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Painter MJ et al. Phenobarbital and phenytoin in neonatalseizures: metabolism and tissue distribution. Neurology.

1981;31:1107.

Gal P et al. The influence of asphyxia on phenobarbital dosing requirements in neonates. Dev Pharmacol Ther.

1984;7:145.

Rane A et al. Plasma protein binding of diphenylhydantoin in normal and hyperbilirubinemic infants. J Pediatr.

1971;78:877.

p. 2193

The most frequent cause of cardiac arrest in pediatric patients is a

terminal result of respiratory failure or shock, not a primary cardiac

event.

Case 106-1 (Question 1)

Developmental changes and immaturity of the respiratory system make

respiratory distress the most common reason for hospital admission in

the first year of life. Nasal flaring and grunting are unique features of

the respiratory examination in infants that indicate respiratory distress.

The normal respiratory rate in children changes over time; therefore, the

respiratory rate that would be of concern varies based on the age of the

patient.

Case 106-2 (Questions 1, 2)

Oxygen should be administered immediately in a child where respiratory

difficulty is suspected. Once the decision is made to intubate the patient,

the choices for pharmacotherapy of intubation vary based on the

cardiovascular stability of the patient, whether the stomach is empty or

full, and the underlying cause of the respiratory distress.

Case 106-2 (Questions 3, 4)

Hypovolemic shock is the most common type of shock seen in pediatric

patients. Septic shock, obstructive shock, and cardiogenic shock occur

in children but are less common. The initial treatment of all forms of

shock is the same. A pediatric patient can present with compensated or

decompensated shock. There are physiologic differences in the pediatric

patient’s response to hypovolemia, with hypotension being the last

physiologic change during decompensation.

Case 106-3 (Questions 1, 2)

Infants have low glycogen stores, so are at high risk for the development

of hypoglycemia when they have poor oral intake or during conditions of

stress. Because hypoglycemia may cause seizures and is linked to poor

neurologic outcome, all critically ill infants should have point-of-care

glucose testing on presentation. If identified, hypoglycemia must be

treated promptly.

Case 106-3 (Question 3)

Due to the immature immune system in the infant, the incidence of

septic shock is the highest in the first year of life. Patients with

underlying medical conditions have a higher mortality rate than

previously healthy children who experience sepsis.

Case 106-4 (Question 1)

Due to physiologic changes during childhood, the definitions of sepsis and

systemic inflammatory response syndrome (SIRS) are different in

children and adults. Tachycardia and tachypnea, pivotal to the adult

definition of SIRS, are common presenting symptoms of many pediatric

disease processes and are not solely indicative of sepsis. Unlike adult

guidelines, temperature variation and leukocyte abnormalities are

included in the pediatric definitions. There are also specific definitions

based on patient age: newborn, neonate, infant, toddler and preschoolaged child, school-aged child, and adolescent.

Case 106-4 (Question 2)

Septic shock can be further defined by the patient’s response to fluid

resuscitation and catecholamine administration. These factors, as well

as physiologic differences in neonatal and pediatric cardiovascular

physiology compared with adults, affect not only the choice of therapy

but also drug dosing and monitoring.

Case 106-4 (Questions 3–6)

p. 2194

p. 2195

Neonates with ductal-dependent congenital heart disease (CHD) may

not be diagnosed immediately after birth. These patients may present

with symptoms of being either in respiratory distress, in cardiogenic or

obstructive shock, or in a combination of both. It is essential to consider

CHD in any neonate who presents with these symptoms.

Case 106-5 (Question 1)

Traumatic brain injury (TBI) is the leading cause of mortality in children

and leads to significant morbidity among survivors. The anatomic

differences of the child’s brain render it more susceptible to certain

types of injuries after head trauma. Causes vary by age, with

nonaccidental trauma seen most commonly in the first year of life.

Quick assessment of the patient on presentation to emergency services

is needed for appropriate diagnosis, stabilization, and treatment.

Case 106-6 (Questions 1–3)

Placement of a ventriculostomy will allow for measurement of

intracranial pressure (ICP) and drainage of cerebralspinal fluid. The

ability to measure ICP will assist in the evaluation of the efficacy of

treatments. Cerebral perfusion pressure (CPP) also must be monitored

closely in patients with TBI. Goal CPP values vary by age. Standard

therapies to reduce ICP include CSF drainage, medically induced

hypertension, and hyperosmolar therapy with mannitol or hypertonic

saline. When standard therapies fail, barbiturate coma, therapeutic

hypothermia, or decompressive craniectomy may be considered.

Case 106-6 (Questions 4–6)

Treatment and/or prevention of early post-traumatic seizures has been

shown to improve outcomes, but long-term use of anticonvulsant

medications (greater than 7 days) has not been shown to improve

outcomes and is associated with adverse effects.

