Caucasians, lowest among Hispanics, and intermediate among African-Americans. There is some genetic predisposition as evi­denced by a family history of another male with hypospadius (Paulozzi, Erickson, & Jackson, 1997). The exact etiology is unknown and may be multifactorial. Some affected boys have defects in testosterone metabolism or testosterone receptors. This suggests that hypospadias can result from an abnormality in endocrine factors that influence the develop­ment of the male genitalia.

Pathophysiology

Hypospadias is a congenital birth defect caused by altered embryogenesis or an insult to the developing fetus during the 3rd through 5th months of gestation. In utero, the penile ure­thra develops from the urogenital sinus. By the 12th week of gestation, the endodermal edges of the secondary urethral groove fuse to form a tube. The urethra fuses in a proximal to distal direction. Failure of this fusion results in the urethral meatus opening other than the tip of the penis, and failure of the foreskin to develop properly. The foreskin usually appears as a hood in children affected with hypospadias.

 

Figure 22-5.   Hypospadias is a congenital anomaly in which the urethral meatus is on the ventral surface (underside) of the penis. Photo courtesy of Casimir Firlit, MD, PhD, William E. Kaplan, MD, Max Maizels, MD, and Jeffrey Palmer, MD, Children’s Urology Ltd.

Clinical Manifestations

The prepuce or skin forming a hood over the glans is abnor­mally small ventrally and may be redundant dorsally. Many caregivers of infants with hypospadias claim it appears that their newborn son has already been circumcised. Associated conditions may include chordee (downward curvature of the penis and an incomplete foreskin), undescended testes, and inguinal hernia. In some cases the urinary stream may be deflected downward secondary to the ventral position of the meatus.

Diagnosis

Diagnosis is based on physical examination. Careful inspec­tion of the external genitalia of all newborn males should be performed at birth.

 

Treatment

Treatment for hypospadias involves surgical correction of chordee, placement of the urethral meatus to the tip of the penis. Successful surgery will enable the child to void in a standing position, have a cosmetically normal appearing penis, and have a sexually adequate penis. Historically, surgery to correct hypospadias was performed in stages and involved lengthy hospitalizations and uncomfortable postop­erative treatments and drains. Currently, because of advances in surgical technique, the surgery can be per­formed in one single outpatient procedure. In more severe cases a two-stage repair also may be performed.

Surgery is usually performed before the child is 18 months of age, prior to toilet training and the development of body image or gender identity, thus minimizing psycho­logical trauma (Sugar, Firlit, & Reisman, 1993). Several sur­gical techniques are available and vary depending on the severity of the anomaly and the surgeon’s preference. All techniques involve reconstruction to elongate the urethra, bring it to the tip of the penis, and straighten the chordee. The foreskin is frequently used as a graft whereby it is rolled into a tube and fashioned into a urethra. Hence, no neonatal circumcision should be performed on these infants. On occasion, the size of the penis is augmented preoperatively with testosterone cream or injections to allow for growth of the tissue and hence facilitate surgery.

Several types of dressings may be utilized postopera-tively. Some may be as extensive as a compression type dressing, most commonly a penile wrap type dressing, and still some may have no application of a dressing at all. Postoperatively, a urethral stent or foley catheter may be used to facilitate urination and prevent obstruction of urine flow secondary to edema.

Nursing Management

Assessment

Preoperatively, the nurse should assess the infant or child for evidence of other genitourinary defects such as undescended testes, inguinal hernia, or hydrocele. The caregivers’ under­standing of hypospadias, the surgical procedure, and their

 expectations of the appearance of the penis after surgery is investigated. The nurse needs to assess their response to having a newborn with a genital defect. Postoperatively, an assessment for adequate urinary output is essential. The nurse observes for signs of wound and urinary tract infec­tion, e.g., penile incision for purulent drainage and excessive erythema, increase in temperature, cloudy urine with a foul odor. The infant or child is assessed for signs and symptoms of pain from incision and bladder spasms.

Nursing Diagnoses

The nursing diagnoses for a child undergoing surgical hypospadias repair are similar to those for many urologic abnormalities. They include:

1.  Pain related to surgical incision.

2.  Deficient knowledge (caregivers) related to the diag­nosis, surgery, postoperative care, and prognosis of hypospadias.

3.  Risk for infection related to indwelling catheter and/or stents and surgical incision.

Outcome Identification

1.  The child will have minimal to no pain postoperatively.

2.  Caregivers will verbalize an understanding of the dis­order, the surgical procedure, and prognosis, and will participate in postoperative care.

3.  The child will be free of infection of the urinary tract and the incision.

Planning/Implementation

Postoperative pain is usually minimal following repair of hypospadias. A dorsal or caudal nerve block provides adequate pain relief for most children; however, occasionally aceta­minophen (Tylenol) may be helpful for a few days to alleviate incisional discomfort. Anticholinergics such as oxybutynin chloride (Ditropan) may be administered if ordered to allevi­ate bladder spasms while the urethral stent is in place. Caregivers should be informed that anticholinergic medica­tion might cause facial flushing and dry mouth. The child should be encouraged to take in adequate fluids to maintain adequate urinary output and the patency of the stent.

Discharge instructions should include information regarding antibiotic use to prevent infections, timing of dress­ing and stent or Foley catheter removal, and anticipatory guidance for the caregiver and older child regarding postop­erative appearance of the penis. They should understand that the penis will look bruised, wrinkled, and swollen because of the trauma and that it will resolve in a few days to weeks.

These instructions may differ between surgeons. Some may remove the dressing in 4-5 days while others may main­tain a larger compression dressing for longer periods depending on the severity of the hypospadias and surgical technique. If a small layered penile dressing is used, the  caregiver will be instructed to have the child soak for 20 minutes in a bathtub filled to the child’s waist with clear warm water prior to the appointment for removal. This allows the dressing to loosen and often fall off at home.

Complications of hypospadias repair can occur. Urethral fistula, or an opening along the urethra that leaks urine to the skin surface, strictures at the anastomosis site, and retru-sion of the urethral meatus to its original position has been reported. If the fistula does not resolve, repeat surgery may be indicated 6 months after the initial repair (Stock, Scherz, & Kaplan, 1995).

Evaluation

The child should be comfortable and participating in age-appropriate activities. The caregivers can explain the surgical intervention and the postoperative course and care involved. They are participating in their child’s care. The child should not exhibit signs of UTI or incisional infection.

Cryptorchidism

Cryptorchidism or undescended testis (UDT) is defined as failure of one or both testes to descend through the inguinal canal into the scrotum (Figure 22-6). Further classification is based on whether the testis is retractable or ectopic. A retractile testis is one that has descended normally but read­ily retracts with physical stimulation and exam, and is often mistakenly diagnosed as UDT. An ectopic testis is one that is found outside the normal path of descent. It may be in the groin, perineum, or abdominal wall.

Incidence and Etiology

UDT is a common urologic problem. The incidence of UDT increases as the degree of prematurity increases. In full-term newborns it is between 3% and 5% (Rozanski & Bloom, 1995). Low birth weight and premature infant boys have a higher incidence of UDT. Incidence of cryptorchidism decreases with age so that by 3 months of age the incidence is 1%, and 0.8% at 9 months of age. In many cases the testes descend spontaneously; however, after 1 year of age, sponta­neous descent does not usually occur.

 

Figure 22-6  Cryptorchidism. Photo courtesy of Casimir Firlit, MD, PhD, William E. Kaplan, MD, Max Maizels, MD, and Jeffrey Palmer, MD, Children’s Urology Ltd.

 

Pathophysiology

Sexually indifferent gonads are found at three to five weeks gestation. During the 7th week of gestation the gonads begin to differentiate into a testis or ovary. As the testes increase in size a network of strands form into the seminiferous tubules where spermatozoa are produced. During the third trimester, the testis begins its descent into the scrotum through the inguinal canal. Many theories attempt to explain the failure of the testes to descend into the scrotum includ­ing increasing abdominal pressure and hormonal influences (Rozanski & Bloom, 1995). In the undescended testis sperm production is decreased and may cause infertility. The child with UDT also has a 20% to 44% increase in risk for devel­oping a malignant testicular tumor in adulthood (Gonzalez, 1996).

Clinical Manifestations

UDT, which may be unilateral or bilateral, is unilateral in 85% of males and most often affects the right testis. Infants diagnosed at birth with bilateral UDT represent 15% of affected boys (Rozanski & Bloom, 1995). One side of the scrotum (unilateral) or the entire scrotum (bilateral) appears flaccid, non-pendulous, and smaller thaormal.

Diagnosis

The diagnosis of cryptorchidism involves primarily the physi­cal examination in which the scrotum is palpated for the testis, a small nodule. It is important to perform the physical examination without stimulating the testicle to retract by the examiner having warm hands and the child being relaxed. If the testis is not palpable, ultrasound may be used to deter­mine its location.

Treatment

Management of cryptorchidism may involve observation while awaiting spontaneous descent of the testis during the first year of life. Human chorionic gonadotropin (HCG) may also be used to stimulate testosterone production to help induce descent of the testis into the scrotum. Limited suc­cess with this technique has been reported. However, HCG does increase testicular vasculature and size thereby assisting in locating the testis either before or during surgery (Sugar & Hoyler-Grant, 1995). If the testis fails to descend sponta­neously or with the administration of HCG, surgery, orchiopexy, is performed. The optimal timing for surgical correction is when the child is between one and two years of age. The goals of surgical correction are to bring the testis into the scrotum and secure it by scrotal fixation without damaging the testicle.

Nursing Management

Assessment

At birth and the first well-child visit the nurse can evaluate for the presence of both testes. By gently compressing both inguinal canals, a small nodule should be felt on both sides. The nurse should assess the caregivers’ understanding of UDT and the importance of timely surgical correction.

Nursing Diagnoses

•      Deficient knowledge (caregiver) related to cryp­torchidism and its treatment.

•      Anxiety (caregiver) related to the possible decreased fertility and increased risk of malignancy.

Outcome Identification

1.  The caregivers will verbalize an understanding of the disorder and treatment.

2.  The caregivers’ anxiety will be decreased by explaining that the child should have appropriate referrals for fer­tility testing when appropriate and should perform tes­ticular self-exam beginning at adolescence.

Planning/Implementation

Education of the caregiver should include clarification and reinforcement of information gleaned from the surgeon, including the use of HCG if ordered. Caregivers need sim­ple explanations regarding how to prepare their child (if age-appropriate) for surgery and what to expect postoperatively. The issue of fertility is of great concern to the caregivers of children with UDT. Biopsies of these testes reveal histologic abnormalities including decreased number of germ cells. Sperm counts in a nondescended testis decrease proportion­ally with age after the second year of life. The contralateral testis even if normally positioned may also demonstrate abnormal histology. Even after successful orchiopexy, the testes may continue with decreased spermatogenesis (Rozanski & Bloom, 1995).

