Initial Impression: “Looks Good” vs. “Looks Bad”

Every skilled critical care nurse and physician develops a systematic method for determining the severity of the patient’s condition, making both qualitative and quantitative assessments. Often, the initial, general impression of how the patient looks is more important than any single vital sign or clinical measurement.^8a

The skilled critical care clinician can determine at a glance whether the patient “looks good” or “looks bad.” This determination requires a rapid visual evaluation of the child’s color, skin perfusion, level of consciousness (activity and responsiveness), breathing, and position of comfort (Box 1-1). Each portion of this assessment is reviewed in detail in this section.

The child’s color is normally consistent over the trunk and extremities. The child’s mucous membranes, nail beds, palms, and soles are normally pink. When cardiorespiratory distress is present, the skin is often mottled and extremities and mucous membranes can be pale. Although the mucous membranes of the adult with hypoxemia often become dusky, such central cyanosis (best observed in the mucous membranes) is not consistently detected in the hypoxemic child. The observation of cyanosis requires the presence of at least 3 to 5 g of desaturated hemoglobin per deciliter of blood, so the anemic child might never appear cyanotic despite the presence of profound hypoxemia. In addition, some healthcare providers have difficulty perceiving subtle color changes.

The child’s extremities are normally warm, with brisk capillary refill (2 s or less). When poor perfusion or stress is present, extremities are cool and capillary refill is often sluggish. Cold stress can also cause peripheral vasoconstriction and cooling of skin, particularly in extremities, so the environmental temperature should be considered when evaluating perfusion. If poor capillary refill is attributed to a cool environment, warm the patient and frequently recheck perfusion to determine whether the compromise in peripheral perfusion was caused by cold stress or if is actually caused by inadequate cardiac output.

A change in the child’s level of activity and responsiveness is often noted when systemic perfusion or neurologic function is compromised. Beyond a few weeks of age, the healthy infant will demonstrate good eye contact, orient preferentially to faces, and visually track brightly colored objects. The healthy infant should move all extremities spontaneously. In contrast, the infant in mild distress may hold all extremities flexed and demonstrate a facial grimace. The critically ill infant often will not sustain eye-to-eye contact and can be more irritable than usual, with a high-pitched or a very weak cry. As the infant deteriorates further, extremities will be flaccid, and the infant may be unresponsive.

The healthy toddler should protest vigorously when separated from the parents and should demonstrate stranger anxiety toward unfamiliar hospital personnel. The seriously ill toddler initially can be extremely irritable and comforted only by parents. With further deterioration, the toddler will be lethargic and unresponsive. The toddler normally will protest when the parents leave the bedside; lack of such protest is abnormal.

The healthy preschooler is typically distrustful or afraid of hospital personnel, but should be curious about equipment and tasks performed by the nurse or physician. At this age the child is usually able to localize and describe pain and symptoms. The school-aged child should be able to cooperate with procedures and answer questions about health, symptoms, and activities of daily living. The healthy school-aged child and adolescent are extremely self-conscious during physical examination. Initially, critical illness can make the child more irritable and uncooperative. As further deterioration occurs, the child will become lethargic and then unresponsive.

The healthy child of any age should respond to a painful stimulus (such as a venipuncture), and most children will attempt to withdraw from the stimulus. Therefore, a decreased response to painful stimuli is abnormal and usually indicates serious cardiorespiratory or neurologic deterioration.

The healthcare provider should evaluate the child’s breathing rate and effort, forming an opinion of the degree of distress that the child is demonstrating. The provider is reassured if the child is breathing at a regular rate that is appropriate for the child’s age and clinical condition. By contrast, the provider should be concerned about the child who is breathing rapidly, irregularly, or at a rate that is too slow for the child’s clinical condition, or if the child demonstrates significant effort (e.g., retractions, nasal flaring).

Most children prefer to sit upright in the hospital bed, particularly if strangers are present. The upright position is typically the position of comfort if respiratory distress is present, and the child will probably resist placement in the supine position. If the child reclines quietly in bed, then fear, pain, and serious illness are probably present. Young infants can’t assume a position of comfort, but may demonstrate less respiratory distress when the head of the bed is elevated.

Evaluation of Vital Signs

In the critical care unit, clinicians constantly evaluate the child’s general appearance (including breathing) and vital signs. Whenever possible the nurse should obtain “resting” information or measurements, including evaluation of heart rate and respiratory rate and effort, before disturbing the child. This resting information can be compared with information obtained when the child is awake and active. The child with upper airway obstruction can breathe comfortably when asleep, but demonstrate increased respiratory rate and effort while awake and active. Alternatively, if the child exhibits tachypnea with severe retractions even during sleep, more significant respiratory distress is present.

Normal vital signs are not always appropriate vital signs when the child is critically ill. The critically ill or stressed child should exhibit tachycardia and tachypnea; a “normal” heart rate and respiratory rate in such a child can indicate deterioration, and cardiorespiratory arrest might be imminent.

The child normally has a faster heart rate and respiratory rate and a lower arterial blood pressure than does an adult. As a result, smaller quantitative changes in the vital signs may be qualitatively more significant in the child than in the adult, particularly if they constitute a trend.

If the adult’s systolic blood pressure falls approximately 15 mm Hg, from 140/80 to 125/80 mm Hg, the mean arterial blood pressure has fallen 5%. However, if the infant’s systolic blood pressure falls 15 mm Hg, from 72/42 to 57/42 mm Hg, the infant’s mean arterial pressure has fallen about 10% and this change may be associated with a compromise in perfusion.

Normal vital signs ranges are provided in Tables 1-1 to 1-3. Evaluation of vital signs requires consideration of normal values for the child’s age,^14a trends in the individual patient’s vital signs, and appropriate vital signs for the child’s condition. Remember that in children, shock can be present despite the observation of a normal blood pressure. Hypotension is often a late sign of shock in the pediatric patient.

Table 1-1 Normal Heart Rates in Children*

* Always consider the patient’s normal range and clinical condition. Heart rate will normally increase with fever or stress.

Table 1-2 Normal Respiratory Rates in Children*^14a

* Consider the patient’s normal range. The child’s respiratory rate is expected to increase in the presence of fever or stress.

The child’s heart rate and respiratory rate normally increase during stress and when the child is frightened or inpain, and they normally decrease when the child is sleeping. If vital signs are obtained when the child is crying, this should be indicated with the vital signs. Attempts should be made to comfort the frightened child, so that resting vital signs can be documented and evaluated.

Assessment Format

Consistent use of a familiar format will facilitate the nurse’s recall of important assessment information. The American Heart Association uses an ABC format to indicate assessment and support of airway, breathing, and circulation, and these priorities are still appropriate for assessment of the critically ill child.^8a In addition, all pediatric life support courses teach an initial assessment by determining the general impression of the child’s consciousness, breathing, and color; this text uses the “looks good versus looks bad” assessment. The skilled critical care clinician repeatedly performs these fundamental assessments.

An additional alphabetical format may be useful for pediatric critical care nurses. This format uses the first seven letters of the alphabet to help the nurse recall the steps in a seven-point check (Box 1-2). The seven essential assessment points include the child’s airway (and aeration), brain (neurologic function), circulation, drips or drugs administered, electrolyte balance, fluids (including fluid balance and fluid administration rate), genitourinary and gastrointestinal function, and growth and development.^17a When caring for the critically ill neonate, this format can be modified to create a nine-point check, with the addition of the letter H for heat, or thermoregulation, and the letter I for immunologic immaturity.

Thermoregulation

Infants and young children have large surface area-to-volume ratios, so they lose more heat to the environment through evaporation, conduction, and convection than do adults. In addition, the small child can lose heat if large quantities of intravenous or dialysis fluids are administered without warming.

Cold-stressed neonates and infants younger than 6 months cannot shiver to generate heat. When the environmental temperature falls, these infants maintain body temperature through nonshivering thermogenesis. This process begins with the secretion of norepinephrine and results in the breakdown of brown fat and creation of heat. Nonshivering thermogenesis is an energy-requiring process, so the infant’s oxygen consumption will increase whenever it develops. Regeneration of brown fat requires adequate nutrition; if the infant’s caloric intake is inadequate, brown fat will not be made to replace that used, and the infant will be less able to maintain body temperature in a cool environment.

