Chapter 51. Pediatric Considerations

Pediatric visits account for 20–25% of visits to emergency departments in the United States. Most of these encounters will occur in general emergency departments, which may have limited capabilities to care for the critically ill child.1,2 The priorities in the assessment and management of the pediatric patient are similar to those of the adult patient. The quoted ABCs of airway, breathing, and circulation still apply and are first and foremost in the evaluation of the young infant and child. There are certain anatomic, physiologic, developmental, and social considerations that are unique to this population and must be taken into account during the evaluation and treatment. This chapter will focus on the key differences in the treatment of the critically ill child. A complete discussion of the many procedures, as well as the presentation of every critical condition in pediatric patients, is well outside the scope of this text. See Table 51-1 for a list of medications used in pediatric resuscitation.

Recognition of Respiratory Distress

Compared with adults, infants and children have anatomic and physiologic characteristics that make them more susceptible to respiratory emergencies. During the first 6 months of life, they are obligate nose breathers, and their nasal passages can easily become occluded with a simple upper respiratory illness that will lead to obstruction. They have weak abdominal muscles and diaphragm, which tire easily during respiratory conditions. In addition, they have faster metabolic rates, which require a higher oxygen demand. This higher oxygen demand, coupled with a decreased functional residual capacity, makes them more vulnerable to decreases in their oxygen levels compared with those of adults.3 It is based on these differences that children tend to have higher respiratory rates, even at rest. One must be familiar with the normal vital signs according to the age (see Table 51-2). Associated fatigue or sweating while feeding and weight changes will prompt the examiner to think of congestive heart failure or hereditary conditions such as cystic fibrosis.3–5

The child's general appearance is the best guide to the level of distress. Patients with mild tachypnea who smile or feed without difficulty and are able to track the examiner (maintain eye movement) are not in extremis. Close attention should be directed to those who look ill and appear irritable or lethargic. See Table 51-3 for a list of findings in the respiratory distressed child.

Initial Airway Management

Failure to adequately manage the airway is a leading cause of preventable deaths in the pediatric population. Unlike adults, in whom cardiac failure is the primary cause of cardiopulmonary arrest, acute respiratory failure is responsible for most cardiopulmonary arrests in children.4,5 Tachypnea is present in all but the most severe respiratory arrests—which will present with no air movement at all. Many illnesses in addition to respiratory disorders in this population can initially present with tachypnea, including sepsis, diabetic ketoacidosis (DKA), and abdominal pain. See Table 51-4 for the anatomic and physiologic differences in the pediatric airways and recommended treatment strategies.

Airway Placement

Nasal and oral airways are used to overcome the mechanical obstruction produced by the tongue in patients with decreased level of consciousness. To place a nasopharyngeal airway, apply some lubricant to the airway and insert gently, angling back toward the pharynx.5 A few drops of a nasal decongestant such as oxymethazoline can be added and may decrease bleeding through the nares. Oropharyngeal airways (OA) can only be used in unconscious patients with an absent cough or gag reflex. Carefully measure the airway to avoid moving the epiglottis or the tongue, worsening the obstruction. To measure the airway, place the OA by the child's cheek and hold one of the OA to the corner of the mouth and the other corner to the angle of the jaw.6

Oxygen Administration

Administration of oxygen is vital in any respiratory illness. Pediatric patients have a very small tolerance for hypoxia. Young infants may benefit from blow-by oxygen by cupping the hand or small nasal cannulas. Cannulas have the advantage of providing oxygen while creating a small amount of positive end-expiratory pressure (PEEP), both of which stimulate the infant while preventing apneic spells. The best way to deliver close to 100% oxygen is with a face mask with a reservoir such as a non-rebreather mask. This may be uncomfortable to very young children, so using alternative methods is recommended.6,7

Medications

Next to oxygen, the most important pharmacologic intervention to consider in respiratory failure is epinephrine. Epinephrine is a natural endogenous catecholamine, both α- and β-agonist. At low dose, it is primarily a β-receptor agonist causing strong bronchodilation, decreasing mucosal edema, and improving cardiovascular status with a very short onset of action.8 It may be administered intramuscularly or intravenously in anaphylactic reaction, depending on the severity of shock. The subcutaneous route is no longer used because of poor delivery. For respiratory distress, upper airway obstruction, or edema, it can be administered in nebulized form. The standard dose is racemic epinephrine 0.5 mL of the 2.25% concentration. “Crash cart” epinephrine (1:1,000) may also be used by administering 5.5 mL in nebulized form. Specific pharmacologic interventions will be discussed with specific conditions below.