Family Teaching

Nurses are helpful in teaching and preparing both the child and caregivers for surgery. If HCG therapy is utilized, the caregiver should be aware of the desired effects as well as secondary effects. For example, caregivers may express con­cern during this treatment when they observe increased penile growth and increased pigmentation of the scrotum as well as growth of pubic hair. Caregivers should be reassured that these side effects will dissipate after therapy is discontinued. They should also be instructed that their child will have discomfort postoperatively. Loose clothing is recommended so as not to apply pressure to the wounds immediately after surgery. Analgesics such as acetaminophen (Tylenol) and acetaminophen with codeine are routinely ordered. The child may appear to have difficulty walking related to tenderness, but this will resolve in a few days. The scrotum will appear quite edematous and ecchymotic. Caregivers need reassur­ance that all these are expected because of surgery but will resolve in a few days to several weeks.

Sutures and dressings are minimal. Usually dissolving sutures are utilized to close the groin and scrotai wound. Hence, the child does not require suture removal that may induce further fear and trauma. Tegaderm, or other clear plastic type dressings, cover the groin wound and may be removed at home one week after surgery. Nurses must teach the caregiver to observe for signs of infection including increased pain, redness, swelling, and drainage from the incisions, along with fever. Frequent diaper changes and proper hygiene will reduce the risk of infections. Lastly, caregivers should be instructed to help the child avoid stren­uous activity, sports, and riding toys that may be straddled until appropriate healing has taken place. The child should be instructed on testicular examination monthly once he reaches puberty to regularly evaluate and assist in early detection of tumors. Nurses are essential in assisting the caregiver to develop a supportive environment in which the child has opportunities to ask questions regarding sexuality and fertility as he becomes an adolescent.

 

Inguinal Hernia and Hydrocele

 

Inguinal hernia and hydroceie are similar disorders, both clinically and in their treatment. An inguinal hernia is a scro­tai or inguinal swelling, or both, that includes the abdominal contents. A hydroceie is a collection of peritoneal fluid in the scrotai sac.

Incidence

Inguinal hernias occur in children at a rate of approximately 10 to 20 per 1,000 live births (3.5% to 5% of term infants) and occur more frequently in boys than girls (ratio of 4:1) (Figure 22-7A). The incidence increases dramatically with other risk factors including prematurity and low birth weight (Skoog & Conlin, 1995). The majority of infantile inguinal hernias are diagnosed in the first month of life. Hydroceles occur in approximately 6% of full-term infant boys (Figure 22-7B). Children who also present with ventriculo-peri-toneal shunts and those receiving dialysis (treatment that acts as a filtration system outside the body to rid the body of waste products) are also at increased risk for development of hernias and hydroceles secondary to the persistence of increased intra-abdominal pressure (Skoog & Conlin, 1995).

Etiology and Pathophysiology

An inguinal hernia is caused by abdominal contents exiting the peritoneal cavity and protruding into the processus vaginalis (a fold of peritoneum that precedes the testicle as it descends through the inguinal canal into the scrotum). An incomplete or abnormal obliteration of the processus vagi-nalis at birth allows peritoneal fluid or abdominal contents to enter the scrotum, resulting in a hydrocele or inguinal her­nia. The processus vaginalis follows the same descending pathway of the testes into the scrotum. Normally fusion of the processus vaginalis occurs spontaneously after the testis is in the scrotum (Skoog & Conlin, 1995).

 

 

Figure 22-7   (A) An inguinal hernia is a scrotai or inguinal swelling, or both, that includes the abdominal contents. (B) A hydroceie is a collection of peritoneal fluid in the scrotai sac.

 

Clinical Manifestations

An inguinal hernia presents as a bulge or a swelling in the scrotum or groin whose size increases because of increased intra-abdominal pressure from crying or straining (Figure 22-8A). Pain is usually not associated with the hernia unless it becomes strangulated. A hernia can become strangulated when the herniated intestines are trapped within the defect and become edematous and twisted. With strangulation, the blood supply to the herniated segment is cut off. There is ischemia and obstruction of the bowel, which can lead to necrosis and possible perforation. Clinical manifestations include scrotal color changes (redness); pain; intense, incon­solable irritability; vomiting; abdominal distention; and tachycardia.

When a hydrocele is present, the scrotal swelling is painless and does not change in size and shape when the infant cries or coughs (Figure 22-8B). It is not reducible but can be easily transilluminated (Sugar & Hoyler-Grant, 1995).

 

Diagnosis

The diagnoses of hernia and hydrocele are based on the physical examination of the scrotum and inguinal area. Differentiation between the two may be made on physical exam. Upon palpation a hernia may feel boggy and may be reduced by applying gentle upward pressure on the enlarged area of the hernia. In contrast, a hydrocele will be fluid filled and feel more tense and is not reducible.

 

Treatment

The treatment of choice for an inguinal hernia is surgery (herniorrhapy), which is usually performed on an outpatient basis. The procedure is done through an incision in the inguinal crease, and the processus vaginalis is identified and ligated. The wound is often covered with a protective sealant after surgery. A hydrocele usually resolves by one year of age. However, if it does not resolve spontaneously by this time, it means a hernia is present and should be surgically repaired. The procedure is called a hydrocelectomy and is the same as for a hernia.

 

Nursing Management and Family Teaching

Nursing care for inguinal hernia and hydrocele focuses on teaching the caregivers about the surgical procedure, preop erative and postoperative care, and signs and symptoms of complications such as wound infection and strangulation (preoperatively). Preoperatively the nurse needs to be vigi­lant for signs of incarceration (strangulation of a portion of the bowel leading to circulation impairment and tissue necrosis). After surgery the surgical site is observed for bleeding, drainage, and recurrence of the hernia. The nurse instructs the caregivers that the infant requires frequent dia­per changes to prevent infection, and that there are no activity or dietary restrictions. They should be instructed to observe the wound for signs of infection, that is, redness, elevated temperature, and drainage.

Figure 22-8A  An inguinal hernia presents as a bulge in the scrotum. Source: Liebert, P. S. (1996). Color atlas of pediatric surgery (2nd ed., p. 1O2). Philadelphia: W. B. Saunders. Used with permission.

Figure 22-8B   Hydrocele. Photo courtesy of Casimir Firlit, MD, PhD, William E. Kaplan, MD, Max Maizels, MD, and Jeffrey Palmer, MD, Children’s Urology Ltd.

 

ACUTE GLOMERULONEPHRITIS

 

Acute glomerulonephritis (AGN) is an acute or sudden inflammation of the glomeruli within the kidney. This inflammation results in acute renal failure. Because the inflammation results in damage to the glomeruli within the kidney, it is often referred to as intrarenal acute renal fail­ure. It is classified further according to the exact site of the damage, for example, the glomerular capillaries or the membrane.

 

Incidence and Etiology

The exact incidence of AGN is not reported. It peaks at seven years of age, is unusual in children younger than three years of age, and occurs more often in males with a ratio of 2:1 (Simckes & Spitzer, 1995). The etiology is usually an infectious agent that has been present in the body for at least 2 to 3 weeks prior to the clinical renal manifestations. There may have been other signs and symptoms that were more systemic prior to the onset of the renal manifestations.

The agents usually involved are bacterial or viral. The most common organism is streptococcus (group A beta). The primary site of infection is typically the throat or the skin. In these cases the disease is referred to as acute poststreptococcal glomerulonephritis (APSGN). Other causes of this condi­tion are systemic or chronic diseases that eventually affect the glomeruli as the disease progresses, such as sickle cell anemia.

 

Pathophysiology

Either a bacterial or viral agent invades the child’s system. The immune system responds by trying to fight the infection and produces antibodies to attack the foreign antigens. This antibody/antigen reaction within the kidney glomeruli forms immune complexes and inflammation occurs. The end result is damaged/scarred glomeruli. Membrane permeability is altered by this immune response, thus allowing protein to leak into the urine. Sodium is retained within the serum and water follows a decrease in the plasma filtration. The accu­mulation of water and sodium leads to edematous tissues. The glomerular filtration rate is slowed as the passage through the kidney gets narrower.

 

Clinical Manifestations

The clinical manifestations of AGN are hematuria (pres­ence of blood in urine), dependent and periorbital edema, diminished urinary output, proteinuria, hypertension, fatigue, diminished glomerular filtration rate, elevated serum sodium levels, and elevated potassium. Hypertension occurs in 60% to 80% of children with APSGN (Simckes & Spitzer, 1995). All these symptoms are related to the inflam­matory process, the changing permeability of the glomerular membrane, and progressive kidney damage. BUN and crea-tinine levels may also be elevated, and a low-grade fever may be present. Again these symptoms are related to progressive kidney damage and loss of protein. Urine may appear grossly bloody or just blood tinged, smoky or tea colored, and greatly reduced in volume depending on the degree of inflammation. Hematuria is essential for the diagnosis.

 

Diagnosis

The diagnosis is dependent upon the clinical manifestations listed above. Other diagnostic tests include the WBC with differential. This count may or may not be withiormal lim­its depending on the length of the infection and its severity. Immunologic tests include (1) serum complement (c3) test for complement cascade of the immune system (usually low); (2) streptozyme, which will be positive if the renal condition is caused by a streptococcal infection; and (3) a culture of the primary site of infection such as the throat. If a culture is not possible or is negative, then the diagnosis is made on the renal symptoms, especially the presence of hematuria and the history of a prior streptococcal infection. The complement system is composed of about 20 serum proteins that assist the specific immune system to fight infection. Because there are so many proteins involved, the system responds in a cascade fashion to enhance the immune response. When infection is present, especially bacterial infection, the complement is depleted from the serum as it moves to create an inflamma­tory effect at the site of infection. Specific renal tests besides the serum chemistries might include a renal biopsy if there is no clear diagnosis from any other source of testing.

 

Treatment

Treatment depends in part on the degree of kidney damage and is symptomatic. The aims of the treatment are: to iden­tify and treat the source of the inflammatory process; to maintain fluid and electrolyte balance; and to maintain the blood pressure within the normal range. As the primary source of glomerulonephritis is usually not renal, a thorough physical examination must be done. A history of symptoms over the past few weeks must be taken. Areas to focus on include: exposures to other sick children/adults; treatment for any minor infections including over-the-counter medica­tions for fever or aches and pains; the respiratory system,, especially the upper respiratory area* the throat for any redness or inflammation; any coughs (productive or non­productive); respiratory difficulties, such as difficulty sleep­ing in a child who usually does not wake up during the night.

Children with normal blood pressure and urine output can usually be managed at home However, those with generalized edema, significant oliguria, hypertension, and gross hematuria should be hospitalized because of the possibility of developing acute renal failure. If the edema is generalized, it may be necessary to give diuretics. Antihypertensive agents are given for hypertension. Dietary restrictions are based on the severity of the disorder, especially the extent of edema and hypertension. Sodium, potassium, and fluids may be restricted. The prognosis for children with APSGN is excellent with most recovering completely.