Case 106-7 (Question 1)

Much of pediatric practice is dedicated to assisting the child in making the transition

from the intrauterine environment through infancy, childhood, and adolescence to

adulthood. One of the greatest challenges in managing pediatric patients is

recognizing the numerous physiologic changes that take place during this time and

understanding how they affect assessment and management of the patient. The

definition and presentation of many disease states encountered in the critical care

setting, including respiratory depression, supraventricular tachycardia, hypotension,

and shock, vary based on the age of the patient as a result of these physiologic

variations. There are also newborn emergencies that are unique to the physiologic

transitions that occur in the first month of life.

Pediatric healthcare providers practicing in critical care settings such as the

emergency department or pediatric intensive care unit (PICU) must be adept at

incorporating these physiologic differences into medication selection, dosing, and

monitoring to optimize patient care.

The epidemiology of patients admitted to either the pediatric emergency

department or PICU differs from that typically seen in adult critical care settings.

1,2

In

an evaluation of 361 children presenting to an emergency department, the most

common medial reasons for admission were cardiocirculatory causes (32%),

neurologic conditions (26%), and respiratory causes (23%).

1 Cardiocirculatory

causes included hypovolemic, septic, cardiac, and anaphylactic shock. Neurologic

conditions consisted primarily of seizures, status epilepticus, and meningitis or

encephalitis. The most common respiratory cause for admission was respiratory

syncytial virus (RSV) bronchiolitis, followed by pneumonia, pleural effusions, and

croup. Eighteen percent (18%) of the patients were admitted after trauma. Diabetic

ketoacidosis accounted for 6% of admissions. Other diagnoses included

intoxications, near drowning, snake bites, and burns. Assessment of the most common

causes for PICU admission has provided similar results. In a review of 1,149

children admitted during a 2-year period to the PICU of a university-affiliated

children’s hospital, the majority (38%) were diagnosed with cardiovascular

diseases, followed by respiratory illnesses (28%), other medical causes (10%),

neurologic illness (8%), and trauma (8%). Another 7% were admitted for

postoperative care.

2 When comparing admissions to pediatric intensive care from

1982, 1995, and 2005 to 2006, the most common medical diagnostic categories have

remained unchanged. However, fewer children were admitted after accidents, with

croup or with epiglottitis.

2 These changes can be explained by mandatory car seats

for children, administration of dexamethasone in the emergency department to

patients with croup and the conjugate Haemophilus influenza type b immunization.

During the same time period, the proportion of patients that died decreased from 11%

to 4.8%; however, the proportion of survivors with moderate or severe disability

increased significantly from 8.4% to 17.9%.

2 With the low rate of mortality in the

PICU, the focus of our research should investigate how to improve patient outcomes.

PEDIATRIC CARDIOPULMONARY

RESUSCITATION

In marked contrast to pediatric cardiac arrest, adult cardiac arrest studies have

focused on the diagnosis and treatment of ventricular fibrillation (VF) in both

inpatient and out-of-hospital cardiac arrest. Studies showed that VF was the most

common initial dysrhythmia in adults with sudden death; in some reports, the

prevalence of VF was 60% to 85%. Cardiac arrest due to VF or pulseless ventricular

tachycardia as the initial cardiac rhythm occurs in only 5% to 15% of pediatric

patients in hospital and out-of hospital cardiac arrest.

3

In contrast to adults, cardiac

arrest in infants and children does not usually result from a primary cardiac cause;

more often it is the terminal result of progressive respiratory failure or shock.

Therefore, it is essential to recognize and treat pediatric patients admitted with

respiratory distress, pneumonia, and shock aggressively to prevent the development

of systemic hypoxemia, hypercapnia, and acidosis that may then progress to

bradycardia, hypotension, and eventually cardiorespiratory arrest.

p. 2195

p. 2196

CASE 106-1

QUESTION 1: Paramedics are transporting C.W., a 5-month-old, 5-kg infant with respiratory distress who

stops breathing en route to the hospital. The patient is bag-mask-ventilated with cardiopulmonary resuscitation in

progress. On arrival in the emergency department, the patient is apneic, asystolic, and pulseless. The infant has

no intravenous (IV) access. After brief bag-mask ventilation, the patient is intubated with an endotracheal tube

(ETT). A colorimetric carbon dioxide capnometer detector device confirms proper ETT placement. Findings

now include breath sounds that are equal bilaterally and good chest movement with ventilation, although there is

still no pulse palpable without chest compressions and no heart sounds are heard. An electrocardiogram shows

asystole. Oxygen saturation is not obtainable. What medication is needed for C.W. at this point in his

resuscitation and what would the appropriate dose be?

Epinephrine is the drug of choice for the management of pediatric asystole.