Although the healthy infant is able to increase oxygen delivery in response to increased oxygen consumption during nonshivering thermogenesis, the critically ill infant may not be able to increase oxygen delivery effectively. As a result, cold stress can produce hypoxemia, lactic acidosis, and hypoglycemia. Cooling of the neonate also can stimulate pulmonary vasoconstriction, resulting in increased right ventricular afterload. For these reasons, cold stress can worsen existing cardiovascular dysfunction, causing increased heart failure or right-to-left intracardiac shunting.

The nurse can reduce cold stress by maintaining a neutral thermal environment for the neonate. A neutral thermal environment is the environmental temperature at which the infant maintains a rectal temperature of 37° C with the lowest oxygen consumption. This neutral temperature should be maintained during all aspects of the infant’s care, especially during transport and diagnostic tests. Over-bed radiant warmers can help maintain the infant’s temperature without interfering with observation and care. The beds are equipped with servo-control devices to adjust heat output in response to changes in the infant’s skin temperature. Adjustable alarms indicate when excessive warming is required to maintain the infant’s temperature or when the infant’s temperature varies from the selected range. (For further information regarding warming devices, see Chapter 21)

Unless there are contraindications (e.g., severe thrombocytopenia), nurses typically monitor both skin (e.g., axillary or via infant skin probe) and central (e.g., oral, esophageal, bladder) temperatures of critically ill infants and young children, because changes in these temperatures may be observed when systemic perfusion is compromised. Bladder temperature monitored via urinary catheter is an additional method of monitoring core body temperature.

Peripheral vasoconstriction and cooling of the skin is often an early sign of cardiovascular dysfunction and low cardiac output. The very young infant also can demonstrate a fall in core body temperature. The older infant or child with low cardiac output can demonstrate a low skin temperature with a normal or increased core body temperature, because heat generated by metabolism cannot be lost through the diminished skin blood flow.

Fluid Requirements and Fluid Therapy

The child’s daily fluid requirement is larger per kilogram body weight than that of the adult, because the child has a higher metabolic rate and greater insensible and evaporative water losses per kilogram body weight. Estimation of these fluid requirements is frequently based on the child’s body weight. However, evaporative water losses are affected directly by the child’s body surface area (BSA), determined by height and weight using a nomogram (see inside back cover), so calculations of fluid requirements are most accurate when based on the BSA.

If a BSA nomogram is not readily available, the BSA can be estimated using body weight and the following formula:

The weight can be estimated from body length using a length-based tape (see section, Cardiac Arrest and Resuscitation) such as the Broselow resuscitation tape (Fig. 1-1; see also Evolve Fig. 1-1 in the Chapter 1 Supplement on the Evolve Website.)

Fig. 1-1 Broselow Pediatric Emergency Tape. A, The two-sided tape allows for rapid identification of doses of emergency drugs, appropriate equipment sizes, and estimated body weight based on child’s body length. B, One side of the tape displays appropriate doses and administration volumes of resuscitation and rapid sequence intubation drugs and estimated weight (determined from child’s length). C, The second (color-coded) side of the tape indicates appropriate sizes of emergency equipment and additional fluid and drug information based on child’s length. (See also Evolve Fig. 1-1 in the Chapter 1 Supplement on the Evolve Website.)

(Used with permission of James Broselow and Vital Signs. Copyright Vital Signs, Inc. All Rights Reserved.)

The estimate of maintenance fluid requirements (Table 1-4) provides a baseline for tailoring the fluid administration rate for each patient. Actual fluid administration is tailored to the child’s clinical condition. Normal insensible water losses average 300 to 400 mL/m² BSA per day. Fever increases insensible water losses by approximately 0.42 mL/kg per hour per degree Celsius elevation in temperature above 37° C.⁴⁰ Radiant warmers, phototherapy, and the presence of diaphoresis or large burns also will increase a child’s insensible water loss. Fluid retention can diminish fluid requirements postoperatively and fluid retention typically develops in the presence of congestive heart failure, respiratory failure, or renal failure.

Table 1-4 Formulas for Estimating Daily Maintenance Fluid and Electrolyte Requirements for Children

* The “maintenance” fluids calculated by these formulas must only be used as a starting point to determine the fluid requirements of an individual patient. If intravascular volume is adequate, children with cardiac, pulmonary, or renal failure or increased intracranial pressure should generally receive less than these calculated “maintenance” fluids. The formula utilizing body weight generally results in a generous “maintenance” fluid total.

Consistent with values from Barakat AY, Ichikawa I: Laboratory data. In Ichikawa I, editor: Pediatric textbook of fluids and electrolytes, Baltimore, 1990, Williams and Wilkins; and Tan JM: Nephrology. In Custer JW, Rau RE, editors: The Johns Hopkins Hospital Harriet Lane Handbook, ed 18, Philadelphia, 2009, Mosby-Elsevier.

Although the child’s fluid requirements per kilogram body weight are higher than those of an adult, the absolute amount of fluid required by the child is small. Excessive fluid administration is avoided through careful regulation and tabulation of all fluids administered to the child. Unrecognized sources of fluid intake can include fluids used to flush monitoring lines or to dilute medications.

When the child is critically ill, hourly (or more frequent) evaluation of the child’s fluid balance is needed to enable rapid modification of fluid therapy in response to changes in the child’s condition. All intravenous and irrigation fluids should be administered through volume-controlled infusion pumps.

Many infusion pumps are programmable, and with entry of the child’s weight and drug concentration, the pumps will calculate drug dose administered by continuous infusion. Each nurse is responsible for all drugs administered during that nurse’s shift, so the accuracy of all infusion devices must be verified at the beginning of each shift and when changes are made in infusion rates, to avoid perpetuation of programming or other errors.

If hydration and fluid intake are adequate, the infant’s urine volume should average 2 mL/kg per hour. The normal urine volume will be 1 to 2 mL/kg per hour in the child and 0.5 to 1 mL/kg per hour in the adolescent. A small reduction in urine volume can indicate significant compromise in renal perfusion or function.

It is important to monitor and document all sources of fluid loss in the critically ill child. Unrecognized fluid loss can result from phlebotomy, nasogastric or pleural drainage, vomiting, diarrhea, or intestinal drainage. If fluid output exceeds intake, notify the appropriate provider; adjustment in fluid administration may be indicated.

Measurement of the child’s weight on a regular basis will aid in evaluation of the child’s fluid balance. You should ideally weigh the child using the same method (e.g., in-bed scale or the same external scale) at the same time each day, and at the same time in relation to diuretic administration, to avoid even small errors in measurement. Small daily weight changes can be significant, particularly if a trend is observed. A weight gain or loss of 50 g/day in the infant, 200 g/day in the child, or 500 g/day in the adolescent should be discussed with a physician or appropriate provider.

If the patient bed incorporates a scale, the bed scale should be zeroed before patient admission with a recorded list of the linens that are on the bed at the time of zeroing. If the linens and weights are not recorded, similar linens can be weighed, but this will obviously introduce error from one measurement to the next. If the bed does not incorporate a scale, sling scales are used. If possible, weigh bulky dressings and equipment before they are placed on the child. If this is impossible, record the weight of similar dressings and equipment to estimate their contribution to the child’s weight.

Children have proportionally more body water than do adults. Total body water constitutes approximately 75% to 80% of the full-term infant’s weight and 60% to 70% of the body weight of the adult. During the first weeks of life, most body water is located in the extracellular compartment, and much of this water is exchanged daily. For this reason and because the infant kidney is less able to concentrate urine (see section, Renal Function), dehydration can develop rapidly if the infant’s fluid intake is compromised or fluid losses are excessive.

Signs of dehydration are approximately the same in patients of any age and include dry mucous membranes, decreased urine volume with increased urine concentration, and poor skin turgor. The dehydrated infant usually will have a sunken fontanelle. Mild dehydration produces weight loss; moderate and severe dehydration generally produce signs of circulatory compromise. Peripheral circulatory compromise will be observed in the infant or child with moderate isotonic dehydration, but it may develop following mild dehydration in patients with hyponatremia. Moderate dehydration is typically associated with a 7% to 10% weight loss in children and a 5% to 7% weight loss in the adolescent or adult.