Ventilation

In some situations, positioning and administration of oxygen or other medications is not enough, and assistance in ventilation may be required. Respiratory failure is described by some authors as hypoxemia (arterial Po2 < 60 mm Hg) and hypercarbia (arterial Pco2 > 55 mm Hg) with associated respiratory acidosis. Intubation is considered a clinical decision and should not be withheld waiting for any laboratory testing.5 Signs of impending respiratory failure include altered sensorium or deterioration in mentation, progressive hypoxemia, severe work of breathing, silent chest, apnea. For a complete list, please refer to Table 51-5.

The ability to provide proper bag–valve ventilation is a vital skill in the airway management of adult and pediatric patients. In the prehospital setting, studies have shown that bag ventilation may be as beneficial, if not more so, as endotracheal intubation.9,10 Ventilations may be provided for a prolonged amount of time with care not to overinflate the stomach. Increasing pressure in the stomach will increase the likelihood of vomiting and, therefore, the risk for aspiration. Overinflating the stomach may also impair ventilation by increasing intra-abdominal pressure, which would not allow the diaphragm to move adequately. Adding a nasogastric tube whenever prolonged bagged ventilation is anticipated may decrease the occurrence of these complications.

Pediatric patients have smaller airways, which lead to higher resistance to flow as well as a higher propensity for obstruction. They also have an increased likelihood of adenoid tissue tonsil hypertrophy. In terms of movement of the lungs, the diaphragm has a smaller zone of apposition and horizontal ribs, which are less efficient and therefore increase the work of breathing. Finally, in younger children especially, immature musculature and higher metabolic rates may predispose to respiratory failure.4,11

Noninvasive Positive Pressure Ventilation (NIPPV)

NIPPV is the administration of a gas mixture at a preset pressure by way of nasal prongs or a face mask. Positive pressure is provided in either continuous or variable pressure to prevent alveolar collapse and maintain an adequate functional residual capacity by decreasing the work of breathing. Based on the modality used, continuous positive airway pressure (CPAP) provides a constant pressure at end expiration or variable/bilevel positive airway pressure (VPAP or BiPAP) that provides two levels of pressure: inspiratory positive airway pressure (IPAP) and a lower expiratory positive airway pressure (EPAP).The level of pressure can be modified based on the patient's need and response. Variable modes also offer the option to activate spontaneous IPAP, which is activated at a set rate, thus time triggered (at set intervals), or spontaneous, which triggers an IPAP when spontaneous inspiratory effort is detected, or a combination of both.

NIPPV is preferred initially in carefully selected groups of patients in order to treat their hypoxemia while reversing the disease process in attempt to avoid endotracheal intubation (see Chapter 6).

Most studies for pediatric applications of NIPPV have been done in neonates, where it is used for conditions such as transient tachypnea of the newborn, apnea of prematurity, and respiratory distress syndrome. Classically, neonates were placed on a continuous NIPPV or CPAP mode. Recent work has shown that BiPAP has a faster resolution of symptoms, is better tolerated, and has fewer side effects.12,13

In infants and older children, it is less established. Similar indications and contraindications apply to use with children than with adults. Patients who could benefit from this modality need to be conscious, have a protected airway with an intact gag reflex, and be able to breathe spontaneously. Contraindications to this therapy are facial injuries, impending respiratory failure, altered mental status, or inability to maintain the airway.13,14

The pediatric patient will need some sedation for optimal management. Ketamine has been established as the sedative of choice. It enables the patient to keep the airway intact. It also has bronchodilator effects and its safety record makes it the best choice for this particular procedure.13 Benzodiazepines are not recommended due to their effects on respiratory depression in an already compromised patient.