3

Ventilation and chest compressions should be continued for C.W., and while one

responder is attempting IV access, another may administer the first dose of

epinephrine down the ETT using a higher dose of 0.5 mg (0.1 mg/kg prepared from

the 1:1,000 or 1 mg/mL concentration) to account for reduced absorption. If two

attempts at IV line placement are unsuccessful, an intraosseous (IO) catheter should

be inserted into the proximal tibia. Blood may be obtained through the IO needle to

perform a rapid glucose check and sent for further studies. After reassessment of the

airway, ventilation and chest compressions should be continued. Subsequent doses of

epinephrine can be administered every 3 to 5 minutes through the IO line, using the

appropriate IV/IO dose of 0.05 mg (0.01 mg/kg using the 1:10,000 or 0.1 mg/mL

concentration).

RESPIRATORY DISTRESS

Respiratory distress, related to problems at all levels of the respiratory tract from the

nose to the lungs, is a frequent occurrence in children.

4

(For a video that shows some

of the signs of respiratory distress in an infant, go to

http://www.youtube.com/watch?v=42jJ18fkZ0Y.) The nose provides nearly half

the total airway resistance in children. Infants under 2 months are obligate nasal

breathers, and their nose is short, soft, and small with nearly circular nares. The

nares will double in size from birth to 6 months but they can easily be occluded from

edema, secretions, or external pressure. Simply clearing the nasal passageways with

saline and bulb suctioning can significantly improve an infant’s respiratory condition.

Other physiologic reasons for a high incidence of respiratory failure in infants and

children are small and collapsible airways, an unstable chest wall, inadequate

collateral ventilation for alveoli, poor control (tone) of the upper airway

(particularly during sleep), tendency for the respiratory muscles to fatigue, reactivity

of the pulmonary vascular bed (increased sensitivity of the vasculature, particularly

in young infants), an inefficient immune system, genetic disorders or syndromes, and

residual problems related to premature birth such as bronchopulmonary dysplasia.

CASE 106-2

QUESTION 1: T.F. is a 7-month-old, previously healthy 12-kg infant who presents to the emergency room

with a 3-day history of upper respiratory tract symptoms. His mother states that he is having increasing

difficulty breathing and has not wanted to drink or eat. On examination, he has a respiratory rate of 70

breaths/minute, an O2

saturation of 90% on 100% FIO2

via nasal cannula, nasal flaring and grunting, and both

intercostal and suprasternal retractions. Initial viral screening reveals positive results for RSV, and his chest Xray is consistent with RSV bronchiolitis. He was agitated and fussy at first presentation, but during the last 30

minutes his respiratory rate has decreased to 40 breaths/minute with a reduction in retractions and he has

become somnolent. What developmental changes in the lung explain why a routine viral infection could result in

the need for an emergency room visit in a 7-month-old previously healthy child?

The most common reason for admission to the hospital in the first year of life is

respiratory distress. This can be explained by the numerous physiologic differences

seen in an infant. Although all the conducting airways are present at birth and the

airway branching pattern is complete, the airways are small.

5 The airways will

increase in size and length throughout childhood. Not only are the airways smaller in

an infant but supporting airway cartilage and elastic tissue are not developed until

school age. For these reasons, the child’s airways are susceptible to collapse and

may easily become obstructed as a result of laryngospasm, bronchospasm, and edema

or mucus accumulation. Normal airway resistance is the highest in infants because it

is inversely proportional to 1/radius

4

. Therefore, any airway narrowing from

bronchospasm, edema, or mucus accumulation will significantly increase the airway

resistance and increase the infant’s work of breathing. The cartilaginous ribs of the

infant and young child are twice as compliant as the bony ribs of the older child or

adult. During episodes of respiratory distress, the infant’s chest wall will retract

further than a patient with a bony ribcage. This will reduce the patient’s ability to

maintain functional residual capacity (FRC) or increase tidal volume, thus further

increasing the patient’s work of breathing.

The respiratory muscles consist of muscles of the upper airway, the lower airway,

and the diaphragm. They contribute to expansion of the lung and maintenance of

airway patency. Lack of development of the small airway muscles may render young

infants less responsive than older children to bronchodilator therapy. Lastly, the

intercostal muscles are not fully developed until school age, so they act primarily to

stabilize the chest wall during the first years of life. Because the intercostal muscles

have neither the leverage nor the strength to lift the rib cage in the young child, the

diaphragm is responsible for the generation of tidal volume. Therefore, anything that

impedes diaphragm movement, such as a large stomach bubble, abdominal

distension, or peritonitis, can result in respiratory failure in the young child.

CASE 106-2, QUESTION 2: What respiratory signs and symptoms are present in T.F. and how do they

define the patient’s respiratory status? What are potential causes of T.F.’s respiratory distress?

To assess a patient for respiratory distress, one should evaluate four areas:

respiratory rate and effort, work of breathing, quality and magnitude of breath sounds,

and the patient’s mental status. Normal respiratory rates vary with age (Table 106-1).

