Many symptoms associated with AOM, such as fever,

irritability, restless sleep, and crying, are neither sensitive

nor specific for AOM, and may be present in children with

a URI with or without AOM. The presence of ear pain

increases the relative risk of a patient having AOM.

Purulent drainage from the ear may be present with AOM

with tympanic membrane perforation or with otitis

externa. Previous episodes of AOM, including timing of

CHAPTER 52

Pars flaccida

Light

reflex

.A. Figure 52-1. Normal tympanic membrane. Cou rtesy Richard A. Chole, MD PhD

most recent infection and antibiotic use may influence

choice of therapy. Persistent fever and headache may be

signs of intracranial complications of AOM.

� Physical Examination

Fever, though nonspecific, is present in 50% of cases

of AOM. Careful examination of the head and neck,

including the oropharynx, teeth, jaw, and lymph nodes,

should be done to search for other causes of pain that may

be referred to the ear. Inspection of the pinna, tragus, and

external auditory canal, as well as palpation of the tragus,

should be performed. Pain with manipulation of the pinna

or tragus, in conjunction with purulent otorrhea and

inflammation of the external auditory canal, suggests otitis

externa. The mastoid process should be examined for swelling, erythema, and tenderness, signs of mastoiditis. With

mastoiditis, the pinna may also be displaced anteriorly.

Diagnosis of AOM or OME is made based on the

appearance of the tympanic membrane (TM) on otoscopic

examination, in conjunction with the clinical presentation.

Adequate visualization of a child's TM requires good

patient immobilization, typically with the child seated on

the parent's lap with the head immobilized against the

parent's chest, as well as use of the largest speculum that

will comfortably fit in the external auditory canal. Removal

of cerumen from the external auditory canal may be

required for good visualization of the TM and can be

accomplished with a cerumen scoop or gentle irrigation.

Ear irrigation should not be performed if there is s uspicion

for a perforated TM. The external auditory canal in

children may be narrow and tortuous, and the tympanic

membrane is located anteriorly and superiorly. Gentle

traction on the pinna in a posterior direction straightens

the ear canal and can aid in visualization of the TM. Once

adequate visualization is obtained, the following tympanic

membrane characteristics should be assessed: translucency

(translucent, opaque, partly opaque), color (clear/grey,

white, amber, red), position (normal, retracted, bulging),

and mobility (normal, decreased or absent). A normal

tympanic membrane is translucent and clear with a

colorless or pearly gray color, and the bony landmarks of

the middle ear are easily visible (Figure 52- 1). In addition,

a normal TM has a neutral position and brisk mobility

with positive and negative pressure on insufflation. Opacity

of the TM often obscures the bony landmarks and s uggests

the presence of fluid in the middle ear or another

abnormality of the TM (tympanosclerosis, cholesteatoma).

Other findings consistent with a middle ear effusion are an

air fluid level or bubbles behind the TM, a bulging TM,

decreased or absent mobility of the TM, or otorrhea. A

middle ear effusion is present with both OME and AOM.

Characteristics associated with OME include a normal or

retracted TM, clear, or amber color, and impaired mobility

on insufflation. Characteristics associated with AOM are a

bulging TM, a purulent effusion, and distinct erythema of

the TM with a middle ear effusion (Figure 52-2). Erythema

alone is a poor predictor of AOM because the TM may

Figure 52-2. I mage showing patient with acute

otitis media. Courtesy Richard A. Chole, MD PhD

appear pink or red with fever or crying. In addition, it is

important to distinguish between distinct erythema of the

TM itself (as in AOM) and increased vascularity with a red

appearance only in the areas of the blood vessels.

DIAGNOSTIC STUDIES

..... Laboratory

AOM is a clinical diagnosis, and laboratory studies are

usually not required. Gram stain and culture of middle ear

fluid obtained by tympanocentesis may be helpful in

directing antibiotic therapy in complicated or resistant

infections, but is not routinely performed.

..... Imaging

A computed tomography (CT) scan of the head may be

needed if there is concern for mastoiditis or other

intracranial complication.