CPAP initial recommended setting is 10–14 cm H2O. “Bubble CPAP,” in addition to the CPAP, provides a high-frequency ventilation effect, producing small vibrations in the infant's chest at the frequency of 15–30 Hz. This modality, if used in neonates, might contribute to gas exchange, reducing the work of breathing.

For BiPAP, the initial recommended settings are an inspiratory pressure of 12–15 cm H2O and an expiratory pressure of 6–7 cm H2O.

Invasive Positive Pressure Ventilation

Definitive airway management entails endotracheal intubation and mechanical ventilation. In the presence of severe trauma, altered mental status leading to coma, organ failure, or respiratory depression, a definitive airway should be considered. There are some crucial differences in ventilation between children and adults. Even if you are familiar with ventilation, consulting an expert in pediatric intensive care is highly recommended whenever you reach this point.

Intubation

The most important considerations for a successful intubation are evaluation of the airway, anticipating complications, and having the necessary equipment. If time permits and the required equipment or staff are unavailable, assist ventilation using bag–valve ventilation until everything is ready.

There are two commonly used laryngeal blade shapes in emergency departments today: Miller, or straight blade, and the Macintosh, or curved blade. Both come in different sizes. For pediatric patients, the Miller blade is generally preferred since it can displace the large floppy epiglottis and may help reach the pediatric vocal chords, which will be superior and anterior. Either blade may be used according to the level of the practitioner's expertise and level of comfort.

Endotracheal tubes (ETTs) also come in different shapes and sizes. There are many ways to calculate the size of the ETT for your patient. A simple way to remember is by using the patient's little finger. The pinky should be as large as the airway, plus or minus a few millimeters. Applying the formula of adding 4 to the patient's age divided by 4 ([age + 4]/4) gives an approximation of the tube size. Multiplying the ETT size by 3 gives an approximation of the number where the tube should rest against the lip commissure. For example, a 4-0 ETT should be introduced with the 12-cm mark at the lip. Recent recommendations state that cuffed tubes should be used in children older than 8 years of age, while both types (cuffed or uncuffed) may be safely used in younger children and infants, except newborns. Under certain conditions such as increased lung resistance, cuffed tubes may actually be preferred.5,6

The most reliable approach in an emergency situation, which can be very stressful, is to use a length-based resuscitation system such as the commercial Broselow™ tape with color-coordinated code cart shelves. These can be used in children 12 years or younger and give information on ETT sizes, blade numbers, indwelling catheters, as well as medication dosages based on the patient's ideal weight. There is current controversy on whether the tapes accurately measure the patient's weight, since children today are heavier than their counterparts 10 or 15 years ago. Even then, it may be useful to utilize this guide. It is also important to remember that these are only guidelines and that ETTs a half a size larger or smaller should be ready and available in case there is any complication.

Rapid Sequence Intubation (RSI)

RSI has become the cornerstone in emergency airway management. Since its advent, outcomes in emergent endotracheal intubations of children and adults have improved greatly. Careful attention should be directed to the patient with a potentially difficult airway. RSI consists of a administering a sedative agent and a paralytic agent followed by endotracheal intubation to minimize complications such as vomiting, aspiration, and hypoxia.15,16 There are a few mnemonics out there that describe the process. It is important to remember that even if the patient is not undergoing paralysis for any particular reason, following the steps is very useful in assuring the best possible outcome. For a list of RSI medications and dosages, please see Table 51-6.

The steps in RSI include:

1. Preparation

2. Preoxygenation

3. Premedication

4. Paralyze

5. Pass the tube

6. Proof of placement

7. Postintubation care

Preparation includes anticipating equipment requirements, calculating dosages, assessing the airway, and testing the equipment. As discussed, always keep in mind the possible complications and unexpected outcomes. At this step, it is crucial to anticipate the need for other services such as anesthesia among other types of airway equipment.