A respiratory rate greater than 60 breaths/minute is abnormal in a child of any age,

but most concerning in an older child. An abnormally slow or decreasing respiratory

rate may herald respiratory failure. Intercostal, subcostal, and supracostal retractions

increase with increasing respiratory distress. Although increased retractions are seen

in infants, they have decreased efficiency of respiratory muscle function during the

first years of life; therefore, the benefit in infants is reduced. Decreasing respiratory

rate and diminished retractions in a child with a history of distress may signal severe

fatigue. Nasal flaring is an effort to increase airway diameter and is often seen with

hypoxemia. T.F. demonstrates all of these physiologic signs of respiratory distress. In

addition to these findings, some infants will exhibit an expiratory grunting noise. This

noise is produced by the child’s involuntary effort to counter the loss of FRC by

closing their glottis on active exhalation. Grunting produces positive end-expiratory

pressure (PEEP) in an effort to prevent airway collapse. An expiratory grunt is

mechanistically similar to “pursed lip breathing” in adults with chronic dyspnea. An

expiratory grunt is classically seen in the presence of extensive alveolar pathology

and is considered a sign of serious disease.

p. 2196

p. 2197

Table 106-1

Normal Respiratory Rates and Definition of Tachypnea for Children, by Age

Age

Respiratory Rate

(breaths/minute)

Tachypnea (breaths/minute)

Newborn–2 months 30–60 >60

2–12 months 25–40 >50

1–3 years 20–30 >40

3–6 years 16–22 >40

7–12 years 14–20 >40

>12 years 12–20 >40

There are numerous causes of respiratory distress in infants and children. Table

106-2 summarizes common respiratory noises in children and their site of origin

which may provide clues to the clinical cause. The most common causes of

respiratory failure in infants and children are infectious diseases, asthma,

malignancies, trauma (both accidental and nonaccidental), poisonings, foreign body

aspiration, anatomic upper airway obstruction, cardiogenic shock, and untreated leftto-right intracardiac shunts. Respiratory syncytial virus is among the most common

causes of respiratory distress in infants and young children, leading to an estimated

90,000 hospitalizations each year.

6 Although RSV can occur at any age, it is most

severe in children under 2 years of age such as T.F. Prematurity, as well as chronic

respiratory disease and congenital heart disease, increases the risk for severe RSV

bronchiolitis requiring hospitalization.

CASE 106-2, QUESTION 3: T.F. is no longer consistently maintaining oxygen saturation values above 90%

on nasal cannula O2

. How should T.F. be managed?

Oxygen should be administered immediately in any patient where respiratory

difficulty is suspected. Infants and children consume 2 to 3 times more oxygen per

kilogram of body weight than adults under normal conditions and even more when

they are ill or distressed. T.F. responded well to oxygen administered via nasal

cannula in the emergency department, but is now increasingly somnolent and has a

decreased respiratory rate along with decreased oxygen saturation values—all signs

of impending respiratory failure. The specific indications for intubation in infants and

children are as follows:

Table 106-2

Common Airway Noises, Site of Origin, and Clinical Causes in Children

Respiratory

Noise Definition Site of Origin

Common Clinical Causes

Acute Persistent

Wheeze A high-pitched, continuous

musical noise, often

associated with prolonged

expiration (can occur with

inspiration or expiration)

Intrathoracic airways Intermittent

asthma/viral-induced

wheeze

Persistent

asthma

2.

3.

4.

1.

Rattle This sound is the result of

excessive secretions in the

large airways, which are

presumably moving with

normal respirations

Either or both

intrathoracic and

extrathoracic

airways

Acute viral bronchitis Chronic sputum

retention

(neuromuscular

disorders)

Stridor This is predominately an

inspiratory noise and

indicates obstruction to

airflow in the extrathoracic

airways (upper airways

obstruction) (can occur with

inspiration or expiration)

Extrathoracic

airways

Acute

laryngotracheobronchitis

(or viral croup)

Laryngomalacia

Snore The noise arises from an

increase to airflow through

the upper airways,

predominately in the region

of the nasopharynx and

oropharynx; it is more

obvious during inspiration, but

may be audible throughout

the respiratory cycle

Oronasopharyngeal

airway

Acute

tonsillitis/pharyngitis

Chronically

enlarged tonsils

and adenoids,

obstructive

sleep apnea

Snuffle/Snort These terms describe

respiratory noises emanating

from the nasal passages;

these noises are audible in

both inspiration and

expiration and are often

associated with visible

secretions from the nares

Nasal

passage/nasopharynx

Acute viral head cold Allergic rhinitis

Grunt This sound occurs with

closure of the glottis during

active exhalation

Alveoli/lung

parenchyma

Any alveolar pathology

in infants and small

children

None

For examples of some of these airway noises, go to the following web links:

Wheeze: http://www.youtube.com/watch?v=YG0-ukhU1xE&feature=related

Rattle/rhonchi: http://www.youtube.com/watch?v=QPBZOohj2a0&feature=related

Stridor

Toddler: http://www.youtube.com/watch?v=Zkau4yHsLLM&feature=related

Infant: http://www.youtube.com/watch?v=73zUjcCzgqA&NR=1

Grunt: http://www.youtube.com/watch?v=aptwttJ6y_4

p. 2197

p. 2198

Apnea

Acute respiratory failure (Pao2 <50 mm Hg in patient with FIO2 >0.5 and Paco2 >55

mm Hg acutely)

Need to control oxygen delivery, with institution of PEEP or to provide accurate

delivery of FIO2 greater than 0.5

Need to control ventilation to decrease work of breathing, control Paco2

, or to

administer neuromuscular blocking agents

5.

7.

6.

Inadequate chest wall function, as in patients with neuromuscular disorders such as

Guillain–Barré syndrome, spinal muscular atrophy, or muscular dystrophy

Upper airway obstruction

Protection of the airway of a patient whose protective reflexes are absent, such as

those with head trauma

Based on the diagnosis of acute respiratory failure and the need to control oxygen

delivery, T.F. should be intubated and placed on mechanical ventilation.

MEDICATIONS FOR INTUBATION AND

MECHANICAL VENTILATION

CASE 106-2, QUESTION 4: What pharmacologic agents are recommended when intubating a pediatric

patient? Develop a plan for the medications to be used during intubation of T.F.

After the decision is made to proceed with intubation, the next decision needs to

be whether pharmacologic agents are appropriate. Most pediatric patients require

sedation before laryngoscopy and intubation. The goal is to depress the infant or

child’s level of consciousness sufficiently to produce appropriate conditions for

intubation. Pharmacologic therapy is used to produce adequate sedation, analgesia,

and amnesia plus a blunting of the physiologic response to airway manipulation.

Intubation in the awake state can elicit protective reflexes that trigger tachycardia,

bradycardia, and elevation of blood pressure, increased intracranial pressure,

intraocular pressure, cough, and bronchospasm. Pharmacologic control promotes a

smoother intubation with less physiologic stress for the patient who often is already

in a compromised state. Ideally, this should be accomplished while producing

minimal hemodynamic compromise.

7

There are many factors to be considered when choosing agents for intubation: the

onset of action of the agent, the patient’s hemodynamic status, the need to prevent

increased intraocular or intracranial pressure that may be caused with intubation, and

whether the stomach is full or empty. A wide variety of medications may be used for

pediatric sedation, each with its own risk and benefits (Table 106-3).

7

In general,

agents that act rapidly and are eliminated quickly are ideal. Often drug choices are

made based on the clinician’s experience with a particular drug and the immediate

availability of the drug. Most importantly, the drug regimen chosen must be based on

the patient’s physiologic state. Agents with adverse effects that would exacerbate any

underlying medical conditions must be avoided. Narcotics used in combination with

anxiolytics are used commonly. To produce optimal conditions for intubation, T.F.

could be given 12 mcg of fentanyl (1 mcg/kg) and 1.2 mg of midazolam (0.1 mg/kg)

IV before the procedure to provide sedation and analgesia. Both agents are relatively

short-acting and reversible if difficulties arise with ETT placement.

Patients with inadequate relaxation despite adequate sedation may require

neuromuscular blockade, although these agents are not without risk. In a patient with

a partial airway obstruction, neuromuscular blockade may worsen pharyngeal

collapse, potentially resulting in complete airway obstruction. Therefore,

neuromuscular blocking agents should only be used if the clinician is absolutely

certain that adequate ventilation can be provided or that the patient can be intubated.

If adequate chest rise and oxygen saturation cannot be readily maintained with bagmask ventilation, neuromuscular blockers should not be used. Infants and children

younger than 5 years have a high vagal tone; therefore, they are more likely to exhibit

bradycardia when intubated. Instrumentation of the airway can directly stimulate

vagal receptors and induce bradycardia. In these patients, it is prudent to administer

atropine 0.02 mg/kg before intubation to blunt the autonomic response. Lidocaine (1–

1.5 mg/kg/dose with a maximum dose of 100 mg) may be administered intravenously

to blunt the airway protective reflexes elicited by instrumentation. This may be

particularly useful in a patient with elevated intracranial pressure (ICP).

In the asthmatic patient, drugs that release histamine (e.g., morphine, atracurium, or

thiopental) and have the potential to produce laryngospasm or bronchospasm should

be avoided. The beneficial bronchodilatory side effects of ketamine, however, make

it a useful choice in these patients. In a child with increased ICP, the choice of

pharmacologic agent depends on the hemodynamic status of the patient. Thiopental or

pentobarbital is an excellent choice in the hemodynamically stable patient whereas

etomidate is preferred if the patient is unstable or hypovolemia is suspected.