Oral intake often is compromised during serious illness, so the critically ill child depends on uninterrupted delivery of intravenous fluids. Because small intravenous catheters can easily kink and become obstructed, they must be handled carefully, anchored securely, and flushed regularly. When intravenous access is difficult to establish during resuscitation, intraosseous access provides a readily accessible and reliable route to administer fluids and medications.

Intravenous fluids are provided to flush monitoring lines, dilute medications, replace volume loss, or provide nutrition. In the past, hypotonic crystalloids (e.g., 5% dextrose with 0.2% sodium chloride) were routinely used for pediatric maintenance and replacement fluids, with the assumption that critically ill patients are likely to retain sodium and water. However, children are much more likely to develop hyponatremia if hypotonic rather than isotonic solutions are used, and isotonic fluids do not increase risk of hypernatremia.^2,9 At this time there is insufficient evidence to identify a single optimal intravenous fluid for pediatric maintenance therapy, so practitioners will need to individualize intravenous fluid selection for each patient.

Providers should monitor serum electrolytes and clinical status during parenteral fluid therapy to enable rapid detection and treatment of any imbalances that develop. The nurse should verify that the volume and content of each infusion is appropriate. If the patient’s status changes, it is often necessary to change the volume and content of the patient’s intravenous infusions.

The nurse should regularly inspect intravenous infusion sites and routinely touch every fluid administration system from beginning to end. With this careful inspection, the nurse will detect any loose connection or leak and can verify correct position of clamps and stopcocks; this inspection can prevent inadvertent interruption of or errors in fluid infusion.

Electrolyte, Glucose, and Calcium Balance

Normal serum electrolyte, glucose, and calcium concentrations are the same for both adults and children, as are renal and cellular mechanisms for maintaining serum electrolyte balance. However, some forms of electrolyte, glucose, and calcium imbalance are more likely to occur or cause complications in children than in adults. In addition, abnormalities of sodium, potassium, glucose, calcium, and magnesium occur frequently in critical care, so the nurse should monitor laboratory values and assess for clinical manifestations of these imbalances. It is important to anticipate the effect of therapy on the child’s electrolytes (e.g., correction of acidosis will be associated with a fall in serum potassium concentration) and attempt to prevent electrolyte imbalances.

Sodium is the major intravascular ion, and acute changes in serum sodium concentration will affect serum osmolality and free water movement. Hyponatremia in the critically ill child can result from antidiuretic hormone excess (i.e., the syndrome of inappropriate antidiuretic hormone secretion) and liberal water administration in excess of sodium, including administration of hypotonic fluids.⁴ Hyponatremia can also result from excess sodium losses, such as those occurring with adrenocortical insufficiency (see Chapter 12).

An acute fall in serum sodium will typically produce an acute fall in serum osmolality; this will produce an osmotic gradient from the extracellular compartment (including the vascular space) to the intracellular compartment, so free water shifts into the cells. A significant intracellular fluid shift can produce cerebral edema, seizures, and coma. The volume of water shift and the severity of clinical manifestations with hyponatremia are directly related to the acuity and the magnitude of the fall in serum sodium and osmolality. As in the adult, hyponatremia associated with neurologic symptoms is a neurologic emergency. In children it is treated with hypertonic saline (3% sodium chloride, 2-4 mL/kg).

Hypernatremia can result from excessive sodium administration or free water loss, such as that occurring with diabetes insipidus or vomiting. Hypernatremia in infants and young children is most frequently observed as a complication of dehydration. Cerebral hemorrhage and cerebral dysfunction have been reported after abrupt correction of hyponatremia in adults (i.e., rapid rise in serum sodium concentration),¹⁸ and similar complications are thought to occur in children. Rapid correction of hypernatremia can produce an acute fall in serum osmolality, with resultant intracellular free water shift and cerebral edema. In general, when correcting hyponatremia or hypernatremia the child’s serum sodium concentration should be changed at a maximum rate of 10 to 12 mEq/24 h (or an average of 0.5 mEq/h).

Changes in the serum potassium concentration occur with changes in acid-base status, use of cardiopulmonary bypass, and administration of diuretics. Hypokalemia can produce cardiac arrhythmias and perpetuate digitalis toxicity. However, cardiac arrhythmias related solely to potassium imbalance rarely occur in children until the serum potassium is extremely low (<3 mEq/L) or high (>7 mEq/L).

The serum potassium should be expected to fall as the child’s pH rises, and it will rise as the pH falls because hydrogen ion moves intracellularly in exchange for potassium. A low serum potassium concentration in a patient with acidosis is problematic, because it will drop even lower as the acidosis is corrected (see Chapter 12).

During periods of stress in adults, epinephrine and cortisol are secreted, resulting in glycogen breakdown and increased serum glucose levels; thus, the critically ill adult often demonstrates hyperglycemia. However, infants have continuously high glucose needs and low glycogen stores, so they often develop hypoglycemia during periods of stress. Hypoglycemia can depress the infant’s cardiovascular or neurologic function. Hypoglycemia or hyperglycemia can be an early sign of sepsis in the infant, and glycosuria can be an early sign of infection in the child.

All critical care clinicians will closely monitor the critically ill infant’s serum glucose concentration and treat hypoglycemia. If point-of-care testing is available, perform heel-stick glucose testing routinely, and treat and repeat as necessary during stabilization of the critically ill infant. A constant glucose infusion is preferable to frequent bolus administration of glucose; the infusion will prevent the wide fluctuations in glucose levels that can result from intermittent bolus glucose administration and reactive hyperinsulinemia. In many critical care units, 10% glucose solutions are used for intravenous maintenance fluid therapy for neonates.

Several case series in adult³⁸ and pediatric patients suggested that uncontrolled hyperglycemia, whether it is endogenous or exogenous in origin, can be harmful to critically ill patients and can increase complication rates and decrease survival. Although this is a significant concern, other studies have found contradictory evidence, and additional studies are underway to clarify these issues. Use of insulin infusion to prevent hyperglycemia was associated with reduced critical care unit mortality in adult studies³⁸ and one multicenter pediatric study,³⁹ but was also associated with increased hypoglycemic episodes.

The relative risk of hyperglycemia and potential harm from hypoglycemia must be considered and are currently being evaluated. If insulin is administered by continuous infusion to control hyperglycemia, it is typically used during the first 12 to 18 hours of pediatric critical care, with careful monitoring of serum glucose concentration using point-of-care testing, if possible. A glucose infusion can be added and titrated to prevent significant hypoglycemia during the insulin infusion.

The serum ionized calcium concentration (normal value is approximately 4.8 to 5.2 mg/dL or 1.2 to 1.38 mmol/L) is the “working” calcium, involved in nerve and muscle function.¹² Therefore, the healthcare team monitors ionized and total calcium concentration during critical illness and provides supplementary calcium for documented hypocalcemia.

A fall in total or ionized calcium is observed frequently in critically ill infants and children. Ionized hypocalcemia has been reported after cardiac arrest in children with septic shock or renal failure.⁴¹ The phosphate in citrate phosphate dextran-preserved blood will precipitate with ionized calcium, so some transfusions may produce ionized hypocalcemia.

The serum ionized calcium concentration is affected by the serum albumin concentration and by the serum pH. The ionized calcium concentration falls when the serum albumin or serum pH rise (both increase binding of calcium to albumin), and the ionized calcium concentration will rise when serum albumin or pH fall.

Abnormalities in magnesium balance are observed frequently in critically ill patients. Magnesium affects parathyroid function and contributes to control of the intracellular potassium concentration. As a result, hypomagnesemia can contribute to refractory hypocalcemia or hypokalemia. In addition, it can be associated with increased neuromuscular excitability, gastrointestinal dysfunction, and arrhythmias.¹⁸

Hypomagnesemia (<1.3 to 2.0 mEq/dL) in the critically ill child is most commonly caused by inadequate magnesium intake, particularly if the child is nutritionally compromised or receiving intravenous fluids without magnesium supplement. Hypomagnesemia is also observed in the child with increased magnesium losses, such as those that occur with chronic congestive heart failure or renal failure or following administration of osmotic diuretics.