 

Family Teaching

 

Caregivers need explanations regarding the prognosis for their child. The normal course of this disorder is one to three weeks of therapy without residual effects. They need to be taught:

1.    Signs of edema or worsening of the renal failure

2.    Dietary and fluid restrictions such as a low sodium diet, which is essential for the care of this child if urinary out­ put is compromised (low or absent) or edema is present

3.    Skin integrity and the need for cleanliness. The care-givers are taught to observe for red areas, excessively dry areas, open areas or abrasions, pressure areas that may appear red or bruised.

4.    Need to reposition the child or encourage the child’s moving about at least every two hours.

5.    Elevation of lower extremities on a pillow when sitting in a chair. This position will decrease the chance of dependent edema and encourage cardiac circulation. Rest periods during activities are important because the child will fatigue easily.

6.    Signs of dehydration and the importance of reporting them immediately to the health care provider

7.    Signs of a worsening condition, which include grossly bloody urine, increased edema, increased lethargy or activity intolerance, restlessness, or any change in res­piratory status. These signs would usually warrant hos-pitalization.

 

NEPHROTIC SYNDROME

 

Nephrotic syndrome (NS) is a clinical entity characterized by massive proteinuria and hypoalbuminemia (low levels of albumin in the blood) leading to edema and hyperlipi-demia. NS can develop during the course of renal or sys­temic diseases and can be classified as either primary or secondary. Primary, or idiopathic, NS results from glomeru-lar disease of the kidney. Secondary NS results in renal mal­functioning as a result of a systemic disease, drugs, or toxins such as liver malfunction, hepatitis, systemic lupus erythe-matosus, lead poisoning, childhood cancer or its therapies, or other diseases that ultimately put a stress on the renal sys­tem. The most common type of NS in children is primary.

 

Incidence and Etiology

The incidence of NS has been reported to be 0.02-0.07 per 1,000 (Bergstein, 1996). It is more common in males than females with a ratio of 2:1 (Constantinescu, Shah, Foote, & Weiss, 2000). It usually affects children between the ages of 2 and 6 years. The etiology of the primary form is believed to be an immune response. The immune response is to glomerular disease or a systemic infection by the body that alters the structure of the glomerulus.

 

Pathophysiology

Nephrotic syndrome results when there is a threat to the immune system and an inflammatory response is evoked. Figure 22-9 illustrates the pathophysiology of NS. The glomeruli become increasingly permeable to plasma protein resulting in massive urinary protein loss or proteinuria. When protein is lost, fluids shift from the intravascular to the interstitial spaces. The result is tissue edema, ascites or accumulation of fluids in the abdominal cavity, and hypo-volemia. Once the volume diminishes in the vascular spaces then renal blood flow declines. Renin production is stimu­lated to maintain volume and systemic pressure. The result is excretion of aldosterone and tubular reabsorption of sodium. Water follows the sodium leading to edema. Serum cholesterol and triglyceride levels rise from the stimulation of lipoprotein production in the face of hypovolemia and falling serum protein levels. This stimulation is an attempt to make up for the lost proteins and is seen in conditions of starvation. If immunoglobulin levels are monitored, IgG lev­els are diminished. As blood volume falls, red blood cell and platelet concentrations are increased. The net result is a slowing of the blood flow and ultimately the clumping or clotting of red blood cells and platelets. That coupled with protein losses puts the child at risk for coagulation or clotting problems.

 

Clinical Manifestations

These children exhibit the same symptoms as any other child with renal failure. Edema is usually the first clinical feature. Initially, it is often mild, being periorbital in the early morn­ing hours and becoming more generalized after the child has been ambulatory (Hogg, et al, 2000). Anorexia, abdominal pain or tenderness caused by the inflammation of the kidney, abdominal swelling, fatigue, history of recent respiratory infection, increased weight or rapid weight gain, and vital signs (initially including blood pressure) within the normal range may also be noted.

 

Diagnosis

The diagnosis is dependent upon proteinuria. Serum albu­min levels are diminished (hypoalbuminemia). Laboratory evaluation includes urinalysis for protein, red blood cell casts, serum albumin (<2.5 g/dl—hypoalbuminemia), serum cholesterol, triglycerides, hemoglobin, hematocrit, platelet count, electrolytes, BUN, creatinine, complement levels, antistreptolysin O (ASO) titer, and streptozyme. The pres­ence of proteinuria, and red blood cells indicates kidney inflammation. The rise in serum cholesterol, triglycerides (in the face of a falling hemoglobin), hematocrit, and platelet count indicates some problem with hypoproteinemia in the serum. The serum electrolytes will be altered as renin and aldosterone levels change and sodium is reabsorbed. The BUN and creatinine rise as kidney function falls. The com­plement level will fall as the condition worsens as comple­ment (serum proteins) move from the serum to the site of inflammation. The ASO titer and streptozyme are tests to determine if there has been a streptococcal infection.

 

Treatment

Treatment focuses on reducing proteinuria, controlling edema, and preventing infection. The mainstay of treatment is corticosteroid therapy with prednisone and prednisolone (Prelone) in order to obtain a remission. Corticosteroids decrease the inflammation and the loss of proteins, thus restoring oncotic pressure and promoting diuresis. Oral preparations of prednisolone allow for accurate dosing and increased palatability in young children. A typical protocol is to start with a high dose of either drug (2 mg/kg/day; maxi­mum of 80 mg/day). Treatment is continued until the child becomes free of proteinuria or for a period of four to eightweeks (Hogg, et al., 2000). The medication is gradually tapered over a period of several weeks and then stopped as long as the child remains asymptomatic. However, the rate of relapses is high, 60-70% (Constantinescu, Shah, Foote, & Weiss, 2000). Relapse is treated with a short course of high-dose daily steroids until the child is free of proteinuria for three days. When there is failure to respond to steroid ther­apy or when their side effects are troublesome, other immunosuppressant medications are given. These include cyclophosphamide (Cytoxan), chlorambucil (Leukeran), or cyclosporin (Sandimmune). If an infection develops as a result of long-term steroids, an antibiotic is ordered.

 

Figure 22-9   Pathophysiology of Nephrotic Syndrome

 

Diuretics, such as furosemide (Lasix), should not be used to treat mild degrees of edema; however, they may be used if the child has severe edema. Because diuretics can precipitate hypovolemia, hyponatremia, and hypokalemia, electrolyte levels should be monitored closely. Albumin may be given if the edema is marked and causes the child to have decreased mobility, poor oral intake, or decreased urine out­put. Albumin helps to restore normal plasma oncotic pres­sure and promotes the movement of interstitial fluid back into the intravascular compartments. The albumin is fol­lowed by furosemide to reduce potential for fluid volume overload and to enhance diuresis. Salt intake is usually lim­ited to control edema and reduce the risk for hypertension especially when daily glucocorticoids are given.

 

Nursing Management

Nursing management focuses on maintaining fluid and elec­trolyte balance, administering medications, preventing infection and skin breakdown, and education. The child’s vital signs should be monitored every 4 hours or at least every shift. Low blood pressure and tachycardia are signs of hypovolemia. Intake and output are documented every shift. The nurse should monitor fluid with special attention to sodium restrictions if ordered. Any urine output less than 1-2 ml/kg/hr is to be reported immediately. Serum and urine electrolytes as ordered need to be evaluated. Nurses should assess for signs of edema and dehydration. These include dry skin, or dry mucous membranes, poor skin tur-gor, slowed capillary refill, pitting edema, sunken eyeballs, or dependent edema. Daily weights should be measured at the same time of day and on the same scale. Assessment of breath sounds for rales or wheezes may indicate pulmonary edema. Medications (diuretics, steroids, or immunosuppres-sive agents) should be administered as ordered. Signs of infection, including elevated temperature, changing CBC with differential, cough, sore throat, or other systemic com­plaints are evaluated. The child should be protected from visitors, personnel, or other clients who may have infections. Nurses should use good handwashing while caring for the child, and give antibiotics as ordered to prevent and/or treat infection. The child’s skieeds to be protected from breakdown especially if edema is present. The child should be repositioned every two hours. The nurse should place an edematous extremity on a pillow or other support making sure the circulation is not impeded. Skin should be assessed for areas of redness or discoloration. For boys with edema­tous scrotums, padding and support to this area should be provided.

 

Family Teaching

Nurses should explain to caregivers what is known about nephrotic syndrome and its expected course. Caregivers should be allowed to ask questions and to express their feel­ings. Nurses must teach caregivers how to perform urine dipstick protein level measurements and the importance of measuring and recording the readings daily. They should be instructed to obtain daily weights for their child. The nurse needs to explain how important their role is in identifying relapses, the first signs of which are increases in weight and levels of protein in the urine. Caregivers should be taught about steroids and their immunosuppressive action and the need to protect their child against infection. They also need to know that steroids can increase appetite, and may benefit from having a nutritionist consultation prior to discharge to help with the child’s diet.

Caregivers should be instructed to notify the health care provider if the child is exposed to chickenpox if she/he has not had the disease or the vaccine. Live viral vaccines should not be given to children receiving high doses of steroids or other immunosuppressive medications, and caregivers need to be cautioned about this.

 

HEMOLYTIC UREMIC SYNDROME

Hemolytic uremic syndrome (HUS), an acute renal disease, is the most frequent cause of acute renal failure (ARF) in children.

 

Incidence and Etiology

Though relatively uncommon, HUS gained attention after children acquired the disorder as a result of an Escherichia coli (E. coli) infection from eating contaminated beef. It is more prevalent in developing countries where sanitation and the undercooking of meats are a problem. It is most com­mon in children ages 6 months to 3 years. About 80% of all cases of HUS are found in children age 4 and under, occur­ring equally in both sexes (Neumann & Urizar, 1994). The exact etiology of HUS has not been determined, but it is thought to be associated with bacterial toxins, viruses, and chemicals. The organisms involved include E. coli, shigella, rickettsia, coxsackievirus, ECHO virus, adenovirus, pneumo-cocci, and salmonella.

 

Pathophysiology

The pathophysiology of HUS is complex. The most fre­quently seen sequence is a bacterial invasion of the gastroin­testinal tract leading to vomiting and diarrhea. The bacteria cling to the intestinal mucosa where they quickly multiply. Intestinal peristaltic action is slowed. An endotoxin is pro­duced from the bacteria. An inflammatory response is cre­ated that leads to capillary wall damage and occlusion of the surrounding blood vessels. This same reaction occurs within the renal system deep in the glomerular arterioles. The endothelial lining of the affected tissues swell, and platelets move to the injured site. This move results in clot formation and intravascular coagulation. In HUS, the platelet clot or aggregate slows the blood flow through the renal system. Renin production is stimulated resulting in systemic hyper­tension. The platelet count falls as these platelets are dam­aged in the same manner as the red blood cells and the result is thrombocytopenia (less than 100,000/pl) which lasts 1 to 2 weeks (Neumann & Urizar, 1994). When the vessels of the glomeruli are affected, the result is a lowered glomerular filtration rate, eventually urine output is lower, and acute renal failure with hypertension follows. These clots and the inflammatory process can occur in any organ of the body, although it is most common in the gastrointestinal, respira­tory, and genitourinary systems.