Etomidate should not be used routinely in pediatric patients because a single dose

administered for intubation has the potential to produce adrenal inhibition.

8

In

children and adults with septic shock, etomidate administration is associated with a

higher mortality rate.

8–10

In all cases of intubation, preoxygenation is carried out to increase the available

oxygen in the lungs during the procedure, thus giving the practitioner some buffer time

to intubate the patient. However, in patients with an elevated ICP or pulmonary

vascular hypertension, hyperventilation is recommended to also produce hypocarbia.

A summary of specific patient conditions and recommended agents for intubation can

be found in Table 106-4. In an infant or child with a full stomach, the risk of

aspiration of gastric contents is high. Rapid sequence intubation (RSI) is used when

there is an aspiration risk, such as the child with a full stomach, and there is no

concern of a difficult intubation.

11 The goal of RSI is to gain airway control with an

ETT as quickly as possible to prevent aspiration. The patient is preoxygenated via

face mask and bag-mask ventilation cannot be used because it causes gastric

distension. Once all necessary intubation equipment is ready, rapidly acting sedative,

analgesic, and paralytic medications are administered simultaneously. Cricoid

pressure must be maintained until the ETT is in place and confirmed to provide

adequate protection from aspiration. An end-tidal CO2 detector should be attached to

the ETT after intubation to confirm proper placement in the trachea. Colorimetric

end-tidal CO2 devices change color from purple to yellow to confirm the presence of

exhaled CO2 and tracheal placement.

Endotracheal intubation and mechanical ventilation can be painful, frightening, and

anxiety provoking, especially in a young child. To improve patient comfort, relieve

anxiety, and lessen the work of breathing, anxiolytics, sedatives, and analgesics are

frequently administered once the patient is intubated and mechanically ventilated.

Maintenance of adequate sedation is essential. Selection of appropriate agents is

based on the physiology of the patient. Guidelines for the use of continuous infusions

are outlined in Table 106-3. In the paralyzed patient, neuromuscular blockade neither

alters consciousness nor provides analgesia; therefore, adequate sedation and

analgesia are essential. Providing effective analgesia and sedation to the pediatric

patient depends on accurate ongoing efforts to assess the intensity of the patient’s

pain or anxiety. The assessment of pain and anxiety in infants and critically ill

children who are unable to communicate relies heavily on physiologic and

behavioral responses. A number of pain and sedation tools have been developed and

validated specifically for use in children.

12 No single standard measure gives a

complete qualitative or quantitative measure. Selection of an appropriate tool is

based on the child’s age, underlying medical condition, and cognition level. It is

essential that these tools are utilized to evaluate the adequacy of the ICU sedation.

Policies and procedures need to be in place for the appropriate selection and use of

each tool, in addition to training of all healthcare professionals to appropriately use

each tool. The goal is to use the minimum amount of sedation needed to adequately

sedate the intubated child, while minimizing adverse effects.

p. 2198

p. 2199

Table 106-3

Pharmacologic Agents Used for Pediatric Intubation and Continuous Sedation

Drug Route Dose Onset Duration Benefits

Adverse

Effects

Narcotics

Morphine IV 0.1 mg/kg/dose

(max: initial dose 2

mg) may repeat to

a maximum total

dose of 15 mg

Neonates: 0.05

mg/kg/dose

Continuous

infusion

Children: 20–50

mcg/kg/hour

Peak: 20

minutes

2–4 hours in

neonates

Reversible

(naloxone)

Histamine

release.

Respiratory

depression

hypotension,

peripheral

vasodilatation,

euphoria,

dysphoria,

itching, central

nausea and

Neonates: 15

mcg/kg/hour

Premature

neonates: 10

mcg/kg/hour

vomiting,

decreased

response to

hypercarbia

Fentanyl IV 1–3 mcg/kg/dose

(max: initial dose

100 mcg, may

repeat to a total

dose of 5 mcg/kg or

250 mcg)

Continuous

infusion

1–3 mcg/kg/hour

(max: initial dose

50–100 mcg/hour)

CHD patient with

an open chest: 5

mcg/kg/hour

1–3 minutes 30–90

minutes

Rapid onset,

short acting,

reversible

(naloxone),

relatively stable

hemodynamic

profile

Bradycardia,

respiratory

depression,

decreased

response to

hypercarbia,

acute chest wall

rigidity, itching

Benzodiazepines

Diazepam IV 0.05 mg/kg/dose

(max: 5 mg) may

repeat in 0.05-

mg/kg increments

(max: 1 mg) to a

total maximum dose

of 10 mg

0.5–2

minutes

3 hours Reversible

(flumazenil)