Renal Function

Kidney weight doubles in the first 10 months of life, more as the result of proximal tubular growth than from an increase in glomerular size. The glomerular filtration rate (GFR) also increases significantly after birth; the GFR of the full-term neonate (per square meter of BSA) is approximately one third that of an adult. Renal blood flow and the GFR double during the first 2 weeks of life, and the GFR continues to increase during the first year. The GFR approaches adult values by approximately 3 years of age (Table 1-5).^3,36 Until that time, the relatively low GFR and reduced tubular secretion can prolong the half-life of administered drugs (see Chapters 4 and 13).

Table 1-5 Changes in Glomerular Filtration Rate with Age

Immediately after birth, the neonate normally has a high urine volume with low osmolality. This is thought to result from the immaturity of renal sodium and fluid regulatory mechanisms. The normal newborn typically demonstrates diuresis of excess body water during the first 72 hours of life. After that time, urine volume normally falls and urine concentration gradually rises.

The newborn kidney is able to conserve sodium and glucose as well as the adult kidney. The newborn kidney is less able to excrete free water and to concentrate urine than the adult kidney, however. As a result, the infant kidney may be less able to excrete a large water load and may be unable to concentrate urine in response to dehydration.

Regulation of acid-base balance by the newborn kidney is relatively efficient, although the infant kidney has less ability to secrete hydrogen ions or fixed acid than the adult kidney (this is exacerbated by limited dietary protein intake). As a result, renal compensation for metabolic acidosis may be limited in the neonate. Dehydration, hypotension, and hypoxemia all produce a marked fall in the infant’s GFR, so renal function can become compromised quickly during critical illness (for further information, see Chapter 13).

Pediatric Pharmacokinetics

Drug absorption, distribution, and elimination will be affected by age and clinical condition. Drug absorption is influenced by maturation of the gastrointestinal tract, liver, and kidney. Because the gastric pH is higher (less acidic) during the first 2 years of life, bioavailability of weak acids administered orally (e.g., phenytoin and phenobarbital) may be reduced in this age group, so higher doses (per kilogram body weight) may be required to achieve target serum concentrations of such drugs.¹

Drug distribution is affected by cardiac output, organ blood flow, composition and relative size of body compartments, pH of body fluids, and extent of drug binding to plasma proteins and tissues. The higher proportion of water in the body during the first years of life increases the volume of distribution for hydrophilic drugs during these years.¹ Even if a drug has a consistent volume of distribution (mg/kg body weight) for patients of all ages, the neonate has limited ability to eliminate some drugs, so those drugs will have longer half-lives and lower clearances when administered to neonates than to older children and adults. Even when loading doses for drugs are similar (per kilogram body weight) for neonates and adults, neonates will likely require lower maintenance doses of the drugs than will be required by adults.

Drug clearance is affected by metabolic, hepatic, and renal blood flow and function.¹ Developmental changes associated with hepatic metabolism and renal secretion or filtration can slow down or speed up drug elimination. Several metabolic processes mature during the first months of life (see Fig. 4-7), and many drug elimination pathways continue to mature during the first years of life. Failure to recognize these developmental changes in children can lead to drug dosing errors and complications. By the end of the first year of life, liver metabolism and drug clearance are similar to those reported in older children and adults.

The nurse should be familiar with the pharmacokinetics and pharmacodynamics of all drugs administered to the patient (see also Chapter 4) and should evaluate drug dose in light of the patient’s organ perfusion and function and in light of clinical factors, such as drugs or conditions that may alter protein binding.

Nutrition and Gastrointestinal Function

The child has a higher metabolic rate than does the adult, and the child requires more calories per kilogram body weight (Table 1-6). Most of a child’s maintenance calories are needed for basal metabolism and growth, so the child typically requires a caloric intake that approaches the typical maintenance caloric intake even if the child is inactive.

Table 1-6 Estimated Normal Maintenance Caloric Requirements for Infants and Children

Nutrient	Percent of total daily calories
Carbohydrates
Fat
Protein	7-15

Critical illness, trauma, or burns will increase the child’s caloric requirements significantly, and fever will increase caloric requirements 12% per hour per degree Celsius elevation in temperature above 37° C.⁴⁰ Unless intolerably large quantities of fluids are administered, maintenance calories cannot be provided through 5% or 10% dextrose intravenous fluids. Therefore, provision of parenteral nutrition or tube feedings must be planned early in the child’s hospitalization.

Liver enzymatic synthesis and degradation are immature in the newborn, and they typically mature during the first months and years of life. The neonatal liver is less able to metabolize toxic substances, which can result in prolongation of beneficial or toxic effects of drugs during the first months of life.

Gastric motility is reduced, but gastric emptying is more rapid in neonates. Although nasogastric or orogastric feeding can be a useful method of providing nutrition during the first weeks of life, some gastroesophageal reflux should be anticipated.

Cardiac Output

Normal cardiac output is higher per kilogram body weight in the child than in the adult. The cardiac output at birth is 400 mL/kg per minute; it falls to approximately 200 mL/kg per minute within the first weeks of life and to 100 mL/kg per minute during adolescence.³²

To allow direct comparison of cardiac outputs for patients of different ages and sizes, the cardiac index is usually calculated. The cardiac index is equal to the cardiac output per square meter of BSA (cardiac output ÷ BSA in m²); normal values are 3.5 to 4.5 L/min per m² BSA in the child and 2.5 to 3.5 L/min per m² BSA in the adult. A cardiac index of less than 2.1 to 2.5 L/min per m² BSA is considered low cardiac output in a patient of any age.³²

When the child is critically ill, cardiac output should be evaluated as either adequate or inadequate to meet metabolic demands; shock can be present despite a normal or high cardiac output. For example, in a patient with high oxygen requirements (e.g., septic shock) and a normal rather than increased cardiac output, metabolic acidosis can develop, indicating inadequate tissue oxygen delivery.

Heart Rate and Rhythm

Cardiac output is the product of heart rate and stroke volume (volume of the blood ejected by the ventricles in each minute). In the child, heart rate is more rapid and stroke volume is smaller than in the adult, so pediatric cardiac output is directly proportional to heart rate.

Tachycardia is the most efficient method of increasing cardiac output in any patient, and it is the chief method of increasing cardiac output in the child. Tachycardia is normally observed when the child is frightened, febrile, or stressed. However, an increase in heart rate to extremely high levels may reduce cardiac output. If the ventricular rate exceeds 180 to 220 beats/min, ventricular diastolic filling time and coronary artery perfusion time are severely compromised, so stroke volume and cardiac output usually fall.³⁰

Transient bradycardia may be normal in the infant or child, particularly during periods of sleep or times of vagal stimulation (such as that produced by suctioning, defecation, or feeding). Profound or persistent bradycardia, however, usually results in a fall in cardiac output and systemic perfusion. The most common cause of bradycardia in the child is hypoxia, so the initial treatment of bradycardia requires assessment and support of airway and ventilation. Symptomatic bradycardia (i.e., bradycardia associated with signs of poor perfusion) despite adequate oxygenation and ventilation is an ominous sign of deterioration and requires immediate resuscitation.^8a,20,30

Many neonatal and pediatric arrhythmias are clinically benign, because they do not compromise systemic perfusion, and they are unlikely to convert to malignant arrhythmias. The significance of any arrhythmia is determined by its effects on the child’s systemic perfusion—the heart rhythm is either stable or unstable.^8a,20,30

Unstable arrhythmias include those in which the ventricular rate is too slow to maintain effective perfusion, too fast to maintain systemic perfusion, or the rhythm results in ineffective perfusion (with loss of pulses). The most common clinically significant unstable arrhythmias observed in children are bradycardia and supraventricular tachycardia; children with cardiovascular disease and some with channelopathies or left ventricular outflow tract obstruction may demonstrate ventricular arrhythmias (see section, Cardiac Arrest and Resuscitation).