 

Clinical Manifestations

The clinical manifestations of HUS are a triad of symptoms, which include acute renal failure, thrombocytopenia, and anemia. The prodromal symptoms are gastrointestinal with diarrhea and vomiting or an upper respiratory infection. Once the hemolytic process starts, it may last from a few days to 2 weeks. The child becomes progressively more irri­table, lethargic, and anorectic. Soon the child experiences anemia, and as it worsens, pallor increases, the hematocrit falls, and urine output diminishes. As the platelet count falls, there is increased chance of bleeding, bruising, and purpura. As the urinary system becomes more restricted with clot for­mation, the blood pressure rises leading to hypertension.

 

Diagnosis

Upon physical examination, hepatosplenomegaly (the enlargement of the liver and spleen) may be present. Edema, hypertension, congestive heart failure, and abdomi­nal tenderness or pain are the common manifestations. The child may be pale, lethargic, dehydrated, and irritable. The history may include bloody diarrhea, vomiting, decreased urinary output, and slight abdominal pain. There may be altered levels of consciousness or seizure activities reported especially if the serum electrolytes, calcium, and phosphorus levels are outside normal limits. The rationale is that if there is an increase in workload on the heart from the edema, the blood pressure rises, and blood flow to the kidneys is dimin­ished. The toxins normally cleared from the kidneys build up and the tubular reabsorption or excretion of ions such as sodium and potassium are altered. The result is an adverse effect on the central nervous system leading to seizures and altered consciousness.

 

Treatment

Primarily the treatment is symptomatic. If the serum elec­trolytes are outside normal limits and renal failure is severe, hemo- or peritoneal dialysis and/or fluid restriction may be necessary to raise the serum sodium levels that have fallen because of dilutional or volume overload. Dialysis is most often reserved for those children who are anuric (without urine output) for 24 hours or have oliguria and are extremely hypertensive or experiencing seizures. If the serum potas­sium level is high because of a decreased excretion of this ion by the renal system, a Kayexalate enema or nasogastric solu­tion may be given. Serum glucose levels may also be low because of increased metabolic needs; therefore, dextrose or total parenteral nutrition must be given. If the pancreas has been affected by clot formation, the insulin production may be altered. Some children may develop hyperglycemia and must receive insulin therapy.

Calcium and phosphorous levels are affected with cal­cium falling and phosphorus rising. Calcium is excreted by the kidney and reabsorbed in the tubules. It is also depen­dent on intestinal function and transport across the epithelial tissue. In HUS these systems fail resulting in falling calcium with the rebound of phosphorus, which is normally filtered by the kidney. Either calcium gluconate or calcium chloride can be given depending on institutional policy or health care provider’s wishes. Aluminum hydroxide gel may be given orally to bind the rising phosphorous. Treatment for hyper­tension is accomplished with hydralazine (Apresoline) and captopril (Capoten). The child may also be acidotic because of metabolic acidosis from the inability of the kidney to buffer normally produced acids in the body, and may require bicarbonate therapy. If there are central nervous system symptoms, such as altered consciousness or seizures, a cen­tral venous line may be placed for central venous pressure (CVP) monitoring. If the bleeding has been severe or the blood counts are low, then blood transfusions with fresh, packed red blood cells are given. Any time that fluids are given, even in the form of packed cells, fluid overload must be considered and prevented, if possible. Some institutions will give plasma products to these children to avoid the increased volume needed with packed red blood cells. Oral feedings may be resumed once the vomiting and diarrhea are controlled. More than 90% of children with HUS recover with normal renal function (Bergstein, 1996). However, there is potential for the development of chronic renal failure.

 

Nursing Management

Nursing management focuses on maintaining renal function and fluid and electrolyte balance, and providing family sup­port. Nurses should assess the child for signs of dehydration: increased temperature, pulse, respirations, falling blood pressure, decreased peripheral perfusion, dry skin and mucous membranes, decreased urine output with a rising urine specific gravity, and poor skin turgor. Intake and out­put should be documented at least every 4 hours. If the child is in intensive care, this may be done every 1 to 2 hours. Nurses should check weights daily, and administer fluids and check serum electrolytes, BUN, creatinine, Hct, Hgb, WBC, and arterial blood gases as ordered. If the child experiences any central nervous system symptoms, a central venous catheter may be placed to measure this pressure. A car-diorespiratory monitor should be placed on the child. Attention should be paid to any changes in EKG tracings, such as a peaked T wave (related to potassium rises) and a widened QRS complex, or signs of heart block.

The child is assessed for signs of edema: tachycardia, tachypnea, hypertension, visible edema, and increased pulmonary secretions. Upon auscultation of the lungs, rales or wheezes may be heard. Weights must be monitored at least daily or more frequently as necessary. Urine output will be low and will need close monitoring. A Foley catheter may be placed for strict intake and output measurements. Chest X rays should be done to determine any pulmonary edema or cardiomegaly. Nurses should monitor electrolytes and blood counts as indicated and monitor CVP. If it measures 15 or greater, dialysis may be necessary. Oxygen may be required to support ventilation.

The child is evaluated for signs of bleeding or injury related to thrombocytopenia, and any signs of petechiae, bleeding, excessive bruising, or rashes are documented. Any invasive procedures should be avoided when possible. Nurses should monitor vital signs for changes from baseline, and assess neurologic status, including increasing restless­ness, irritability, or lethargy, difficulty in arousal, or decreased sensation to touch or pain.

Nurses should assess the child for signs of possible increased intracranial pressure. These include changes in level of consciousness; inability to respond appropriately to verbal cues, touch, or pain; and changes in movements of the extremities or a decreased muscle tone in one or all four extremities. Pupillary changes or seizure activity should be noted also. The head of the bed should be elevated at least 30 degrees, and the room should be quiet and without excessive lights. If the neurologic status is impaired and the central venous pressure is rising, hypotonic IV solutions should be avoided. Osmotic diuretics should also be avoided as they add to problems of hypervolemia caused by fluid shifts.

Nurses should assess for gastrointestinal disturbances, document any vomitus and stools and describe the charac­teristics, and auscultate for bowel sounds. If none are pre­sent, a nasogastric tube may need to be placed to assist with gastric decompression. Antacids are used if the gastric pH is less than 5. Once feeding can be tolerated, small frequent feedings should be started and increased as tolerated.

 

Family Teaching

The caregivers may feel guilty that they missed something and did not know their child was so sick. They need reassur­ance that the symptoms are very subtle. They should be told as much of the pathophysiology as is known and helped to understand the normal course of HUS. They should be encouraged to participate in their child’s care (MacPhee, 1995).

 

RENAL FAILURE

Renal failure refers to a condition that adversely affects the kidney resulting in decreased functioning of this organ sys­tem. It may take two main forms: acute or chronic.

 

Acute Renal Failure

Acute renal failure is a sudden onset of impaired renal func­tion. Most children with ARF regain renal function. ARF is classified according to the part of the renal system that is affected. Three main types exist: prerenal, intrarenal, and postrenal.

 

Incidence

ARF is uncommon in children, but it can be life-threatening when it does develop.

 

Etiology and Pathophysiology

Prerenal ARF is characterized by a sudden decrease in renal blood flow or perfusion to the kidneys. This type of renal fail­ure can result from dehydration, hypovolemia or shock, sep­sis, renal artery obstruction, or perinatal asphyxia (Stewart & Barnett, 1997). Intrarenal ARF is associated with damage to the tissues of the kidney. The causes are iatrogenic secondary to antibiotic therapy (aminoglycosides or other nephrotoxic medications), contrasts dyes, ureterovesical obstruction, glomerulonephritis, pyelonephritis, hemolytic uremic syn­drome, or other infections that affect renal tissue. Postrenal ARF results from an obstruction of urine at some point between the kidney and the urinary meatus. It is usually an outflow obstruction that causes a “back-up” of urine within the kidney, putting pressure on the endothelial lining and ultimately diminishing renal function. The causes that can occur in utero or during postnatal liie are:

·                           Posterior ureteral valves

·                           Ureterovesical obstruction—an obstruction at the junction of the ureters into the bladder

·   Ureteropelvic obstruction—an obstruction at the junction of the ureters into the renal pelvis

·                           Neurogenic bladder, primarily one without innervation

·                           Wilms tumor—a nephroblastoma or solid mass, which is the most common renal tumor in children

·               Renal calculi

 

Clinical Manifestations

The most common clinical manifestations are fluid and elec­trolyte imbalance, metabolic acidosis, and signs of dehydration or edema. Pallor, listlessness, lethargy, anorexia, vomiting, and in some cases seizures may also be observed. The child’s vitals signs mayor may not be withiormal limits depending upon the cause and duration of the renal dysfunction.

 

Diagnosis

The diagnosis is based on history, laboratory evaluation, and physical examination. Anuria or a urine output of <1 ml/kg/hr is a potential finding, although some children will have a normal volume of urinary output. Renal serum panel usually reveals a rising BUN and creatinine; serum electrolytes, especially sodium and potassium, may also be elevated. As the renal blood flow falls, the glomerular filtration rate falls, and the amount of sodium that is filtered by the kidney diminishes. The child may have dependent, pitting, or peri-orbital edema. There may be hypertension accompanying the edema. This hypertension is caused by changes in blood flow throughout the body and the build up of edema. As the blood flow to the kidneys decreases, renin production increases leading to vasoconstriction. The heart works harder to pump the blood thus raising the blood pressure. Pulmonary edema occurs in some children presenting with increasing respiratory distress.

 

Treatment

As with nephrotic syndrome, the aims of the treatment for the child with acute renal failure are to increase renal perfu­sion and to restore and maintain fluid and electrolyte bal­ance. This treatment may be with or without dialysis. The treatment without dialysis is as follows. If the sodium level is too high and edema is present, fluid and sodium restriction are necessary. If the potassium level is too high, then poly­styrene sodium sulfonate (Kayexalate) orally or per rectum is given. This resin binds potassium and removes it from the body. If metabolic acidosis is present, treatment is sodium bicarbonate to replace the lacking renal buffer.

If these interventions do not control the fluid and elec­trolyte balance or pulmonary edema or if congestive heart failure is present, then dialysis must be considered. Other indications for dialysis are severe systemic hypertension, a BUN >120 mg/dl, hyperkalemia, and increasing metabolic acidosis. There are three main types of dialysis: hemodialysis, peritoneal dialysis, and hemofiltration.

Hemodialysis is a hemofiltration system that occurs outside the body. It requires an arteriovenous (AV) fistula or shunt to be placed in a large vessel. This central line pro­vides access to the blood system to pump the blood out from the body to an external extracorporeal circuit and through a filtration system. This serves to remove the body’s waste products that cao longer be effectively filtered through the kidneys. This arteriovenous shunt in a large vessel requires surgical placement. The nurse must aseptically maintain it. Hemodialysis can be performed on an intermit­tent time-cycled basis, either in a hospital, dialysis center, or home setting. It is usually a 3 to 4 hour procedure repeated 3 to 4 times per week. It is more efficient at removing nitrogenous wastes than any other form of dialysis (Madder & Milberger, 1996).