Respiratory

depression,

lacks analgesic

properties,

hypotension and

bradycardia,

Local irritation,

pain

Lorazepam IV 0.05–0.15

mg/kg/dose (max: 4

mg)

15–30

minutes

0.5–3 hours Reversible

(flumazenil)

Respiratory

depression,

lacks analgesic

properties,

hypotension and

bradycardia

Midazolam IV/IM 0.05–0.15

mg/kg/dose (max:

initial dose 2 mg,

may repeat in 1-mg

increments to a

total dose of 5 mg)

Continuous

infusion

0.05–0.1

mg/kg/hour (max:

initial dose 2

mg/hour)

1–5 minutes 20–30

minutes

Rapid onset,

short acting,

provides

amnesia,

reversible

(flumazenil)

Respiratory

depression,

lacks analgesic

properties,

hypotension and

bradycardia

Intranasal 0.1–0.3 mg/kg/dose

(max: 10 mg)

Use the 5-mg/mL

concentration

2–5 minutes 30–60

minutes

PO 0.5–0.75

mg/kg/dose

(max:10–20 mg)

30 minutes 2–6 hours

Barbiturates

Pentobarbital IV 2 mg/kg/dose (max:

100 mg). May

repeat in 1-

mg/kg/dose

increments to a

total dose of 7

mg/kg. Do not

exceed 200 mg

total dose

Continuous

infusion

0.5–1 mg/kg/hour

1 minute 15 minutes Decreases

intracranial

pressure

Cardiovascular

and respiratory

depression

IM/PO/PR 2–6 mg/kg/dose IM: 10–15

minutes

PR/PO: 15–

60 minutes

1–4 hours

p. 2199

p. 2200

Miscellaneous

Ketamine IV 1 mg/kg/dose

every 5 minutes

titrated to effect

Continuous

infusion

0.5–1 mg/kg/hour

1–2

minutes

10–30

minutes

Rapid onset,

airway

protective

reflexes stay

intact, no

hypotension or

bradycardia

Bronchodilation

is useful to

intubate

asthmatics

Increases

airway

secretions and

laryngospasm

(blunted with

atropine).

Elevated

intracranial and

intraocular

pressure.

Emergence

reactions are

possible.

IM 4–5 mg/kg/dose 3–5

minutes

12–25

minutes

PO 6–10 mg/kg (mixed

in cola or other

beverage)

30 minutes 30–60

minutes

Etomidate IV 0.3 mg/kg/dose

initially, then 0.1

mg/kg/dose every

5 minutes to titrate

to effect

10–20

seconds

4–10

minutes

Rapid onset

Short acting

Stable

hemodynamic

profile,

decreased ICP

Potential for

adrenal

inhibition,

nausea, and

vomiting on

emergence

Propofol IV 1–2 mg/kg/dose

initially, then 0.5–2

mg/kg/dose every

3–5 minutes to

30–60

seconds

5–10

minutes

Intravenous

general

anesthetic, rapid

onset and

Cardiovascular

and respiratory

depression

(propofol-

titrate to effect

Continuous

infusion

Infants and

children: 50–150

mcg/kg/minute

Adolescents: 10–

50 mcg/kg/minute

recovery related infusion

syndrome),

contraindicated

in patients with

egg allergy, pain

on injection

Dexmedetomidine IV 0.5–1 mg/kg/dose

Continuous

infusion

0.4–0.7

mcg/kg/hour

Doses as high as

2.5 mcg/kg/hour

have been used

30 minutes 4 hours Minimal to no

respiratory

depression

Hypotension

and bradycardia

Use with

caution in

patients with

advanced heart

block

Neuromuscular Blockers

Succinylcholine IV 1 mg/kg/dose 30–60

seconds

4–7

minutes

Rapid onset

Short duration

Potentiates

hyperkalemia.

Contraindicated

in head trauma

(↑ ICP), crush

injury, burns,

hyperkalemia.

May induce

neuroleptic

malignant

syndrome

Vecuronium IV 0.1 mg/kg/dose

Continuous

infusion:

0.1 mg/kg/hour

1–3

minutes

30–40

minutes

Cardiovascular

stable

Slower onset

Longer duration

of action

Rocuronium IV/IM 0.6–1 mg/kg/dose 60–75

seconds

20–30

minutes

Cardiovascular

stable

Reversal Agents

Naloxone IV For opioid

overdose: 0.1

mg/kg/dose (max:

2 mg)