Preoxygenation is performed by administering 100% oxygen for at least 3 minutes, which will “wash out the nitrogen” and provide an oxygen reserve for most patients for up to several minutes of apnea. As discussed, younger patients have a smaller reserve and will reach hypoxia faster. Oxygen can be applied by non-rebreather mask or by bag–valve ventilation. It is important to note that self-inflating bags will not provide flow unless ventilations are given. If this equipment is being used, attempts to synchronize with the patient's breathing effort will maximize oxygen delivery.

Premedication includes administration of medications to avoid increases in intracranial pressure as well as depolarizing agents and sedatives. In pediatric patients, atropine is administered to blunt the vasovagal hypotension that can occur during laryngoscopy. Intravenous lidocaine is also given, especially in head trauma patients, in order to decrease the gag reflex, thereby minimizing the rise in ICP that the procedure may cause. At this phase, a sedative may also be administered, prior to paralytics.16

For sedation purposes, there are many pharmacologic options. Ketamine is well studied in the pediatric population and it is safe in patients with hypotension or shock. It is also recommended in patients with respiratory conditions such as asthma, as it induces bronchodilation and increases blood flow. Although controversial, it is still not recommended in patients with increased ICP since it is thought to worsen their conditions.17 Benzodiazepines are safe in patients who are to be intubated but should be avoided in the presence of hypotension. Etomidate is safe in patients undergoing intubation since it does not affect cerebral blood flow or blood pressure and lasts less than 20 minutes. Side effects include transient myoclonic movements. The clinical relevance of etomidate-related adrenal insufficiency has been called into question by several studies. But patient populations especially at risk are the septic shock patients in an already suppressed state, in whom it causes adrenal suppression. Largely prospective trials are needed for validation.18 Propofol is another candidate that is neuroprotective by decreasing neuronal metabolism but may induce hypotension. The brand name Diprivan™ should be avoided in patients with egg allergy, but the generic drug is safe. Barbiturates, especially Thiopental™, have the same safety profile as propofol but with higher neuroprotective action by reducing ICP, cerebral metabolism, and cerebral oxygen demands. However, the vasodilation and myocardial depression causing hypotension and the real potential risk of bronchospasms made the barbiturates fall out of favor during RSI.

Paralyzing is the process of total muscle relaxation; yet the patient might still be conscious, thus the sedation. The two most commonly used paralytic agents are: the depolarizing agent, that is, succinylcholine, and the nondepolarizing agents, that is, rocuronium, pancuronium, and vecuronium. Succinylcholine is a fast-acting, short-lasting depolarizing agent; you can see the onset of action as the membranes get depolarized and the patient fasciculates. There is a relative contraindication in patients with an increased ICP. It is contraindicated in patients with potential hyperkalemia or causes that can cause hyperkalemia such as suspected renal failure, muscular disorders, prolonged bed rest, and subacute burns, since these conditions may cause a transient rise in potassium. On the other hand, rocuronium is one of many nondepolarizing agents available for RSI. It is has a very short onset of action and, since it does not depolarize the membranes, does not affect potassium or rise in increased ICP.19

In passing the tube, the best way to verify placement is by visualizing passing of the ETT through the vocal cords. In pediatric patients, the narrower part of the airway is the subglottic space, while in the adult population, it is the vocal cords. The tube should be visualized just past the cords. The previously described formula can be used to approximate position.

Placement confirmation: auscultate the epigastrium first and then verify that breath sounds are symmetric in both lung fields. The use of a colorimetric or end-tidal CO2 detector to confirm adequate ventilation is now the recommended method and the most sensitive method for confirming tube placement.5 A chest radiograph is always ordered to verify the depth of placement: the end of the ETT should be 2–3 cm above the carina.

Postintubation care includes placing the patient on a mechanical ventilator (see below) and introducing a nasogastric tube to decompress the stomach. Arterial blood gasses are sent 10–15 minutes after intubation to assess oxygenation and ventilation status. The head of the bed should be kept at 45° to decrease the risk of aspiration. This is also important in patients with increased ICP as this maneuver alone may greatly improve this condition. Order restrain and appropriate sedation.