 

 

Figure 22-10  Peritoneal Dialysis Setup

 

Peritoneal dialysis requires the placement of a catheter into the peritoneal cavity for the purposes of removing excess fluids, solutes, and nitrogenous wastes (Figure 22-10). This placement may or may not require an open surgical proce­dure. It usually does not require a heparinized line. The treatment or filtration process involves the slow flow of fluid through the catheter into the peritoneal cavity until the desired fluid level has been administered. At that time a clamp is put in place allowing the fluid to dwell for a time in the peritoneal cavity to remove waste products. When the clamp is released, the fluid drains into the dialysis system. This cycle is repeated either automatically or manually four to five times per day. The procedure is usually repeated for several days and is normally done at home. Peritoneal dialy­sis is problematic for infants requiring dialysis, as the clear­ance of toxic wastes, solutes, and fluids is slow. Their abdominal areas are small and, if the treatment is not suc­cessful, the hypervolemia may be worse, a condition not tol­erated well by small infants. Hemofiltration is a continuous form of dialysis by means of a continuous arteriovenous (CAV) or venovenous (CW) shunt. These shunts, like hemodialysis, require an extracorporeal circuit through which the blood flows into a filter system. The filter is placed between the arterial and venous lines along with a collecting bag. The blood flows from the child through the circuit continuously to remove nitrogenous wastes, solutes, and fluid. When the arteriove­nous shunt is used, movement of the fluid is caused by the body’s own pressure gradient (hydrostatic pressure from cardiac output and oncotic pressure from plasma proteins) rather than an external pumping device. If the venovenous shunt is used, a pump is necessary to move the blood through two separate venous cannulas or two ports in mul-tilumen cannula (Madder & Milberger, 1996). Both ports are in veins so blood leaves through a venous route and returns via a vein. Either of these ultrafiltration systems has the advantage of using a very slow process that continu­ously adjusts as the body’s solute load changes. The pressure of the body’s own plasma proteins helps regulate the system so there is less stress on it. The circuit is heparinized so there is a danger of bleeding with this type of dialysis. However, this danger is less than with hemodial­ysis because less volume of blood flows through the circuit at any one time with hemofiltration. This process is slow and is not as effective at removing large molecules such as urea. When any form of dialysis is used, there are risks. Morbidity and mortality for children on dialysis are most often related to intraperitoneal bleeding, peritonitis, or ves­sel blockage (Kohli, et al., 1997).

 

Nursing Management

This section will be divided into two parts. The first will be for the child and family that does not require dialysis but is experiencing acute renal failure. The second part will be for the child and family with acute renal failure who requires dialysis. The nursing care for both groups of children is aimed at restoring and maintaining fluid and electrolyte bal­ance. In addition, for the child and family undergoing dialy­sis, the focus is also on maintaining the integrity of the circuit, protecting the child from bleeding at the shunt site, and preventing injury or infection. For both groups of chil­dren, a thorough history must be taken to elicit the underly­ing cause of the acute renal failure. Questions should focus on those conditions described as potential etiologies of prer-enal, intrarenal, and postrenal acute renal failure, such as, have there been any previous urinary tract infection, episodes of low oxygen levels as with a premature infant, any antibiotic therapy, or renal stones? Physical examination, ini­tially and subsequently, includes vital signs, weight, intake and output, urine specific gravity, and laboratory values, especially BUN and creatinine. The remainder of the nurs­ing management is the same as that described for the child with nephrotic syndrome.

 

Family Teaching

Fear and anxiety are very real emotions for caregivers of a child with acute renal failure. They need honest and thorough explanations about what is known about the cause and the expected course of the illness. They need time to express their feelings. They may benefit from referrals to clergy or to support groups, especially if the treatment will be prolonged. Encourage them to participate in the child’s care as they feel comfortable.

For the child and family undergoing dialysis, teaching regarding medications is necessary. They must be aware that if the urine output diminishes from what they have come to accept as normal, the health care provider should be called prior to medication administration. They need to be taught to maintain the routine schedule or cycling of the dialysis, either at the clinic or in the home, and to maintain meticulous clean care of the catheter site to protect the child from infection. If the dialysis is to be performed in the home, there must be a telephone and running water avail­able. The electric company as well as the police and fire departments need to be notified to make sure that power is restored immediately to this family in case of electrical fail­ure. A backup generator should also be available in the home to be used until power can be restored. It is also nec­essary for the nurse to assess the child and family for signs of depression or severe anxiety as these are common find­ings that may require a mental health consultation. This child and family will require a lot of emotional support. If the child is school age, encourage discussion of his or her fears, concerns about peers, and any self-esteem issues he or she may have.

            Instruct the child and family about the need for a low protein diet if this is to be maintained at home.

            Teach the child and family about signs of infection or the worsening of the renal problem. Signs would include weight gain caused by edema, headache that could indicate hypertension, flank pain, decreased urine output, fever, sore throat, or flu like symptoms.

            Instruct the family that the child can pursue activities as tolerated each day.

            Encourage the caregivers to teach the child to stay away from other children who have obvious colds, flu, or other infections.

            Encourage the caregivers to teach the child about good handwashing especially at school where there are many other people.

            Allow the child to decide whether the teachers or friends will be told about the renal problem.

            Refer the child and family to resource groups such as the National Kidney Foundation or local support
groups.

 

Chronic Renal Failure and End Stage Renal Failure

Chronic renal failure (CRF) is a progressive disease. The damage that is done to the renal system in some cases is irre­versible. This condition is considered chronic when approxi­mately 50% of the renal function remains and the condition has lasted for at least several months. If it is considered to be permanent and irreversible, then it is classified as end stage renal failure (ESRF). All chronic renal failure will first progress to uremia. Uremia is a condition where toxic nitrogenous waste products, blood urea, and creatinine build up in the system. If this condition is not reversed, it pro­gresses to ESRF.

 

Incidence and Etiology

The incidence of CRF is between 1.5 and 3.0 per million in the pediatric population (Fogo & Kon, 1994). The etiology of CRF and ESRF varies but may be caused by prematurity, use of nephrotoxic medications such as aminoglycosides, genetic syndromes with congenital urinary or renal obstruc­tions, hemolytic uremic syndrome, glomerulonephritis, pyelonephritis, and other systemic infections. Some children experience CRF or ESRF as a result of immunologic dys­function that causes actual injury to renal tissue.

 

Pathophysiology

The exact pathophysiology depends on the etiology of the condition that began to disrupt the kidney function. In any case, eventually the renal system is compromised, as is renal blood flow through the kidney, leading to loss of oxygen to the tissues and ultimately to destruction of portions of the nephron. The nephron is the working unit of the kidney and functions to create urine, filter substances through the kid­ney, and reabsorb and excrete solutes in the body. The nephron is composed of the glomerulus and the renal tubule. Nephrons once destroyed cannot be regenerated. As portions of the nephrons die, the renal function becomes less efficient. The remaining nephrons attempt to take over the complete function so they hypertrophy. The glomerular pressure increases, as does the arterial pressure in the glomerular capillaries and renal arteries. Eventually the glorneruli sclerose and die. If this cycle is not stopped and the arterial pressure lowered, ESRF results.

 

Clinical Manifestations

As with acute renal failure, the main clinical manifestations of CRF and ESRF include fluid and electrolyte imbalance, dehydration or edema, metabolic acidosis, and systemic hypertension. The child may also experience anemia, pallor, fatigue, anorexia, vomiting, slowed linear growth, organic failure to thrive, and renal bone disease or osteodystrophy (Watkins, 1997).

 

Diagnosis

The diagnosis is based on the history of either long-standing renal problems or growth problems accompanied by altered laboratory values. The child’s presentation may be one of dehydration, edema, hypertension, electrolyte imbalance, altered calcium phosphorus ratios, elevated BUN and creati­nine levels, low hematocrit and hemoglobin, and long bone X rays revealing osteodystrophy. Pallor, lethargy, anorexia, and vomiting may or may not be present.

 

Treatment

Treatment for the child with CRF and ESRF is aimed at restoring or maintaining fluid and electrolyte balance. If edema is present, then fluid restriction and sodium and potassium restriction may be necessary. Diuretics are used if edema is significant. Antihypertensive medications are given if hypertension is present. Protein intake may be restricted because of the kidney’s inability to rid the body of waste products. Phosphorus is restricted in order to increase the calcium levels. If calcium levels are maintained, then there is less chance of bone disease that can result when calcium lev­els are low. Vitamin D supplementation may be given. The result is that vitamin D will be present to boost the calcium levels to prevent bone disease. Aluminum hydroxy gel may be given to bind with phosphorus and decrease the gastroin­testinal absorption. This medication should only be used on a short-term basis as aluminum levels can become high and result in seizures. Calcium carbonate will achieve the same result and is not toxic even to infants.

Experimental therapies include erythropoietin to combat anemia and growth hormone to boost linear growth. Immunosuppressive therapy is also used especially if the child is going to require renal transplantation. While this immuno-suppressive therapy is not experimental, the combination of medications (more than one immunosuppressive medication at a time) is undergoing research. For those children  ESRF, dialysis and/or renal transplantation are the only treatment options.

Renal transplantation is usually reserved for children for whom medication and dietary management of fluid and elec­trolyte balance and hypertension have been unsuccessful. These children have ESRF. They may or may not have been maintained on dialysis for a long period of time prior to the transplant. Transplants can be performed on infants. The surgical team and the family make the determination of the candidate for a transplant. In some institutions an ethics committee also looks at quality of life issues to help in the decision-making process. The question they usually ask is “What will the long-term quality of life be for this child if the transplant is done?” Unfortunately there are no guarantees with this type of surgery. The usual candidates for trans­plants are those who can withstand a surgical intervention, are in good nutritional status, and are not severely immuno-compromised (Ryckman & Pedersen-Ryckman, 1998; Tyden, Berg, Bohlin, & Sandberg, 1997).

Kidneys for transplantation are obtained either through living donors—usually close relatives—or cadavers. Tissue typing to determine a match requires meticulous tests simi­lar to crossmatching for blood transfusions. Close relatives are most likely to be a very good tissue match, but even then there is a chance of graft (the transplanted kidney) or organ rejection. Cyclosporine, azathioprine (Imuran) and pred-nisone or prednisolone are used to suppress the natural immune response. Organ rejection is known as graft versus host disease, which occurs when the transplanted organ fights against its host, creating an exaggerated immune response to rid the body of the foreign organ. This reaction can be life-threatening. Most renal transplants are not lost by rejection but the tissue dies from vascular thrombus or clots in the renal vessels (Singh, Stablein, & Tejani, 1997).