MEDICAL DECISION MAKING

History and physical examination should be sufficient to

diagnose AOM and distinguish it from OME. If the

tympanic membrane is normal, consider alternative

causes of ear pain or fever (Figure 52-3). Inflammation of

the mastoid process with anterior displacement of the

pinna or other signs and symptoms of intracranial extension of infection should warrant investigation with a

head CT.

 

A complete history is necessary to determine the severity of

illness and to identify the type of dehydration present.

Obtain as much information from the child, and elicit

217

CHAPTER 51

further details and clarifications from the parent or care ­

giver. Obtain a detailed description of intake (types of

liquids and solids, volume, frequency) and output of urine

(frequency, amount, color, odor, hematuria), stool

(number, consistency, presence of blood or mucous), and

emesis (frequency, volume, bilious or nonbilious,

hematemesis). Estimate urine output by the number and

saturation of wet diapers in infants and young children.

Note the presence of abdominal pain (duration, location,

intensity, quality, and radiation). Inquire about weight loss

and activity level. Note the time interval of symptoms. The

last episode of vomiting is important in determining when

the initiation of an oral trial is advisable.

Ask about associated symptoms (fever, headache, neck

pain, throat pain, dysuria, urinary frequency, rash). Travel

and recent antibiotic use are also pertinent.

Note underlying diseases that could contribute to dehydration (kidney disease, diabetes mellitus, cystic fibrosis, hyperthyroidism). Contact with ill people and daycare attendance

should be considered. Important elements of the past medical

history include immunocompromise and malignancy.

� Physical Examination

The examination begins with assessment of the general

appearance of the child. Lethargy or listlessness can warn

of impending circulatory collapse. Examine the throat for

erythema, ulcerations, or tonsillar exudates. Assess the

abdomen for tenderness, rebound, or guarding.

Neurologic exam should include mental status, cranial

nerves, strength, and reflexes. Altered mental status or

focal neurologic findings can indicate increased intracra ­

nial pressure. Capillary refill and skin turgor should be

noted. The gold standard for the diagnosis of dehydration

is measurement of acute weight loss. True pre-illness

weight is rarely known in the acute care setting. An

estimate of the fluid deficit is thus made based on clinical

assessment ( Table 5 1 -1). Any of the two following findings

are predictive of clinically significant dehydration in children: ill appearance, absence of t ears, dry mucous mem ­

branes, and delayed capillary refill ( > 2 seconds). Other

important considerations are abnormal respiratory

pattern and skin tenting.

Vital signs are an important objective measure and can

be normal in a child with dehydration. The first sign of

mild dehydration in children is tachycardia. Hypotension

is a late sign of severe dehydration.

DIAGNOSTIC STUDIES

� Laboratory

Laboratory studies are not required if the etiology is apparent and mild-to-moderate dehydration is present. A bedside glucose is indicated for all infants and children with

altered mental status. Blood sugar may be low (poor

intake) or high (diabetic ketoacidosis [DKA) ). With moderate-to-severe dehydration, electrolyte abnormalities may

point to a specific diagnosis: high K (congenital adrenal

hyperplasia, renal failure), low K (pyloric stenosis), low

bicarbonate (acidosis, HC03 loss in diarrhea), high blood

urea nitrogen/creatinine (renal hypoperfusion). Urinalysis

may show glucose, ketones, or signs of infection. Urine ­

specific gravity may be elevated in patients with dehydra ­

tion, but it is not a reliable measure. Serum sodium should

be determined because hypo/hypernatrernia requires spe ­

cific treatment regimens.

� Imaging

No imaging is required for most patients presenting to the

ED with dehydration. Consider flat/upright abdominal

x-rays if there is suspicion for obstruction. Ultrasound or

computed tomography ( CT) scan of the pelvis is indicated

if appendicitis suspected. Noncontrast head CT scan is

indicated when evaluating severe headache or if exam

reveals signs of intracranial pressure.

Table 51-1. Cli nical assessment of severity of dehydration in the pediatric patient.