For reversal of

mild respiratory

depression: 0.01–

0.02 mg/kg/dose

(max: 0.4 mg) may

repeat every 2–3

minutes

2 minutes 20–60

minutes

Rapid onset Shorter duration

than most

opioids,

therefore

repeated doses

may be needed

Flumazenil IV 0.01 mg/kg/dose

(max: 0.2 mg), may

repeat 0.005

mg/kg/dose at 1-

minute intervals to

1–3

minutes

6–10

minutes

Rapid onset Shorter duration

than most

benzodiazepines,

therefore

repeated doses

a max total dose of

1 mg

may be needed

p. 2200

p. 2201

Table 106-4

Management Examples of Specific Patient Cases

Condition

Treatment Goal During

Intubation Medications

Fullstomach Prevent passive regurgitation and

aspiration after airway protective

reflexes lost

Rocuronium, succinylcholine

Bronchospasm Eliminate or treat stimuli that would

induce or increase bronchospasm

Ketamine, vecuronium, lidocaine,

atropine

Increased intracranial pressure No increase in heart rate or blood

pressure

Thiopental/pentobarbital, etomidate,

vecuronium, rocuronium, lidocaine

Pulmonary vascular hypertension Avoid decreased pulmonary blood

flow

Midazolam, fentanyl, vecuronium

Hypokalemia or depressed cardiac

output

Maintain blood pressure without

heart rate changes

Etomidate or midazolam with

fentanyl

PEDIATRIC SHOCK

CASE 106-3

QUESTION 1: M.M., a 3-month-old, 6-kg male infant, presents with a history of decreased oral intake and

progressive lethargy. Physical examination revealed an irritable infant with a respiratory rate of 50

breaths/minute, heart rate of 150 beats/minute, blood pressure of 80/50 mm Hg, and temperature of 39°C. He

has cool extremities with a capillary refill of 3 seconds. The mother reports that her baby has had no wet

diapers for the last 4 hours. A small purpuric rash has appeared on his trunk in the last half hour because the

parents left home to bring him to the emergency room. Initial electrolytes obtained in the emergency room on

placement of IV access were as follows:

Sodium, 136 mEq/L

Potassium, 4.9 mEq/L

Chloride, 111 mEq/L

CO2

content, 13 mEq/L

Blood urea nitrogen, 31 mg/dL

Serum creatinine, 0.8 mg/dL

Serum glucose, 50 mg/dL

What type of shock might M.M. be experiencing?

Shock may be classified as hypovolemic, distributive, cardiogenic, or obstructive.

Based on his presentation, M.M. is most likely presenting with hypovolemic shock,

the most frequent type of shock seen in pediatric patients. Hypovolemic shock occurs

when circulating intravascular volume decreases to a point at which adequate tissue

perfusion can no longer be maintained. Hypovolemia causes a decrease in preload

and adversely affects cardiac output. Initially, hypovolemia activates peripheral and

central baroreceptors that cause catecholamine-mediated vasoconstriction and

tachycardia. This initial response can maintain adequate circulation and blood

pressure even after acute loss of as much as 15% of the circulating blood volume.

Shock results from inadequate blood flow and oxygen delivery to meet the metabolic

demands of the tissues.

3 Shock will progress from an initial compensated state to

decompensated state. Typical signs of compensated shock include tachycardia, cool

and pale distal extremities, prolonged (>2 seconds) capillary refill, weak peripheral

pulses compared with central pulses, and normal systolic blood pressure. As shock

progresses, the patient will exhaust his ability to compensate. The patient will exhibit

signs of inadequate end-organ perfusion, including depressed mental status,

decreased urine output, metabolic acidosis, tachypnea, weak central pulses, and

mottling of extremities. M.M. shows evidence of having progressed to this later

stage, with lethargy and decreased urine output.

CASE 106-3, QUESTION 2: How should M.M. be initially managed and monitored?

All patients presenting with shock should be placed on high-flow oxygen while

their initial evaluation is being performed. Initial volume resuscitation in all forms of

shock is the same. It is recommended to push isotonic crystalloid fluid (normal saline

or lactated Ringer’s solution) in 20 mL/kg boluses administered over 5-10 minutes.

Immediately reassess the patient for signs of improved perfusion, using clinical

criteria such as reduction in heart rate, improvement of blood pressure, capillary

refill, quality of pulses, and mental status. If the clinical signs of shock persist,

another 20 mL/kg of isotonic fluid should be administered, reaching, if necessary, at

least 60 mL/kg within the first 15 to 30 minutes of treatment.

3,13 Therapeutic end

points of fluid resuscitation in patients with shock are capillary refill less than 2

seconds, normal pulses with no difference between central and peripheral pulses,

warm limbs, urine output greater than 1 mL/kg/hour, normal mental status, decreased

lactate as measured on arterial blood gases (ABG), and increased base deficit.

Children normally have a lower blood pressure than adults and are better able to

preserve adequate blood pressure by vasoconstriction and increasing heart rate;

therefore, blood pressure by itself is not a reliable end point for evaluating the

adequacy of resuscitation. Hypotension is the last thing to occur in pediatric shock

states. The definition of hypotension, defined as the 5% for systolic blood pressure

for

p. 2201

p. 2202

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