Transplantation is just one aspect of ESRF treatment. Post-transplantation, immunosuppressive medications are required for life. Dietary restrictions may still be necessary especially regarding protein intake. Medications for hyper­tension and diuretics may still be needed following surgery.

These clients need to be followed for serum and urine chemistries, immunologic examination for signs of rejection and aggressive infections, and growth and development follow-up care. As they are on immunosuppressive medication along with steroids to decrease the chance of rejection, these children must be followed for any side effects of the steroids. There are several concerns about the long-term effects of steroid or cyclosporine therapy. Both of these medications increase the susceptibility to infection as mentioned above. They both affect other glucocorticosteroids that in turn alter serum glucose and insulin levels. Adrenal suppression is common often resulting in glucose intolerance (Haffner, Blum, Heinrich, Mehls, & Tonshoff, 1997). Cushing syn­drome or round moon face and deposition of fat around the scapular region caused by the glucocorticosteroid effects has most often been associated with long-term steroid therapy, but can also come from cyclosporine use. Other effects from steroids are seen in bone mineralization and strength, which are concerns for a growing, active child. The effects on growth hormone of the renal disease itself are made worse by some of the therapies. All these questions need further research to either substantiate or refute these clinical obser­vations. Use of growth hormone is just becoming popular to stimulate continued growth, but again the long-term effects are ieed of research (Watkins, 1997).

 

Nursing Management

This section will be divided into two sections. The first will be the management of the child and family with CRF or ESRF. The second part will be the management of the child and family undergoing a renal transplant. The goals of the nursing care are to restore and maintain fluid and electrolyte balance; restore and maintaiutrition and growth; and decrease the anxiety of the child and family. Most of the nursing management is the same as with acute renal failure. Other points of nursing management are discussed below.

Nurses should administer medications (diuretics, steroids, or immunosuppressive agents) as ordered, and assess for signs of infection: elevated temperature, changing

CBC with differential, cough, sore throat, or other systemic complaints. The child should be protected from visitors or personnel who may have infections. Antibiotics are adminis­tered as ordered. Nurses should always consider if these medications are cleared through the kidney, and if so, then peak and trough levels must be monitored as some medica­tions are nephrotoxic.

If anemia is severe, blood transfusions with packed red blood cells may be administered, but this presents the dan­ger of fluid overload. Newer therapies include the use of erythropoietin to boost the reticulocyte development. This therapy is used in the predialysis phase and is associated with delaying renal function deterioration. Erythropoietin boosts the hemoglobin by about 3 g/dl when a maintenance dose of between 70 and 300 U/kg per week is given (Krmar, Gretz, Klare, Wyhl, & Scharer, 1997). Many practitioners consider this treatment to be experimental and the long-term effectiveness has not been widely studied. This child may also need dialysis and should be assessed for signs indi­cating the need for this form of treatment.

The assessment and care remains the same as that described for the child and family with CRF and ESRF. These children are at risk for the development of vesi-courethral reflux in the graft, which may lead to pyelonephritis (Neuhaus, et al, 1997). Signs of a kidney infection such as fever, flank pain, burning on urination, cloudy or blood-tinged urine, and sometimes abdominal cramping, must be moni­tored, and the caregivers must be taught these signs as well.

 

Family Teaching

Because either CRF or ESRF is a chronic, life-long prob­lem, the family will have many learning needs, especially related to the need for meticulous follow-up care. They need to understand the etiology of the problem and the course of treatment. They will need to be taught about dietary restrictions, use and side effects of medications, signs of further deterioration of the renal function, and pos­sibly how to perform dialysis in their homes. The side effects from steroids and immunosuppressive therapies include a depressed immune system so the child is more vulnerable to infection, growth retardation, and bone dem-ineralization. There is a greater risk for fractures. Some children will feel hyperactive with high doses of steroids. If they take the steroids for a long time, they may develop a moon face, fat deposits along the shoulders, and generally gain weight. If the child is on diuretics, the individual may lose potassium and feel weak or faint or experience heart palpitations. Caregivers need to know that these side effects are possible but do not always occur.

 

They may benefit from financial counseling as these are costly problems and are not always covered by health insur­ance policies or managed care contracts. They need to understand the impact that a chronic illness has on them­selves and their child. They should be encouraged to take advantage of psychological counseling or participate in a support group. For the family whose child has undergone a transplant additional teaching is needed. The family must be taught signs of rejection and a kidney infection. They must also understand the need for lifelong follow-up care and medications given on the established schedule. It will be necessary to arrange for home care and nursing follow-up in the home. Quality of life issues need to be addressed. The child and family can be reassured that current research indi­cates that childhood transplant recipients can achieve a good quality of life in their adult years (Krmar, Eymann, Ramirez& Ferraris, 1997). Families also need to know that generally the immunizations should be given and that there is no, adverse affect on the kidney (Enke, Bokenkamp, Offner Bartmann, & Brodehl, 1997). The rationale is that while these children may be immunosuppressed, their immune system still can respond to the vaccines in the immuniza tions. It is better to have the children challenged by a labora tory, controlled dose of the “disease” than to actually acquire the childhood disease itself

 

BLADDER EXSTROPHY-EPISPADIAS COMPLEX

 

Bladder exstrophy-epispadias complex is a rare serious con-genital anomaly affecting the urologic and musculoskeletal systems. In early fetal life the abdominal wall and underlying structures fail to fuse producing an exposed bladder and ure­thra, pubic bone separation, and associated genital and anal abnormalities. This complex occurs in males more frequently than in females. Epispadias is considered a mild form of bladder exstrophy, and in more severe cases the two coexist (McAninch, 1995). In males, epispadias is characterized by the urethral opening on the dorsal side of the penis in con­trast to hypospadias where it is on the ventral surface (Figure 22-11). Females with epispadias present with sepa­ration of the labia and a bifid (split into two parts) clitoris. If the internal bladder sphincter is affected, total incontinence results. In exstrophy the lower urinary tract is exposed, and the everted bladder appears bright red through the abdomi­nal opening. There is also a widening of the symphysis pubis. Musculoskeletal anomalies seen in these children include an outward rotation of the hips and widening of the pelvis. Male infants have a short penis with dorsal chordee, or upward curvature, and a ventral prepuce. Females pre­sent with a bifid clitoris and nonfused labia. At birth the bladder mucosa is thin, reddened, and susceptible to injury. Various techniques are utilized to protect the mucosa and preserve hydration.

 

 

 

Figure 22-1. 1    Bladder Exstrophy with Epispadias. Photo courtesy of Casimir Firlit, MD, PhD, William E. Kaplan, MD, Max Maizels, MD, and Jeffrey Palmer, MD, Children’s Urology Ltd.

 

Surgical management of bladder exstrophy is usually performed within the first 48 hours of life but may be deferred secondarily to the infant’s stability or until further testing is performed. Goals of management include preser­vation of the primary bladder and abdominal wall and provi­sion of an adequate pelvic structure to support the bladder. Other goals include the achievement of a functional bladder and cosmetic reconstruction (Bowers, Hannigan, & Kushner, 1995). Initially, the bladder, abdominal wall, and symphysis are closed surgically.

Long-term care focuses on continence issues and social adjustment. In its severest forms continence may only be achieved through augmentation of the bladder to increase its storage capacity and in some cases a urinary diversion proce­dure. Issues of sexuality need to be addressed as the child approaches adolescence, including information regarding reproduction. Research indicates that most clients with exstrophy do not develop long-standing maladjustment and have a high level of sexual functioning (Bowers, Hannigan, & Kushner, 1995). Management of exstrophy is one of the most complex of all urologic disorders.

 

Key Concepts

 

            The genitourinary system of the infant and child is immature compared to an adult’s; therefore, medica­tions and therapies must be considered in terms of renal maturation.

            Embryologieally, the genital and urinary systems are interrelated; hence, any insult during fetal develop­ment can have devastating consequences for the child and family.

        Common manifestations of genitourinary alterations in children include vague symptoms such as abdominal pain, nausea, vomiting, and diarrhea.

        Nursing assessment of the child with genitourinary alterations  includes  a  history  about  diet  and feeding/eating pattern, elimination pattern (stool and urine), growth pattern, gastrointestinal symptoms, and a physical examination.

        Untreated UTIs can lead to progressive infections with kidney involvement, subsequent renal scarring, and decreased kidney function.

        Enuresis is the involuntary voiding of urine in children over the age of 5 years without a structural defect. Incontinence is wetting that results from a structural defect or abnormality.

        Vesicoureteral reflux is the backflow of urine from the bladder into the upper urinary tract. Clinically these children may be diagnosed only after a full radiographic workup after UTI.

        Hypospadias is a congenital malformation and displacement of the urethra to the underside or ventral surface of the penis, requiring surgical repair.

        Cryptorchidism is synonymous with undescended testes. It may be unilateral or bilateral and is often treated before the age of 2 in an attempt to preserve spermatogenesis. Children with UDT must be followed through puberty and into adulthood secondary to issues regarding fertility and increased tumor potential.

        Hernias present as a bulge or a swelling in the scrotum or groin and may fluctuate with increased intraabdominal pressure such as crying.

       Acute glomerulonephritis is an inflammation of glomeruli within the kidney caused by a viral or bacterial agent.

       Nephrotic syndrome manifests as massive proteinuria and hypoalbuminemia that leads to edema and hyperlipidemia.

       Hemolytic uremic syndrome though rarely seen in children has been found to be secondary to E. coli infection.

       The three types of acute renal failure are prerenal, intrarenal, and postrenal.

       Chronic renal failure is a progressive disease that can lead to end-stage renal failure.

       Nursing management of children undergoing urologic procedures generally involve extensive family education and anticipatory guidance preoperatively along with postoperative issues of accurate fluid management, care of various drainage tubes, and meticulous wound care and assessment.

       Teaching for the child and family undergoing dialysis must include dietary needs, infection control, and performing the dialysis. The nurse must also emphasize the signs and symptoms of worsening renal failure and the need for close follow-up.

       Nursing management for the child with a renal transplant is directed toward teaching the family about dietary needs, infection control, and signs and symptoms of rejection.

 

Review Questions

           Identify the signs and symptoms of urinary tract infections including the standard clarification between cystitis or bladder infection and pyelonephritis.

       Describe the necessary urologic workup for a child post-first-documented UTI and the rationale for this further testing.

       Describe the differences between the terms enuresis and incontinence. What questions should be asked when obtaining a history for a child with wetting problems?

       Describe the conservative medical management for a child with vesicoureteral reflux.

       Describe the clinical manifestations of hypospadias in the newborn period and nursing interventions that should be instituted.

     Develop a teaching plan regarding the importance of long-term follow-up for a boy with UDT.

        Develop a teaching plan for caregivers regarding signs and symptoms of increasing problems and risk of incarceration in a child with hernias and/or hydrocele.

     Describe the pathophysiology of hemolytic uremic syndrome.

        What should the nurse advise caregivers about fluid restrictions and dietary restrictions for the child with acute or chronic renal failure?

        List the clinical indicators for dialysis.