Mechanical Ventilation

Mechanical ventilators have many different settings that go beyond the scope of this chapter.

For infants and neonates younger than 1 year or weighing less than 10 kg, the ventilator is usually set in pressure limited cycles since most ventilators cannot deliver a restricted low tidal volume, as small as 40–60 mL. Pressure cycles have always been the preferred mode in young patients and neonates, since they deliver a set pressure, and flow stops once the pressure is reached, thus limiting barotrauma and decreasing the rate of ventilator-induced lung injury (VILI). The downside of this modality is that tidal volumes (Vt) are variable and not guaranteed, with potential for hypoxemia. In situations with decreased lung compliance a decrease in the Vt reaching the lungs is seen, whereas in situations with increased compliance the Vt will exceed the expected. To begin ventilation with this modality, pick either synchronized intermittent mandatory ventilation (SIMV) or assist control (AC) mode. The trigger will be a pressure, so set positive inspiratory pressure (PIP) between 15 and 20 cm H2O and titrate just enough to get an adequate chest rise. Set the PEEP at 3–5 cm H2O.7 Maintaining oxygen saturation above 92% guarantees appropriate oxygenation.

In older children and adults, volume cycles seem to be the preferred mode; the ventilator will deliver a set Vt regardless of the pressure necessary to achieve that delivery.

The peak pressure at end inspiration, (PIP) is a function of the inflation volume, flow resistance, and the elastic recoil of the lung and chest wall, but has nothing to do with the plateau pressure that in turn is at end inspiration when there is no air flow. Plateau pressure is a surrogate for transalveolar pressure and is directly proportional to the elasticity of the lungs and chest wall. The rapid, repetitive opening of alveoli has been associated with barotraumas and VILI. For initial settings, consider: Vt of 5–8 mL/kg, the respiratory rate at 12–20 adjusted for age, with a PEEP of 3–5 cm H2O. Different modalities and modifications should be done depending on the etiology requiring this therapy and changed according to clinical condition. See Table 51-7 for initial ventilation settings in pediatric patients. Something to remember: there are very limited evidence-based data on specific modalities. Choice of modality is user driven, and the users should use the mode they feel most comfortable with. The goal should be to ventilate and oxygenate with minimal lung damage.

Avoid unnecessarily high levels of oxygen by keeping the fraction of inspired oxygen (FiO2) at the lowest level to maintain adequate oxygenation to avoid oxygen toxicity. There is a higher correlation of oxygen toxicity and FiO2 above 70, so it is reasonable to titrate the FiO2 using O2 saturation or the ABG's.18

Acute respiratory distress syndrome is defined as a Pao2/FiO2 ratio of less than 200, with the presence of bilateral infiltrates on chest radiography (radiographically similar to pulmonary edema) without left atrial pressure elevation (wedge should be less than 18 mm Hg). In the advent of ARDS or to prevent it, lung-protective ventilation is recommended using Vt 4–6 mL/kg in conjunction with a higher respiratory rate to achieve an adequate minute ventilation, limiting plateau pressure to <30 cm H2O. Hypercapnia is expected, and the term permissive hypercapnia is tolerated as long the arterial pH is kept above 7.20. This trial in adults and pediatric populations showed a significant decrease in mortality. Pediatric patients who have worsening hypoxemia should be referred early for extracorporeal membrane oxygenation (ECMO) (see Chapter 7).

Shock is a state of inadequate tissue perfusion of oxygen and normal cellular function. The causes of shock include: pump failure (i.e., cardiogenic shock), hypovolemia (i.e., dehydration, bleeding), or vasodilation (i.e., anaphylaxis or sepsis). The body will adjust to maintain perfusion and O2 delivery via the microcirculatory and macrocirculatory systems. In the event of hypovolemia, several mechanisms are employed in order to compensate for the resulting decrease in venous return that, itself, results in decreased CO. Such mechanisms include adrenal release of catecholamines, which induce tachycardia (increased heart rate), increased cardiac contractility leading to increased stroke volume (SV), and peripheral vasoconstriction. This is in response to insufficient stretch sensed by carotid and aortic baroreceptors. In reference to vasoconstriction, venoconstriction will support intrathoracic volume and produce an increase in preload, whereas arterial constriction will increase perfusion pressure that in turn directly increases organ blood flow. The renin–angiotensin system is activated to increase sodium and water reabsorption and augment systemic vascular resistance. Glucagon is excreted leading to hyperglycemia by increasing gluconeogenesis and glycogenolysis that, coupled with decreased renal blood flow and lactic acid production from anaerobic metabolism, may lead to acidosis.19