Factors Influencing Stroke Volume

Cardiac output can be affected by changes in the stroke volume. The stroke volume in the neonate is extremely small, averaging 1.5 mL/kg, or 5 mL, in the full-term newborn. This stroke volume increases with age and averages approximately 75 to 90 mL in the adolescent or adult.³²

As in the adult, the child’s stroke volume is affected by cardiac preload, contractility, and afterload. Ventricular preload is increased by increasing myocardial fiber length before ventricular contraction; this is accomplished in the critical care unit with intravenous volume administration.

There is not a linear relationship between volume administered and preload (ventricular end-diastolic pressure [VEDP]) produced. The effect of volume administration on VEDP is influenced by ventricular compliance (i.e., the distensibility of the ventricle); compliance varies from patient to patient and can vary in the same patient. Neonatal myocardium is less compliant and has a smaller response to volume loading than the myocardium of older children and adults.²⁷ When treating shock with bolus fluid administration, the critical care provider will titrate volume administration to patient response.

Early studies of isolated and nonhuman myocardium led to the conclusion that the neonate and young infant are incapable of increasing stroke volume in response to volume administration. We now know, however, that infants and children can increase stroke volume and cardiac output in response to increases in preload, provided that ventricular function remains adequate and ventricular afterload is normal or low. The heart rate, however, is the major factor that determines cardiac output in infants and children.

Cardiac contractility refers to efficiency of myocardial fiber shortening. Contractility can be impaired in postoperative patients or patients with ischemia, electrolyte or acid-base imbalance, coronary artery insufficiency, or infection. Neonatal myocardium is less compliant and contains less contractile mass than does adult myocardium, and the neonatal ventricle is thought to require higher VEDP to maximize stroke volume. Infant myocardium, however, actually has a higher ejection fraction than that of the older child or adult.³²

Ventricular afterload is ventricular wall stress, commonly considered as impedance to ventricular ejection. Infants and children tolerate mild increases in ventricular afterload (such as may result from mild pulmonary or aortic stenosis), provided the afterload does not develop acutely. As in the adult, significant increases in ventricular afterload can produce heart failure and decreased cardiac output (see Chapters 6 and 8 for more information).

Response to Catecholamines

The developmental response to exogenous catecholamine administration is still under investigation. Published studies of catecholamine administration in children have used heterogeneous groups of patients (many ages, sizes, and clinical conditions), so it is difficult to generalize observations. The response of the myocardium and vascular tone to exogenous catecholamine administration will probably be affected more by the child’s clinical condition (e.g., whether downgrading or upgrading of receptors or in hepatic and renal dysfunction) than by the child’s age (see Chapters 6 and 8). Therefore, the correct dose of any vasoactive drug must be determined at the patient’s bedside with careful titration according to patient response. This drug titration requires ongoing assessment to maximize therapeutic effects and minimize side or toxic effects.

Signs of Shock

Signs of low cardiac output or poor systemic perfusion are generally the same in any patient, regardless of age. Most patients develop tachycardia, pallor, cool skin, and decreased urine output. Peripheral pulses are usually diminished in intensity, and metabolic acidosis develops. In patients with sepsis, the skin may be warm with brisk capillary refill and pulses may be bounding.

As noted previously, the infant with poor systemic perfusion can demonstrate temperature instability, and the child can develop a high core temperature in the face of profound reduction in skin blood flow. Subtle signs of poor systemic perfusion in the infant or young child include a change in level of consciousness or responsiveness and hypoglycemia (Box 1-3). Unlike in adults, however, hypotension is usually only a late sign of poor systemic perfusion in the child.

The American Heart Association (AHA) Pediatric Advanced Life Support Guidelines²⁰ define hypotension as a systolic blood pressure less than 60 mm Hg in term neonates (up to 28 days of age), and a systolic blood pressure less than 70 mm Hg in infants (1 to 12 months of age). In children 1 to 10 years old, systolic hypotension is present if the systolic pressure is less than 70 mm Hg plus twice the age in years.^8a,20 This estimate corresponds to slightly higher than the fifth percentile systolic blood pressure for children of median height.¹⁷ For the same age group, the critically low mean arterial pressure (the fifth percentile mean arterial pressure for children of median height) can be estimated by the following formula¹⁷:

For children 10 years of age and older, a systolic blood pressure less than 90 mm Hg is considered hypotensive.^8a,20,30

Signs of congestive heart failure, similar in the adult and the child, include the signs of adrenergic stimulation and evidence of high systemic and pulmonary venous pressures. Pulmonary venous congestion will produce tachypnea and increased respiratory effort, and in infants it can result in difficulty feeding.

Treatment of congestive heart failure in any patient requires eliminating excess intravascular fluid and improving myocardial function. Diuretic therapy and limitation of fluid intake will eliminate excess intravascular fluid. Administration (and titration) of inotropic agents, inodilators or vasodilators can improve cardiovascular function. Digoxin derivatives are used less often in children than in adults, and potential benefits of use must be weighed against risk of toxicity. Because risk of toxicity is high in premature infants, digoxin is less likely to be used in this population. Digoxin can be used in infants with large ventricular septal defects and preoperative congestive heart failure and in older children who have structurally normal hearts and cardiomyopathy (see section, Congestive Heart Failure in Chapter 8).

Circulating Blood Volume

The child’s circulating blood volume is larger per kilogram body weight than that of the adult (Table 1-7). However, the child’s absolute blood volume is small, so quantitatively small blood loss can significantly reduce blood volume and systemic perfusion. A 25-mL blood loss in a 70-kg adult would represent loss of only 0.5% to 0.6% of blood volume. The same 25-mL blood loss in the 3-kg neonate constitutes a 10% hemorrhage.

Table 1-7 Estimated Circulating Blood Volume in Children

Calculate the child’s total circulating blood volume on admission, and consider all blood lost or drawn for laboratory analysis as a percentage of this blood volume. Unit protocols should establish a consistent technique for withdrawing blood samples from indwelling lines to minimize blood loss and net fluid administration (particularly for neonates). When frequent blood sampling is required, include a running total of blood lost or drawn in the patient record. Notify a provider if acute blood loss totals 5% to 10% of the child’s circulating blood volume; blood administration may be necessary.

As in the adult, systemic oxygen delivery is a product of arterial oxygen content and cardiac output. A threshold hemoglobin concentration for red blood cell (RBC) transfusion of approximately 7 g/dL (typically associated with a hematocrit of 20% to 21% or less) was found to be sufficient in stable critically ill children with adequate cardiovascular function.²² However, there are insufficient data to recommend a threshold hemoglobin concentration for premature infants or children with conditions such as severe hypoxemia, hemodynamic instability, or heart disease. The healthcare team must individualize transfusion approach, weighing the potential risks of transfusion and the need to optimize the hemoglobin concentration to support the child’s systemic oxygen delivery and cardiac output (see Chapter 15).

Cardiac Arrest and Resuscitation

Although there are differences in the epidemiology of out-of-hospital versus in-hospital pediatric cardiac arrest, most episodes of cardiac arrest in infants and children are associated with a terminal rhythm of bradycardia or pulseless electrical activity which, if untreated, progresses to asystole. Sudden arrhythmic arrest is much less common in infants and children than in adults.³⁰

Recent analysis of in-hospital pediatric resuscitation data from the American Heart Association National Registry of Cardiopulmonary Resuscitation (NRCPR) in the United States,²⁶ and data downloaded from automated external defibrillators in the prehospital setting³³ support many of the widely held concepts regarding the epidemiology of pediatric arrest, reinforce the need to prevent arrest, and raise questions for additional studies.