 

 

 GASTROINTERSTINAL ALTERATIONS

 

Alterations of the gastrointestinal system can involve the esopha- gus, stomach, small and large intestine or the accessory organs, the liver, gallbladder, and pancreas. The primary function of the system is ingestion, digestion, absorption of nutrients essential for normal growth and maintenance of fluid and electrolyte balance, and elimination of waste products. These functions are vital for normal growth and develop­ment of infants and children. Gastrointestinal complaints are common in this age group. Alterations of function can be expressions of congenital anatomic abnormalities or alterations acquired after birth from disease or infection. The severity of gastrointestinal problems ranges from minor ill­nesses causing inconvenience to severe, life-threatening disorders such as intestinal obstruction.

 

ANATOMY AND PHYSIOLOGY

In comparison with adults, the newborn has a very ineffective gastrointestinal system because of its immaturity at birth. Sucking and swallowing are auto­matic reflexes initially, gradually coming under voluntary control as the nerves and muscles develop by 6 weeks of age. The newborn’s stomach capacity is only 10 to 20 ml, but expands rapidly to 200 ml by one month of

age and reaches adult capacity of 2000-3000 ml by late ado­lescence. Peristalsis, the coordinated, rhythmic, serial con­traction of the smooth muscle of the GI tract, is greater in the infant than in the older child. The emptying time of the stomach increases from 2 to 3 hours in the newborn to 3 to 6 hours by one to two months of age. These factors, the small stomach capacity, increased peristalsis, and increased stom­ach emptying rate, result in the need for small, frequent feedings. The infants metabolic rate is faster than an adults, thus requiring approximately 100 calories per kilogram of body weight compared with 30 to 40 for an adult. Regurgitation is common in the infant because the lower esophageal sphincter tone is decreased or relaxed.

The length of the small intestine is proportionately greater in an infant than an adult: six times the body length in infancy as opposed to four times the height of the adult. However, the infant’s intestine is supplied with an adult’s proportion of functional secretory glands per unit of area; therefore, an infant secretes proportionately more fluids and electrolytes into the intestine than does an adult. Similarly, the infant’s small intestine has a larger surface for absorption relative to body size than does an adult’s. Therefore, if diar­rhea develops, more electrolytes will be lost from the intesti­nal secretions. In contrast, the large intestine of the infant is proportionately shorter than an adult’s, resulting in less epithelial lining available for absorption of water from the feces. These two characteristics, more secretions and less absorption, are responsible for the soft, frequent stools of infants. Liver functions are also immature at birth; therefore, toxic substances are inefficiently detoxified and medications are inefficiently processed. Hence, the therapeutic dosage of drugs must be adjusted during the first few months of life to prevent them from reaching toxic levels. The processes of gluconeogenesis, deamination, plasma protein and ketone formation, and vitamin storage are immature during the infant’s first year.

The infant is deficient in several digestive enzymes that are usually not sufficient until 4-6 months of age. The pan­creatic enzyme amylase, responsible for the initial digestion of carbohydrates, is insufficient resulting in an intolerance of starches. If cereals are given before 4—6 months, the infant may develop gas and diarrhea. The enzyme lactase breaks down or hydrolyzes lactose, the primary source of carbohy­drates in infant formula and breast milk. Lactase levels are low in the preterm infant, increase in infancy, and decline after early childhood. This initial decreased level results in incomplete absorption of lactose, which can cause gas, abdominal distention, and diarrhea. Digestion and absorp­tion of fats is impaired because of low levels of the enzyme lipase. Fat in breast milk is absorbed more readily than in formula because human milk contains lipase. Protein diges­tion and absorption are fairly efficient in the newborn and infant. The infant intestine is more permeable to proteins than the older child or adult, thus allowing passage into the bloodstream of cow’s milk protein and other potential aller­gens. Therefore, infants ingesting formula instead of breast milk are more susceptible to food protein allergens. Breast­fed infants receive protective immunoglobulin proteins from human milk whereas formula-fed infants do not. Figure 23-1 illustrates the gastrointestinal tract of the child.

 

UPPER GASTROINTESTINAL ALTERATIONS

 

Upper gastrointestinal alterations commonly found in chil­dren include hypertrophic pyloric stenosis, cleft lip and cleft palate, and esophageal atresia and tracheoesophageal fistula.

 

Hypertrophic Pyloric Stenosis

Hypertropic pyloric stenosis (HPS) is the most common intra-abdominal condition requiring surgery during the neonatal period. Figure 23-2A illustrates a normal pyloric opening; Figure 23-2B shows pyloric stenosis.

 

Incidence and Etiology

HPS affects 1 to 3 per 1,000 live births and four to five times as many males as females. Caucasian males, especially first born, are the group most commonly affected. It is more common among Caucasians of Northern European ancestry, less common among African-Americans, and rare in Asians. The exact cause is not known; however, several theories have been proposed to explain the etiology. Environmental factors, allergies, pylorospasm, and muscle enzymes are just a few of the unproven etiologies. Genetic predisposition seems to increase the risk of HPS (Cook, Lopez, & Manfredi, 1996).

 

Figure 23-1.   Gastrointestinal Tract of a Child

 

Figure 23-2.   (A) Normal Pyloric Opening; (B) Pyloric Stenosis

 

Pathophysioiogy

The pylorus is the opening through which food passes from the stomach to the intestines. This opening is surrounded by a muscular ring, the pyloric sphincter. In HPS the pyloric sphincter hypertrophies and increases to four times its nor­mal width, resulting in a narrowed opening and gastric outlet obstruction (Cook, et al, 1996). This obstruction prevents gastric contents from emptying into the duodenum.

Clinical Manifestations

Symptoms usually develop during the third and fourth weeks of life. Nonbilious vomiting beginning between the second and fourth week of life is the initial symptom. Because of the progressive nature of the obstruction, the vomiting increases in frequency and eventually becomes projectile with vomitus being propelled up to several feet. The emesis is not bile stained because the obstruction occurs above the outlet of the bile duct. The infant is hungry in spite of the vomiting and will usually feed again. Because food does not pass through the pylorus, bowel movements are small. As vomit­ing continues, there is loss of fluid, leading to dehydration, and hydrogen and chloride ions are lost, leading to hypochloremic metabolic alkalosis. Serum potassium levels are usually maintained, but there may be a total body potas­sium deficit. The infant has poor weight gain or experiences weight loss and becomes increasingly irritable and lethargic as dehydration and electrolyte imbalances worsen.

Diagnosis

Diagnosis may be made on history and physical identification of the hypertrophic pylorus, which can usually be palpated as an olive-shaped mass in the epigastrum, above and to the right of the umbilicus. If the olive-shaped mass is felt, the diagnosis is confirmed. However, in many cases the enlarged muscle cannot be felt and prompt diagnostic imaging is required for further evaluation. The diagnosis may be con­firmed with a barium upper gastrointestinal (UGI) series or an abdominal ultrasound. The UGI, if positive, will reveal a delay in gastric emptying and a narrow, elongated pyloric channel, referred to as a “railroad track” sign (two narrow channels) or a “string sign” (one narrow channel). Ultrasonography is becoming the diagnostic method of choice because it is highly accurate (direct visualization of the muscle hypertrophy and the pyloric channel) and lacks the ionizing radiation inherent in a radiologic procedure such as the upper gastrointestinal contrast series (Deluca, 1993).

Treatment

A surgical procedure called a pyloromyotomy is the treat­ment of choice in which the circular muscle fibers are released opening the passage from the stomach into the duo­denum. Preoperatively, a nasogastric (NG) tube may be inserted, and the stomach emptied. Fluid, acid-base, and electrolyte losses must be corrected for 24 to 48 hours before surgery. Intravenous fluids and electrolytes are administered until the infant is rehydrated and the serum bicarbonate concentrations are less than 30 mEq/dl, indicat­ing that the alkalosis has been corrected.

Postoperatively, the NG tube should be removed, unless there is a reason to keep it in place, such as injury to or per­foration of the duodenum. The blood glucose, electrolytes, and complete blood count (CBC) should be monitored. Intravenous glucose should be continued until the infant is able to feed normally. Gastric motility is delayed for up to 24 hours following anesthesia. Therefore, feeding should begin slowly and advance cautiously. The surgical treatment for HPS has a high success rate and is considered curative.

Nursing Management

Assessment

In the nursing history the relationship of feeding to vomiting is determined, and the frequency, color, and amount of eme­sis is documented. Strict intake and output records are essential to assess the status of the infant’s hydration. Signs of dehydration are noted such as inelastic skin turgor, crying without tears, dry mucous membranes, a depressed anterior fontanel, urine output <1 cc/kg/hr, increased pulse, decreased blood pressure, and weight loss. The infant is observed for evidence of pain or discomfort, which does not occur except that of chronic hunger.

 

Nursing Diagnoses

Nursing diagnoses for the infant with HPS include:

Deficient fluid volume related to the effects of frequent vomiting.

Imbalanced nutrition: Less than body requirements related to vomiting and gradual reintroduction of feedings.

Pain related to surgical trauma.

Risk for infection related to surgical incision.

Deficient knowledge (caregivers) related to care of infant after discharge.

 

Outcome Identification

     The infant will demonstrate improved fluid and electrolyte balance.

     The infant will tolerate feedings and will demonstrate adequate nutrition by maintaining or regaining pre­admission weight.

    The infant will experience minimal postoperative pain.

    The infant’s surgical incision will remain free of infec­tion as evidenced by decreased swelling without red­ness or purulent discharge.

     Caregivers will verbalize an understanding of incision care, feeding techniques, and signs and symptoms of complications (recurrent vomiting, wound infection, failure to gain weight).

 

Planning/Implementation

Preoperative nursing care focuses on rehydration and cor­rection of the electrolyte imbalance. Daily weights obtained at the same time of day using the same scale are the best indicator of extracellular deficient fluid volume. Because vomiting will continue until surgical correction, the infant is giveothing by mouth; thus, maintaining a patent intra­venous infusion is essential. Monitoring the infusion, intake and output, and urine specific gravity are important nursing activities in fluid replacement. Family members need to be reminded to save diapers for weighing to measure urine out­put. If NG suction is used to decompress the stomach pre-operatively, the nurse’s responsibility is to maintain its patency and record the amount, color, and type of drainage. Laboratory data are assessed for electrolyte abnormalities. The nurse continually assesses the infant’s hvdration status.

Postoperative care includes maintaining fluid and elec­trolyte balance by (1) monitoring intravenous infusion until oral fluids are tolerated; (2) monitoring infant’s response to feedings by mouth; and (3) assessing for signs of dehydra­tion. Appropriate analgesics are given for pain. The incision site is monitored for signs of infection, such as redness, inflammation, purulent drainage, or temperature of 101°F or higher. Most surgeons remove the NG tube immediately after surgery and begin feeding within 4 to 6 hours if bowel sounds are normal. Initial feedings consist of small amounts of an electrolyte solution such as Pedialyte, and the volume is gradually increased. If greater volumes are tolerated with­out vomiting, formula or breast milk is offered. Most infants experience some vomiting in the first 24 to 36 hours after surgery; therefore, intravenous fluids are administered until full feedings are tolerated.