Prolonged failure to maintain adequate perfusion pressure to critical organs is incompatible with life. In light of this, blood perfusion may be redirected and limited to organs essential to life with nonvital organs suffering the detrimental effect of lack of blood perfusion. This is a method of maintaining mean arterial pressure (MAP) under the conditions of hypovolemia and, ultimately, organ hypoperfusion.19–21

Pediatric patients respond differently to shock than do adults. The first and most sensitive response to shock in a pediatric patient is tachycardia. The myocardium is underdeveloped that prevents them from modifying their SV as needed. Therefore, the only way that cardiac output is increased is by raising the heart rate. It is important to note that in children, blood pressure in itself should not be used to monitor severity of illness or response to treatment. Young patients have a very strong response to a decrease in effective circulatory volume. They have lower baseline blood pressures and are able to increase their systemic vascular resistance and heart rate to compensate. This benefit, at the same time, gives the examiner a false sense of security since hypotension may not be observed until approaching cardiac arrest. Prompt recognition and reversal of shock is warranted to avoid morbidity and mortality.20

Categorizing and Treating Shock

The many etiologies responsible for shock can be divided into different categories based on the type of dysfunction present. Shock may be categorized as cardiogenic, hemorrhagic, neurogenic, obstructive, dissociative, or distributive in nature. See Table 51-8 for shock etiologies and their treatment.

Hemorrhagic or hypovolemic shock occurs whenever intravascular volume is depleted. It can ensue from bleeding or dehydration with associated electrolytic disturbances. In pediatric patients, the most common cause worldwide is secondary to vomiting and/or diarrhea. Other common causes include burns, trauma, and metabolic disorders such as DKA. Treatment includes isotonic volume expansion followed by blood transfusion in the trauma setting. In the presence of shock, the initial bolus is 20 mL/kg over 5–10 minutes followed by reassessment of vital signs and mental status. Studies have shown similar outcomes whenever crystalloids or colloids are used, as long as resuscitation is adequate.22–25 In the trauma setting, blood is administered at 10-mL/kg aliquots after initial expansion of 40 mL/kg of normal saline or Ringer's lactate. Younger infants and children with cardiac or renal conditions should receive smaller boluses of 10 mL/kg with close monitoring to avoid fluid overload.

In obstructive shock, intravascular volume is normal but the flowing process is affected. Causes of obstructive shock include pericardial tamponade, pulmonary embolism, pneumothorax, or congenital heart disease (CHD) (i.e., ductal dependent lesions). Other causes of obstructive shock will be discussed elsewhere in this book.

Cardiogenic shock occurs when the pump fails to propel the blood due to intrinsic myocyte dysfunction. In pediatric patients, the common causes include infectious etiologies such as myocarditis or pericarditis, cardiac dysrhythmias, and those secondary to CHD. Depending on the etiology, different therapies are warranted. Arrhythmias should be corrected with the use of amiodarone, β-blockers, calcium channel blockers, or adenosine. Pericarditis and myocarditis may benefit from inotropic medications such as dopamine. For a list of vasopressors, see Table 51-8. CHD requires a particular set of treatments depending on the pathophysiology involved. Shock within the first 4–6 weeks should prompt examiners to consider CHD. In these situations, the administration of prostaglandin E1 may be life saving with the goal of maintaing the ductus arteriosus open.25

Distributive shock involves patients with normal plasma volume that has been displaced by loss of vascular tone or increased capillary leakage. Patients with this type of shock usually have anaphylactic reactions, infectious processes such as sepsis or dengue shock syndrome, or an acute inflammatory state, all of which will increase capillary leakage as a third-spacing phenomenon.