In-hospital cardiac arrest often develops as a progression of respiratory failure and shock. Typically half or more of pediatric victims of in-hospital arrest have preexisting respiratory failure, and one third or more have shock, although these figures vary somewhat among reporting hospitals.^25,26 When pediatric in-hospital respiratory failure or arrest with bradycardia is treated before the development of (pulseless) cardiac arrest, survival is generally high.^14,25

Bradycardia, asystole, or pulseless electrical activity were recorded as initial rhythms in half or more of recent reports of in-hospital pediatric cardiac arrest, with survival to hospital discharge ranging from 22% to 40%.^25,26 In the NRCPR analysis of first rhythm in cardiac arrest, children who received chest compressions for severe bradycardia with pulses had a significantly higher rate of survival to hospital discharge than those who had a pulseless arrest (60% versus 27%).^14,26 In addition, children with bradycardia who received chest compressions had a higher survival rate than adults who arrested with a terminal bradycardic rhythm.²⁶

An analysis of the initial rhythm of in-hospital cardiac arrest in the NRCPR confirmed age-related differences in initial in-hospital arrest rhythms and outcomes. Pediatric patients were more likely than adults to exhibit asystole and only about half as likely to exhibit ventricular fibrillation (VF). Pulseless electrical activity was also less common in children than in adults.²⁶

Although VF and pulseless ventricular tachycardia (VT) are uncommon presenting rhythms for pediatric patients with in-hospital pulseless arrest, a “shockable” rhythm was present sometime during the course of one fourth of attempted in-hospital resuscitations in children.²⁶ This report confirms the importance of training pediatric resuscitation team members in coordination of high-quality chest compressions with shock delivery.

Pediatric advanced life support includes accurate and rapid preparation of appropriate drugs. Use of emergency drug and supply tables and tapes (see Fig. 1-1 earlier in chapter) will improve accuracy and eliminate the need for rapid calculations at a stressful time.²³

Although retrospective pediatric arrest series have provided important information about the epidemiology of pediatric cardiac arrest, many uncontrolled factors (e.g., definitions of arrest, patient comorbidities, quality of cardiopulmonary resuscitation [CPR], and system factors) can influence outcome. The quality of prearrest, arrest, and postarrest care influences survival. Rapid response teams can reduce the incidence of cardiac arrests outside the pediatric critical care unit, particularly respiratory arrests, although success rates of rapid response teams vary based on activation criteria, team members, and hospital type.

Outcome of in-hospital pediatric resuscitation is undoubtedly influenced by the quality of CPR provided, including duration of “hands off” intervals, and specific periarrest interventions such as extracorporeal membrane oxygenation support, cardiorespiratory support and attempted defibrillation (including technique and dose). Each healthcare system that provides resuscitation is responsible for monitoring outcome and identifying areas for improvement (see Chapter 6).

There are limited data to characterize pediatric out-of-hospital cardiac arrest, although existing data (most recently obtained with automated external defibrillators) support the long-held belief that brady-asystolic rhythms are far more common than “shockable rhythms.”³³ VF and VT are not common pediatric arrest rhythms in the out-of-hospital setting, especially in children 7 years of age and younger. Shockable rhythms are more likely to be present with sudden, witnessed collapse, particularly among adolescents.³³

Although the frequency of sudden cardiac arrest in athletes is not known, extrapolation from a statewide survey in Minnesota suggests the annual incidence is approximately 1 per 200,000 athletes, with more than half of deaths attributed to hypertrophic cardiomyopathy (the leading cause), commotio cordis, or coronary artery anomalies.²⁴ More recently, channelopathies causing long-QT syndrome have been identified as causes of sudden cardiac arrest.²⁰ Sudden cardiac arrest in athletes is likely associated with VF or VT, and many episodes are witnessed. Immediate bystander CPR and early defibrillation with an automated external defibrillator can improve the chance of survival. Infants with congenital heart disease often develop ventricular arrhythmias. More data are needed regarding any modifications in resuscitation approach that these children might require.²⁹

For adults with a return of spontaneous circulation after cardiac arrest, therapeutic hypothermia and protocols for hemodynamic support and respiratory care improved outcomes of patients admitted after cardiopulmonary arrest and return of spontaneous circulation.³⁵ Although similar studies have not been reported in children, it is likely that improving post-resuscitation care can increase the rates of survival following cardiopulmonary arrest.

Central Nervous System Control of Breathing

Although central and peripheral respiratory chemoreceptors for response to hypoxemia and hypercarbia are present at birth, infants possess fewer peripheral chemoreceptors than do adults. Healthy infants and children typically develop tachypnea and hyperpnea in response to hypoxemia. Premature infants, however, often demonstrate a biphasic response to hypoxemia, with initial hyperpnea followed by a slowing of the respiratory rate and apnea. Careful monitoring of the infant’s rate and effort is needed to detect early evidence of deterioration.

If central nervous system depression results from trauma, disease, narcotic administration, or cerebral edema, the nurse must be prepared to support the child’s airway and respiratory function. It is always better to initiate support of ventilation while the patient’s respiratory effort is adequate than to delay support until respiratory failure or arrest occur and the patient exhibits apnea or is gasping.

Airways

At birth, the full “adult” complement of conducting airways is present and the airway branching pattern is complete. These airways grow in size and length during childhood. Alveoli and respiratory bronchioles multiply after birth. The number of alveoli increases by more than 10-fold by adulthood, and the alveolar surface area increases by a factor of 20.^6,37

Supporting airway cartilage and small airway muscles are incompletely developed until school age, so laryngospasm and bronchospasm can produce airway obstruction in the young child. Although it was previously thought that the lack of small airway muscle development contributed to the lack of infant response to bronchodilator therapy, this concept has generally been dispelled.

All airways of infants and children are smaller than airways of adults. Because resistance to air flow (R) is inversely related to 1/radius (r)⁴ during quiet breathing (laminar air flow), reduction in airway radius will increase resistance to air flow exponentially, and will increase work of breathing.

Small amounts of accumulated mucus, edema or airway constriction can have a minimal effect on the adult airway, but will often produce critical reduction in airway radius and critical increase in resistance to air flow and work of breathing in infants and young children (Fig. 1-2). Pediatric artificial airways are also small; they provide greater resistance to airflow than a normal natural airway and can quickly become obstructed by mucus.

Fig. 1-2 Effects of 1 mm of circumferential edema in neonates and young adults. A, The diameter of the larynx of the neonate is approximately 4 mm in diameter. If 1 mm of circumferential edema develops, it will halve the airway radius and increase resistance to airflow by a factor of 16 during quiet breathing (and more if airflow is turbulent). B, The larynx of the young adult is approximately 10 mm in diameter and 5 mm in radius. If the young adult develops 1 mm of circumferential edema, it will reduce the radius by about 20% (from 5 to 4 mm), and increase resistance to air flow by a factor of 2.4 during quiet breathing (more if airflow is turbulent).

The position and shape of the pediatric larynx is different from that of the adult. The pediatric larynx is more anterior and cephalad, and the articulation of the epiglottis with the larynx is more acute in children than in adults. These differences make the upper airway of infants more funnel-shaped than columnar. Pediatric intubation is often difficult for these reasons, and application of slight pressure on the cricoid cartilage may be necessary to displace the larynx posteriorly to facilitate intubation (although excessive pressure may make intubation more difficult).^8a,20,30

Until a child is approximately 8 years old, the smallest diameter of the pediatric larynx is at the level of the cricoid cartilage, and maximum endotracheal tube size is limited by the size of this area. By comparison, the cricoid area of the adult larynx is relatively wide, so maximal adult endotracheal tube size usually is limited by the diameter of the adult larynx at the level of the vocal cords (Fig. 1-3). In the past, fear of tracheal injury prevented the use of cuffed endotracheal tubes in children. However, cuffed tubes are now used for children in the prehospital and hospital settings, and may be preferable to uncuffed tubes, particularly when there is a high risk of aspiration or when it is difficult to maintain sufficient airway pressures during assisted ventilation in a child with poor lung compliance or when a large glottic leak is present.²⁰ The tube cuff pressure must be monitored and maintained per manufacturer’s recommendation (usually less than 20 to 25 cm H₂O).³⁰

Fig. 1-3 Comparison of infant A, and adult B, larynx.

There are several formulas to estimate pediatric endotracheal tube size, depth of insertion, and suction catheter size (Box 1-4). However, body length provides the most reliable parameter for selection of accurate endotracheal tube size.²³

After an endotracheal tube is inserted, the provider should verify correct position (using clinical assessment and a device such as an exhaled carbon dioxide detector or end-tidal carbon dioxide capnography) and appropriate size. If an uncuffed endotracheal tube is of appropriate size, positive pressure ventilation should produce an air leak when 25 cm H₂O is provided during hand ventilation. If no leak is detected, it might be necessary to replace the tube (when patient condition allows) with a tube that is 0.5 mm (internal diameter) smaller. Cuffed tubes should still allow a slight glottic air leak.