 

Evaluation

Evaluation of nursing care is based on how effectively the identified outcomes were met. When feedings are resumed, the infant should be able to tolerate feedings without vomit­ing, and weight should be gained to the pre-illness amount. The surgical incision should heal without signs of infection. The caregivers need to be able to demonstrate correct care of the incision, state plans for feeding and caring for the infant at home, and verbalize the signs and symptoms of complications and when to contact their health care provider.

 

Family Teaching

Caregivers often feel ineffective because their baby has been hungry and, yet, they have not been able to satisfy this hunger. They may believe they have done something wrong. Nurses can support them by explaining that they are not at fault and the condition is caused by a structural defect. They need to be encouraged to be involved in caring for the baby before and after surgery. Prior to surgery the infant is irrita­ble, hungry, and cries often. Caregivers can be involved by holding, rocking, and cuddling their baby. A pacifier may sat­isfy the infant’s sucking needs.

Nurses should instruct caregivers about the care of the incision (if any is required) and signs of infection. The infant’s response to feedings should be observed. Vomiting may still be present; however, if it persists beyond 48 hours, the health care provider should be notified.

 

Cleft Lip (CL) and Cleft Palate (CP)

A cleft is a fissure or elongated opening. A cleft of the lip, palate, or both is one of the most common congenital anom­alies of newborns. Most afflicted will have both cleft lip and palate; some have only a cleft of the lip and others only of the palate. Any type of cleft interferes with the development of the normal anatomic structures of the lips, nose, muscles, and palate. The degree to which these structures are incom­plete or malformed depends on the type, placement, and severity of the cleft(s).

 

Incidence and Etiology

The incidence of cleft lip and/or palate (CL/CP) is 1.5 in 1,000 births (Czeizel, Timar, & Sarkozi, 1999). The inci­dence is highest in Asians, followed by Caucasians, and is lowest in African-Americans. Clefts of the lip with or without cleft palate are more common in males, while clefts of the palate alone are more common in females.

Possible etiologies include genetic and environmental factors. If there is a family history of a cleft, the risk of other children also having a cleft is higher. Environmental factors have also been identified as a possible etiology of CL/CP including parental age, maternal intake of excessive alcohol, maternal drug exposure to phenytoin (Dilantin) or diazepam (Valium), and dietary factors such as folic acid and vitamin deficiencies.

 

Pathophysiology

The hard palate is the bony front part of the roof of the mouth. The soft palate lies behind the hard palate and is composed of muscle and fibrous tissue. The flap of mucosa that hangs down from the soft palate is the uvula. Cleft lip is caused by a failure of the nasal and maxillary processes to fuse between the 5th and 8th week of gestation. The lip and palate develop independently; therefore, it is possible to have either a cleft of the lip or the palate separately or together. Cleft palate is caused by the failure of the palatine plates to fuse between the 7th and 12th weeks of gestation.

 

Clinical Manifestations

Cleft lip can occur as either unilateral (only on one side) or bilateral (both sides) and can vary from a slight notch in the red portion of the lip to a complete separation extending into the nostril. Cleft palate can occur in the hard or bony palate and/or in the soft palate, with or without a cleft lip being present (Figures 23-3A and 23-3B).

 

Diagnosis

Cleft lip, and in most cases, cleft palate are obvious at birth. Even a small cleft of the palate can be detected by visual inspection and palpation. When cleft palate is not diagnosed at birth, formula coming from the nose may be the first sign. Both of these defects can be diagnosed in utero by ultrasound, and if present, the family will be referred to a multidiscipli-nary team at a cleft palate, craniofacial, or orofacial center.

 

Treatment

The treatment for a child with a cleft lip and palate is com­plex and involves many specialists, including a plastic sur­geon, neurosurgeon, orthodontist, otolaryngologist, pediatrician, nurse, speech pathologist, and audiologist. Reconstruction begins in infancy and can continue through adulthood. Wide variations exist in the timing and technique for surgical repair. Closure of the lip is usually performed when the infant is approximately 3 months of age or 12 pounds. The goal of surgery is to close the cleft so scarring will be minimal, and the face will have an increased chance to develop normally. Clefts of the hard and/or soft palate are surgically closed at approximately one year of age to assist feeding and to promote speech and language development. Additionally, good nutritional status and general health are essential factors influencing timing for surgery. Long-term consequences of cleft lip and palate may include speech dif­ficulties, malocclusion problems (abnormal tooth eruption pattern), and hearing problems from recurrent otitis media caused by abnormalities of the eustachian tube.

 

 

                                                        A                                             B

 

Figure 23-3   (A) Cleft Lip. Courtesy of Dr. Joseph Konzelman, School of Dentistry, Medical College of Georgia. (B) Cleft Palate. Courtesy of Dr. Joseph Konzelman, School of Dentistry, Medical College of Georgia.

 

Nursing Management

Assessment

A cleft of the lip and usually the palate are observable at birth. During the newborn assessment the nurse examines the palate by visualization and palpation with a gloved finger. A description of the location and extent of the defects is doc­umented. The neonate’s ability to suck, swallow, and feed are also noted. Nurses must also assess the caregiver’s reactions as the birth of a baby with a cleft may be devastating.

 

Nursing Diagnoses

Nursing diagnoses for the infant with cleft lip and/or palate include:

 Preoperative:

     Imbalanced nutrition: Less than body requirements related to feeding difficulties.

     Altered parenting related to interruption in the bond­ing process.

Postoperative:

     Risk of injury and infection to the surgical site related to surgical procedure.

     Pain related to surgical correction of clefts.

     Deficient knowledge related to the condition, treatment, and long-term care.

 

Outcome Identification

    Infant will consume adequate nutrients.

    Caregivers will demonstrate feeding techniques that provide adequate nutrients.

    Caregivers will begin to adjust and bond to their infant.

    Infant will maintain optimum comfort.

    Infants incision will heal without disruption or infection.

    Caregivers will verbalize understanding of treatment plan, feeding and restraint techniques, surgical site care, and need for possible later surgeries and speech therapy.

 

Planning/Implementation

Preoperatively, nursing care focuses on providing support for the caregivers, preventing aspiration and infection, and ensuring adequate nutrition. The birth of a child is usually a time of joy and celebration; however, the birth of a child with craniofacial anomaly has potentially devastating effects on a family. The initial reactions are shock, grief, feelings of isolation, feelings of failure or inadequacy. Shock is usually followed by anger, guilt, frustration, and depression. Caregivers may become preoccupied with the baby’s appear­ance and experience negative feelings toward the infant, which may disrupt or delay attachment. Nurses working with these families must realize that these are normal reactions and that they can aid in the bonding process by demonstrat­ing acceptance of the baby and by encouraging the care­givers to hold and touch their infant. Fears may be allayed by seeing before and after photographs of successful surgical repairs. Providing an opportunity to talk with other families who have a child with a cleft is also important. Agencies such as the Cleft Palate Foundation provide information and sup­port for children and their families (see Resources).

Once the initial shock has been dealt with, the care­givers usually have many questions pertaining to the child’s condition. The four most frequently asked are:

            Why did this happen?

            Is this hereditary?

            What can be done? Can anything be done right away?

            What about our baby’s future? Will my child be normal?

Feeding problems, such as poor or inadequate suction, prolonged feeding time, frequent nasal regurgitation, and inadequate weight gain, can be a frustrating and exhausting experience for many caregivers. Early teaching by nurses about the anatomy and functioning of the palate and suc­cessful feeding techniques can decrease caregiver anxiety. When an infant sucks, the soft palate rises up closing off the nasopharynx from the oropharynx, thereby creating negative pressure. This mechanical vacuum draws liquid into the mouth and delivers it to the back of the throat where it is swallowed.

Breastfeeding an infant with a CL/CP is one option for the mother. The infant with only a CL will probably have no more difficulty than other babies in achieving effective breastfeeding. The breast itself tends to fill the opening in the lip because it has the capacity to mold to the shape of the oral cavity. It may be possible to breastfeed an infant with both CL and CP; however, if this method is unsuccess­ful, a breast pump may be used to express the milk and bot­tle feeding with special nipples should be used.

If the method chosen is bottle feeding, it is important for caregivers to initially try a regular nipple and bottle as some infants with small clefts may feed satisfactorily without special adaptations. One method using readily available stan­dard nipples and bottles that is inexpensive and convenient is the Enlarge, Stimulate, Swallow, and Rest (ESSR) method. Enlarging the nipple hole by making a cross cut allows the infant to receive formula in the back of the throat for swallowing, thus bypassing the sucking problem. The next step, stimulate, refers to stimulating the sucking reflex by rubbing the nipple on the lower lip. The nipple is inserted into the mouth, and then the bottle is inverted. The infant swallows the fluid normally. The last step is a rest.

Shortly before infants choke or gag, their facial expression will signal a need for a short break to finish swallowing for­mula already in their mouth. The signal consists of elevating eyebrows and wrinkling of the forehead. The nipple should be removed slowly and gently from the mouth. Frequent burping is needed. These steps are repeated until the infant has consumed normal amounts of formula, 3 or 4 ounces, in a normal amount of time, 15 to 30 minutes (Richard, 1991). Figure 23-4 illustrates a cross-cut nipple.

If standard nipples are ineffective for feeding, a variety of special nipples, for example, soft, “preemie,” or elongated, are commercially available. If the infant is unable to ingest adequate milk using any of these types of nipples, an asepto syringe with a rubber tip may be effective.

The major emphasis after surgery for cleft lip repair is the protection of the operative area. A small metal strip called a Logan bow or a butterfly adhesive may be placed over the upper lip and taped to the infant’s cheeks to pre­vent tension on the suture line (Figure 23-5). The infant should be placed only on the back or side and arm or elbow restraints applied to prevent touching or pulling the site. These restraints should be removed periodically to exercise the anus (Figure 23-6). Adequate pain medicatioeeds to be administered to minimize crying and stress on the suture line.

 

Evaluation

Evaluation is based on how effectively the outcomes of nurs­ing management are met. The infant consumes adequate nutrients and gains weight along a normal growth curve. Caregivers demonstrate increased feelings of confidence with feeding techniques and routine. Caregivers begin to bond with their infant by stroking, touching, and nurturing appropriately. The infant appears content while resting and displays behaviors consistent with comfort. Caregivers ver­balize understanding of CL/CP pathology, treatment plan, home care, and long-term care.

 

Figure 23-4   Cross-cut in Nipple. When the nipple is squeezed, the hole can be seen to have been enlarged slightly. From Golding-Kushner, K. J. (2001). Therapy techniques for cleft palate, speech, & related disorders. San Diego, CA: Singular Thomson Learning.

 

Figure 23-5.   Infant with Logan Bow to Protect Suture Line After Repair of Unilateral Cleft Lip