Anaphylaxis is a common cause of distributive shock. Pediatric patients most commonly develop anaphylactic reactions from exposure to exogenous antigens such as food and medications.26 Signs and symptoms can be cutaneous, respiratory, cardiovascular, gastrointestinal, and generalized. A list of signs and symptoms can be found in Table 51-9. It is important to note that in many instances, the urticaria and flushing may lag presentation of more severe symptoms by minutes to hours. Treatment involves epinephrine (1:1,000) 0.15 (< 30kg) or 0.3–0.5 mL (> 30 kg) delivered into the medial thigh region. Recent studies have shown that the IM route achieves a faster peak in delivery and better symptom response than subcutaneous administration. In addition, corticosteroids, H2 blocking agents, and antihistamines should be administered. If symptoms persist, repeated doses of epinephrine should be continued every 5–15 minutes. In the presence of hypotension, epinephrine should be administered IV and an epinephrine drip considered for persistent shock. Delayed reactions may occur up to 72 hours after the initial reaction. Close observation and follow-up are advised.27

Neurogenic shock is observed in the setting of spine trauma at the T6 level and above. Findings include hypotension, bradycardia, and flushed extremities associated to a decreased CO. Treatment includes spine immobilization, normal saline boluses, and vasopressors such as norepinephrine or epinephrine.

In dissociative shock, there is an uncoupling between oxygen demand and energy production caused by poisoning and intoxication such as cyanide, aspirin, or methemoglobin. The definite treatment includes IV fluid boluses and administration of a specific antidote.

IV access is vital in the treatment of any kind of shock. Placement of two peripheral lines is usually more than enough but in cases of severe shock and dehydration, it may prove difficult. Classic teaching states that in the critically ill child, inability to gain vascular access within three attempts or 90 seconds should prompt placement of an intraosseous (IO) line. Newer systems make this process easier and anticipating a difficult line may be more than enough. Through an IO, fluids and resuscitation drugs may be administered easily. For a more definite access, performing a central line using the Seldinger technique will also provide the ability to get blood for sampling. In children and infants, the preferred approach is the femoral and external jugular veins.28

Septic Shock

Sepsis is defined as a suspected or confirmed source of infection in a patient with two or more of the following systems involved:

1. Temperature >38.3°C (>101°F) or <36°C (<96.8°F)

2. Heart rate >90 beats/min

3. Respiratory rate >20 breaths/min

4. Acute mental status change

5. Hyperglycemia in the absence of diabetes

6. WBC count >12,000 and <4,000/mm3, or >10% immature (bands)

Severe sepsis is defined as an acute sepsis causing organ dysfunction, hypoperfusion, or hypotension before fluid challenge, whereas septic shock is the evidence of persistent hypoperfusion after fluid challenge in a patient with severe sepsis. This has been closely studied in both the adult and the pediatric populations. In a study by Han et al, approximately 3% of pediatric transports to a pediatric emergency department had a final diagnosis of septic shock. In this article, mortality approached 25% in this population.29 According to new pediatric guidelines, the use of resuscitation protocols as recommended by the Society of Critical Care Medicine decreased mortality to approximately 2% in previously healthy children and 10% in chronically ill children, with a number needed to treat of 3.3. Pediatric patients will require proportionally more fluid in resuscitation due to their usual hypovolemic state and earlier intubation strategies due to their low functional residual capacity.21

Other differences include variations in their capacity to respond to SV requirements and their cardiovascular response to septic shock. For instance, based on the formula CO = SVR × HR, if an adult faces a need for increased SV, doubling the resting heart rate from 70 to 140 will more than double the CO. On the other hand, infants and children have, at baseline, higher resting heart rates and doubling the resting heart rate from 150 to 300 will not be as effective, shortening diastolic time leading to decreased coronary artery perfusion and cardiac preload time.22 Further, the clinical presentation of septic shock in young children or infants will present different variations leading to cold or warm shock, whereas adults usually present with a state of elevated CO with decreased SVR. These differences may be observed in the initial physical exam but may become more evident once the initial resuscitation has taken place in the emergency department. Finally, most pediatric septic shock is linked to volume depletion, which is the reason they require comparatively more fluid than do adults, usually 40–60 mL/kg, and to some extremes up to 200 mL/kg in the first hours or resuscitation.20