Signs and Symptoms Mild (3-5% body weight) Moderate (5-1 0% body weight) Severe (>l OOfo body weight)

Mental status Alert/restless Irritable and drowsy Lethargic

Respirations Normal Deep ± rapid Deep and rapid

Pulse Normal Rapid and weak Weak to absent

Blood pressure Normal Normal with orthostasis Low

Mucous membranes Moist Dry Very dry

Tears Present Decreased Absent

Skin turgor Pinch and retract Tenting Tenting to doughy

Urine output Normal Decreased Absent

Capillary refill <2 sec 2-3 sec >3 sec

MEDICAL DECISION MAKING

History and physical examination are generally sufficient

to identify signs or symptoms of dehydration. Shock needs

immediate recognition and treatment with fluid resuscitation. Determine severity of dehydration using clinical

assessment (Figure 51-1).

The underlying cause of dehydration should be identified,

and electrolyte abnormalities require correction. Further testing is guided by clinical suspicion of more serious problems.

TREATMENT

Identify patients with signs of shock and resuscitate with

fluid immediately (20 mL/kg normal saline [NS] or

Lactated Ringer's over a 20 - to 30-minute period). Reassess

and repeat fluid bolus until perfusion is adequate and vital

DEHYDRATION

signs normalize (fluid bolus x 3 if necessary). Urine output

is the most important indicator of restored intravascular

volume (minimum = 1 mL/kg!hr). If 60-80 mL/kg of isotonic fluid is given with no improvement, consider other

causes of shock (sepsis, hemorrhage, cardiac disease). Treat

hypoglycemia promptly (2.5 mL/kg of 10o/o dextrose or

1 mL/kg of 25o/o dextrose). Once vital sign abnormalities

are corrected, the rate of fluid administration for treatment

is determined by the estimated fluid losses plus ongoing

maintenance fluid requirements (Table 51-2).

The literature supports the use of a single dose of oral

 

SUGGESTED READING

Cantor RM, Wittick L. Upper airway emergencies. ln: Wiebe RA,

Ahrens WR, Strange GR, Schafermeyer RW, eds. Pediatric

Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill,

2009. http:/ /www.accessemergencymedicine.com/ content

.aspx?aiD=5332700. Accessed March 29, 20 12.

Rodrigo GJ, Pollack CV, Rodrigo C, Rowe BH. Heliox for nonintubated acute asthma patients. Cochrane Database of Syst Rev.

2006;( 4):CD002884.

Schibler A, Pharo TMT, Dunster KR, et al. Reduced intubation

rates for infants after introduction of high-flow nasal prong

oxygen delivery. Intens Care Med. 201 1;37:847-852.

Weiner DL. Respiratory distress. ln: Fleisher GR, Ludwig SL.

Textbook of Pediatric Emergency Medicine. 6th ed. Philadelphia,

PA: Lippincott Williams & Wilkins, 20 10, pp. 55 1-563.

Zhang L, Mendoza-Sassi RA, Wainwright C, Klassen TP.

Nebulized hypertonic saline solution for acute bronchiolitis

in infants. Cochrane Database Syst Rev. 2008;(4):CD006458.

Abdominal Pain

Russ Horowitz, MD

Key Points

• Currant jelly stool is a late finding in intussusception.

• In appendicitis, young children have a very high rate of

rupture on presentation.

INTRODUCTION

Abdominal pain in children is one of the most common

complaints in pediatrics. Etiologies range from benign

conditions such as constipation to surgical emergencies

such as malrotation with volvulus. The challenge for the

clinician is to distinguish between these diseases in

preverbal children and in those with limited ability to

describe their symptoms. Some conditions such as pyloric

stenosis are unique to young children, but others, such as

appendicitis which occur in all ages, have dramatically

different presentations in the very young. Although less

common than in adults, children may still suffer from

gallstones, peptic ulcer disease, and kidney stones. Pelvic

disorders including ovarian cysts and torsion must be

considered in all girls over the age of menarche.

� Surgical Causes of Abdominal Pain

Pyloric stenosis. Usually presents in the newborn period

from 2 to 6 weeks of age. It is more common in first-born

male children (4:1) and has a familial inheritance. The

typical presentation is with postprandial projectile vomiting. After vomiting, children still appear hungry and will

readily feed. Early on they seem well, but as symptoms

progress they become dehydrated and develop the stereo ­

typical electrolyte abnormality of hypokalemic, hypochloremic metabolic alkalosis.