The pediatric trachea is much shorter than the adult trachea. The slightest downward or upward displacement of a pediatric endotracheal tube can move the tube into a mainstem bronchus or out of the trachea. Artificial airways must be securely taped in place, and nurses and therapists should monitor the tube insertion depth at the lip or nares, verifying position with auscultation and exhaled CO₂ tension hourly and with any change in patient condition. Continuous monitoring of waveform capnography will enable immediate detection of inadvertent extubation (see Chapter 9) and may assist in evaluating the quality of resuscitation (see Chapter 6).

The tip of an orotracheal tube will move with changes in the child’s head position. Flexion of the neck will displace an orotracheal tube further into the trachea, and extension of the neck will move the tip of the orotracheal tube further out of the trachea (see Fig. 10-19).

The cartilage supporting the infant’s larynx is compliant and can be easily compressed anteriorly or posteriorly when the neck is flexed or extended, respectively. When respiratory distress develops during spontaneous breathing, slight neck extension (with or without a jaw lift) can improve airway patency. It is important to avoid neck flexion or hyperextension when distress is present.

During childhood, growth of the peripheral airways lags behind growth of the larger airways, so peripheral airway resistance constitutes a greater portion of total airway resistance than in adults. Because the smaller bronchioles provide high resistance to air flow, the alveolar units served by these bronchioles require long filling and emptying times. If inadequate exhalation time is provided during mechanical ventilation, air trapping and alveolar distension can develop, producing complications such as increased positive end-expiratory pressure and pneumothorax. During pediatric mechanical ventilation, an optimal inspiratory:expiratory time ratio of 1:3 is usually provided. Mechanical ventilators must be capable of delivering small tidal volumes in short inspiratory times at low peak airway pressures.

Chest Wall

The cartilaginous chest wall of the infant and child is twice as compliant as the chest wall of the adult. As a result, during episodes of respiratory distress the chest wall can retract, compromising the child’s ability to maintain functional residual capacity or increase tidal volume. Chest retractions will also increase the work of breathing.

The shape of the infant’s chest and the orientation of the ribs also reduce the efficiency of ventilation during episodes of respiratory distress. The ribs are horizontal in orientation, and they articulate linearly with the vertebrae and sternum, so the intercostal muscles do not have the leverage to lift the ribs effectively. After the child reaches school age, the 45-degree orientation of the ribs enables the intercostal muscles to lift the ribs with a lever effect to elevate the chest wall.

During effective positive pressure ventilation, the child’s chest should expand easily outward. Positive pressure ventilation is ineffective if the child’s chest does not rise bilaterally. When evaluating effectiveness of positive pressure ventilation, if the nurse stands at the head or the foot of the bed and compares chest expansion bilaterally it will be easy to see if chest expansion is inadequate. If one side of the chest is not expanding, endotracheal tube migration, pneumothorax, or atelectasis may be present.

The chest wall is extremely thin in children, so respiratory sounds are easily transmitted throughout all lung fields. As a result, respiratory sounds from other areas of the lung can be heard over an area of atelectasis or pneumothorax. When assessing respiratory sounds and aeration, the nurse should auscultate all lung fields, and compare respiratory sounds heard over one side of the chest with those heard over the contralateral chest. Unilateral pathologic findings (e.g., atelectasis, pneumothorax, pleural effusion) can produce a change in pitch rather than a change in intensity of respiratory sounds.

Respiratory Muscles

Respiratory muscles consist of the diaphragm, the chest wall muscles, and the muscles of the upper and lower airways. These muscles contribute to expansion of the lung and to maintenance of airway patency. Loss of tone, power, and coordination in respiratory muscles will contribute to respiratory failure.

The diaphragm is the chief muscle of respiration. Diaphragm contraction results in an increase in intrathoracic volume and a fall in intrathoracic pressure, so that air enters the lungs. In neonates, the diaphragm is located higher in the thorax and has a smaller radius of curvature than in adults, and so it contracts less efficiently.

The diaphragm inserts obliquely in adults but horizontally in infants. Contraction of the infant diaphragm will tend to draw the lower ribs inward especially if the infant is supine. During episodes of respiratory distress, diaphragm movement will likely be optimized if the infant is placed prone or on the side, with the head of the bed elevated.

Anything that impedes diaphragm contraction or movement, such as abdominal distension, decreased abdominal wall compliance or diaphragm paralysis or paresis can contribute to respiratory failure in children. Paradoxic abdominal motion during inspiration (retraction of the chest wall and expansion of the abdomen) can indicate severe respiratory distress and usually results in rapid fatigue and decompensation.

In adults, the intercostal muscles function as accessory muscles of respiration and can lift the ribs if diaphragm function is impaired. In children, however, the intercostal muscles are not fully developed, so they function largely to stabilize rather than to lift the chest wall.

Lung Tissue

Lung compliance is low in neonates but increases during childhood. Low lung compliance and high chest wall compliance make respiratory function inefficient during episodes of respiratory distress. During childhood, respiratory efficiency improves as chest wall compliance decreases (i.e., the chest wall becomes more stiff) and lung compliance increases.

Closing volume (the minimum lung volume required to maintain peripheral airway patency) constitutes a higher percentage of total lung volume in children than in adults. Some infant airways remain closed during normal breathing; this can render the infant more susceptible to atelectasis.

Elastic tissue in the septae of the alveoli that surround smaller airways contributes to the maintenance of airway patency. There is a smaller amount of elastic and collagen tissue in the pediatric lung than in the adult lung; this can contribute to the increased incidence of pulmonary edema, pneumomediastinum, and pneumothorax in infants and young children. The relative paucity of elastic fibers, in combination with the low elastic recoil of the thorax and lung in the infant and toddler, can contribute to premature airway closure and atelectasis.

Collateral pathways of ventilation, including the intraalveolar Kohn’s pores and bronchoalveolar canals of Lambert, are incompletely developed during infancy. As a result, small airway obstruction can produce significant respiratory distress, because collateral pathways cannot ensure ventilation of alveoli distal to the obstruction.

Neonates may be more susceptible to pulmonary edema than older children or adults. Pulmonary edema may be observed frequently during episodes of respiratory distress, even when pulmonary capillary pressure is low. As a result, limitation of fluid intake and possible diuresis is often advisable when caring for euvolemic infants with respiratory failure.

Signs of Respiratory Distress

Signs of respiratory distress in children include: tachypnea, tachycardia, retractions, nasal flaring, grunting, mottled color, and change in responsiveness (Box 1-5). The infant may also demonstrate a weak cry. Hypercarbia, hypoxemia, or a fall in oxyhemoglobin saturation may also be documented. Apnea or gasping, decreased air movement, and alteration in perfusion can be late signs of respiratory distress, indicating impending arrest.

Brain and Skull Growth

All major structures of the brain and all cranial nerves are present and developed at birth. The infant’s neurologic system functions largely at a subcortical level. Brainstem functions and spinal cord reflexes are present, but cortical functions (e.g., memory and fine motor coordination) are incompletely developed. The autonomic nervous system is intact but immature; the infant has limited ability to control body temperature in response to changes in environmental temperature.

At birth, the brain is 25% of its mature adult weight. By 2½ years of age, the brain has achieved 75% of its mature adult weight.¹³ The growth in brain size is largely due to the development of fiber tracts and myelinization of neurons. This tremendous central nervous system growth during the first years of life adds uncertainty to the prediction of long-term consequences of early neurologic insults or injury. The child may recover with fewer sequelae than anticipated, because other areas of the brain begin to compensate for the injured areas; this is called plasticity. Subtle signs of unsuspected neurologic sequelae can manifest as learning disabilities when the child enters school.

Mortality is approximately the same following similar head injury in adults and children. However, children who survive head injury often demonstrate more complete recovery than do adult victims with similar injury. The Glasgow Coma Scale is less accurate in predicting the outcome of severe head injury in children than it is in adults, so modified pediatric coma scales have been published (see Chapter 11). A poor prognosis is indicated following head injury in children by the absence of spontaneous respiration, cardiovascular instability despite adequate volume resuscitation, flaccid paralysis, and fixed and dilated pupils. The presence of diabetes insipidus or disseminated intravascular coagulation can also indicate a poor prognosis.