Recognition

Diagnosis in pediatric septic shock is mainly clinical. Children commonly present with tachycardia, vasodilation, and fever. In septic shock, additional findings include hypothermia or hyperthermia, changes in mental status, oliguria, prolonged capillary refill (more than 2 seconds) in cold shock, and peripheral vasodilation in warm shock. Hypotension with bounding pulses is considered warm shock; diminished peripheral perfusion with prolonged CR is considered compensated cold shock, while hypotension with associated prolonged CR is considered decompensated shock. The expected heart rate should be between 90 and 160 bpm in young infants and between 70 and 150 bpm in children. These have the same goal: to monitor with improvement in condition.20

The workup should be directed at finding a source. Bacterial etiologies are usually sought, but viral syndromes are seen as common agents as well. Along with the usual workup, there should be other considerations. Although the adult literature recommends that lactate be sampled and monitored as evidence of hypoperfusion, there is no consensus for this in the pediatric literature. This test should probably be added to the initial evaluation, but its benefit has not been clearly established. On the other hand, according to the recent literature, elevated troponin levels in pediatric patients may be useful in predicting myocardial dysfunction and a subsequent decrease in CO.30

The main goal of treatment in pediatric septic shock is early recognition, followed by aggressive fluid resuscitation with early administration of antibiotics. Manage the airway and get vascular access as previously discussed. Approximately 40% of CO is dedicated to the work of breathing. Intubating and sedating the patient will allow the CO to be dedicated to vital organs. Administer an initial fluid bolus of 20 mL/kg of normal saline or 5% albumin over 5–10 minutes and repeat if there is no improvement. These patients may require close to 60 mL/kg or more, in certain situations. Reassess after each bolus. Palpable hepatomegaly or rales on lung examination will be found in fluid overload. If signs of fluid overload are present, boluses should be of only 10-mL/kg aliquots and careful monitoring should take place. Diuretics, peritoneal dialysis, and continuous renal replacement therapy may be considered in patients who have undergone stabilization but are unable to manage the fluid overload.

Inotropic agents should be added to patients who present with fluid-resistant shock (Table 51-10). Fluid-refractory shock is the presence of clinical signs of shock after 60 mL/kg of fluid administration. In most patients, dopamine remains the first-line agent for fluid-refractory shock, although some studies suggest that infants younger than 6 months may not have enough norepinephrine stores due to an immature sympathetic innervention.22,31 Adding dobutamine to this initial intervention will be beneficial. In the presence of dopamine-resistant shock, titrating epinephrine (cold shock) or norepinephrine (warm shock) is beneficial in most cases. If no central line access is available, inotropes may be administered peripherally as long as there is close monitoring of the area for any signs of necrosis (Figure 51-1).19

In the presence of catecholamine, dexamethasone at a dose of 1–2 mg/kg may be administered in patients at risk for adrenal insufficiency. Very young infants have low glycogen stores and underdeveloped thermoregulatory systems. Close attention should be paid to hypothermia and electrolyte disturbances such as hyperglycemia or hypoglycemia and hypocalcemia. Vasodilator therapies with agents such as nitroprusside, nitroglycerine, and milrinone should be considered in patients with persistent shock despite the above interventions.

Goals of Intervention

Therapeutic goals of intervention in septic pediatric patients in the emergency department include restoration of capillary refill to less than 2 seconds and normal mental status, pulses, and blood pressure, with an adequate urine output of >1 mL/kg/h. Even if the patient improves significantly during the first hour, admission to a pediatric intensive care unit is warranted.

The differences in pediatric and adult critical care management stem from complex social, developmental, and physiologic interactions. Knowledge of these differences and adequate preparation are key in improving care for this important population.