The infant’s skull is not rigid during infancy, and the bones of the cranium normally fuse at approximately 16 to 18 months old. As a result, to a point, gradual increases in intracranial volume can be accommodated by skull expansion. Cranial enlargement can indicate the presence of a slow-growing tumor, hydrocephalus, or other mass lesions. Skull expansion does not, however, prevent the development of increased intracranial pressure.

The infant’s head circumference is documented on admission to the hospital. If the infant has central nervous system disease or injury (e.g., meningitis, head trauma), the head circumference is recorded frequently (intervals to be determined by protocol or by the healthcare team), and an increase should be reported to a physician or other on-call provider.

Because the fontanelles are not covered by the skull, palpation of the fontanelles can provide information about intracranial pressure or volume. The anterior fontanelle should feel flat and firm but not tense. It will typically bulge with any condition that increases superior vena cava pressure (including congestive heart failure) or intracranial volume or pressure (such as meningitis). If the anterior fontanelle is sunken, significant dehydration may be present.

Normal cerebral blood flow and cerebral perfusion pressure in the infant have not been definitively established. Adult cerebral blood flow averages approximately 50 mL/100 g brain tissue per minute, and the infant’s cerebral blood flow is thought to approximate 60% of that amount.¹⁹ The normal volume of cerebrospinal fluid production in children is unknown.

Criteria for brain death pronouncement in children require the use of accepted pediatric brain death criteria that are fundamentally the same as those used for adult. Clinical brain death criteria include absence of reversible cause and complete cessation of brain function (e.g., absence of cranial nerve function and absence of brainstem function, including absence of spontaneous respirations). For further information, see Chapter 11.

Neurologic Evaluation

Because infants demonstrate primarily reflexive behavior, a large part of the infant neurologic examination consists of evaluation of reflexes. It is important to note that some reflexes (e.g., a positive Babinski’s reflex) that are pathologic in the older child or adult may be normally present in the infant. Examination of cranial nerve function—especially the presence of pupil response to light, blinking, coughing, and gag reflex—is possible during routine nursing care of the critically ill or injured child.

Evaluation of the infant’s level of consciousness is based largely on evaluation of the infant’s alertness, response to the environment and parents, level of activity, and cry. Extreme sensitivity to stimuli usually indicates irritability, and extreme irritability or lethargy is abnormal. Infants with neurologic disease or injury often demonstrate a high-pitched cry.

Once the child is sufficiently mature to comprehend and answer questions, it will be possible to assess level of consciousness, orientation to time and place, and ability to follow commands. If the names of the child’s family members and favorite pets and friends are recorded in the care plan, every member of the healthcare team will be able to question the child about familiar people and quickly determine the accuracy of the child’s responses. The child’s responsiveness must also be evaluated in light of the child’s fatigue and clinical condition. A 5-year old might be sleepy after spending most of the night in the emergency department, but should still respond to a painful procedure.

Decreased response to painful stimuli is abnormal and can indicate deterioration in neurologic function. When assessing the child’s response, provide a central pain stimulus over the trunk. Withdrawal of extremities from a peripheral pain stimulus can be mediated by a spinal reflex; such reflex withdrawal does not enable verification of higher brain activity.

The neurologic examination includes evaluation of the child’s muscle tone. The term newborn and infant usually demonstrate dominance of flexor muscles, so extremities will be flexed even during sleep. Hypotonia or paralysis is abnormal in a patient of any age. When evaluating muscle strength, discrepancies can be appreciated most easily when antigravity muscles are used (e.g., instruct the child to simultaneously extend both arms with eyes closed; unilateral weakness is present if one arm falls). Small tremors may be normal during infancy, but tonic-clonic movements are abnormal.

Assessing the child’s ability to follow commands is a critical part of the assessment of responsiveness and motor function. Ask the child to raise two fingers, stick out his or her tongue or wiggle toes; these movements cannot be accomplished reflexively. Reflex curling of the fingers in response to palmar pressure may be misinterpreted as a voluntary hand squeeze, so this is not a reliable method to evaluate response to commands.

When using the Glasgow Coma Scale to score motor function, withdrawal of extremities is evaluated by pinching the medial aspect of each extremity in turn. Appropriate withdrawal occurs if the child adducts extremities (i.e., moves them away from the stimulus, away from midline).

Signs of increased intracranial pressure (Box 1-6) are the same in patients of all ages and include change in level of consciousness; decrease in spontaneous movement, movement in response to commands, and movement in response to painful stimulus; and pupil dilation with decreased constriction to light. In children, bradycardia, systolic hypertension, and altered breathing pattern are usually late signs of increased intracranial pressure and often indicate impending cerebral herniation.

Healthcare-Acquired (Nosocomial) Infections

Nosocomial infections can develop in as many as 12% of pediatric critical care patients.¹⁶ The sources of nosocomial infections in children differ from those reported in adults. Whereas the most common nosocomial infections observed in adult patients are urinary tract and wound infections, the most common nosocomial infections in pediatric patients are bloodstream infections (including catheter-related bloodstream infections [CRBSIs]) and ventilator-associated pneumonias (VAPs).^8,31 The risk of pediatric nosocomial infection and sepsis increases with increased length of stay, each invasive device day, illness severity at admission, and depressed immune status.⁷

As in adults, nosocomial infections are reduced by strict hand washing before and after every patient contact, strict attention to aseptic technique, and specific bundled care to target common causes of infection such as CRBSIs and VAP (see section, Care of Vascular Monitoring Lines, and Chapters 16 and 22).^8,15,28,31

Care of Vascular Monitoring Lines

CRBSIs are among the most common nosocomial infections in pediatric critical care. Risk factors include parenteral nutrition and antimicrobial therapy.³⁴ Risk factors for patients in the pediatric cardiac critical care unit include unscheduled medical admission, noncardiac comorbidities, prolonged device use, and medical therapies such as extracorporeal membrane oxygenation.¹¹

Although there is limited evidence to support specific strategies to prevent CRBSI in children, bundled therapies have been effective. Most multifaceted approaches are based on adult studies and include: (1) use of maximal sterile barrier precautions (e.g., cap, mask, sterile gown, sterile gloves, large sterile drape) during catheter placement; (2) use of 2% to 3% chlorhexidine gluconate/70% isopropyl alcohol or other appropriate antiseptic agents to prepare the skin before catheter placement and during routine care of the catheter insertion site; (3) prompt removal of catheters as soon as they are no longer required; and (4) strict adherence to appropriate hand hygiene practices, with annual handwashing campaigns.^21,28,34 For additional information, see Chapters 16.

In studies performed in adult intensive care units, antiseptic impregnated catheters were associated with reduced rates of CRBSI (see Chapter 22). Studies performed in children have described delayed time to infection, but not reduced infection rate associated with the use of antibiotic-impregnated catheters.

Catheters should be taped or secured to prevent inadvertent dislodging. Use of volume-controlled infusion pumps to provide continuous irrigation of each vascular catheter allows precise regulation of the volume of fluids administered hourly. Arterial catheters should be irrigated gently, especially in neonates and young infants, because forceful irrigation in small patients can result in retrograde delivery of air or particulate matter into the arch of the aorta and cerebral arteries.

Ventilator-Associated Pneumonia

Although the incidence of VAP is lower in children than adults, VAP remains the second most common cause of nosocomial infections children. The pathogenesis is poorly understood, but in children it is likely related to aspiration and immunodeficiency.¹⁵ VAP is a significant cause of increased critical care length of stay, increased mechanical ventilation days, and mortality in pediatric and adult critical care.

As with prevention of CRBSIs, the use of a multidisciplinary approach with bundled care protocols has been associated with a decreased prevalence of VAP. Strategies documented to reduce the risk of VAP in children include hand hygiene, elevation of the head of the bed, scheduled mouth care, and changing the ventilator circuit only when soiled.⁵ Use of heated ventilator circuits can reduce the pooling of water within the circuit.⁵ Additional factors associated with reduction of VAP in adults include: avoidance of nasotracheal intubation and the use of in-line suctioning to prevent the aspiration of pooled tracheal sections.¹⁰