• If bilious vomiting is present, think malrotation with

volvu lus.

 

Meckel diverticulum. Surgical resection is curative.

Transfusion may be necessary in cases of significant blood

loss.

Malrotation and volvulus. Emergent surgical repair is

essential to minimize bowel necrosis.

Constipation. Treatments range from mild (laxatives

for home use) to invasive (enema, disimpaction). Rarely,

children require admission for continued enemas and

nasogastric administration of laxatives.

DISPOSITION

..... Admission

Children with surgical or suspected surgical causes of

abdominal pain should be admitted to the hospital under

the care of a surgeon. To prevent exposure to ionizing

radiation, children with equivocal examinations or

ultrasound findings may be admitted for serial abdominal

examinations. Intussusception has up to a lOo/o recurrence

risk in the first 24 hours after reduction. Most often children are admitted after reduction, but the potential exists

for discharge from the ED with thorough instructions on

when to return.

..... Discharge

Children with medical causes of abdominal pain (pharyngitis, urinary tract infection, pneumonia, gastroenteritis)

who tolerate oral fluids can be discharged home with

close follow-up. The first presentation of etiologies of

abdominal pain such as appendicitis or intussusception

may be misinterpreted as viral illness. Therefore, very

specific return instructions must be provided to the caregivers on discharge. These include bilious vomiting, worsening pain, localization to the right lower quadrant, and

inability to tolerate oral fluids.

SUGGESTED READING

Bachur RG. Abdominal emergencies. In Fleischer GR, Ludwig S.

Textbook of Pediatric Emergency Medicine. 6th ed. Philadelphia,

PA: Lippincott Williams & Wilkins, 20 10, pp. 1515-1 538.

Kharbanda AK, Sawaya RD. Acute abdominal pain in children.

In: Tintinalli's Emergency Medicine: A Comprehensive Study

Guide. 7tb ed. New York, NY: McGraw-Hill, New York, 2011,

839-848.

Ross S, LeLeiko NS. Acute abdominal pain. Pediatr Rev.

2010;3 1:135-144.

Rothrock SG, Pagane J. Acute appendicitis in children: Emergency

department diagnosis and management. Ann Emerg Med.

2000;36:39-5 1.

Dehydration

Kristi ne Cieslak, MD

Key Points

• Dehydration is not a disease; the underlying cause must

be identified and treated.

• Severity of dehydration can be classified using clinical

assessment.

• Management priorities in the emergency department

are stabil ization of vita l signs, replacement of

INTRODUCTION

Acute evaluation and treatment of children presenting

with dehydration represents one of the most common

situations in the pediatric emergency department (ED).

Dehydration in sick children is often a combination of

refusing to eat or drink and losing fluid from vomiting,

diarrhea, or fever. In children with vomiting and diarrhea,

the underlying problem is actually intravascular volume

depletion, not dehydration. Volume depletion represents

an equal loss of water and solutes (mainly sodium) from

the blood plasma, whereas dehydration denotes a disproportional loss of plasma free water.

Children have higher morbidity and mortality rates

associated with dehydration than adults due to a higher

turnover of fluids and solutes (higher metabolic rates,

increased body surface area/mass index, larger total body

water content, immature kidneys with relative inability to

produce concentrated urine, reliance on caregivers for basic

needs). In clinical practice, the clinician attempts to determine the degree of volume depletion and the underlying

cause of dehydration to initiate proper treatment.

Gastroenteritis is the most common cause of dehydra ­

tion and is due to viruses in 80% of cases (rotavirus

30-50%). The clinical diagnosis of gastroenteritis by defi ­

nition requires the presence of diarrhea. However, many

intravascu lar volume deficit and ongoing losses, and

correction of electrolyte abnormal ities.

• Frequent reassessment of clinical status is necessary to

mon itor the response to treatment.

infants with viral gastroenteritis present with isolated diarrhea or isolated vomiting. Rotavirus infections are responsible for approximately 3 million cases of diarrhea and

55,000 hospitalizations for diarrhea and dehydration in

children <5 years of age each year in the United States. The

majority of children with dehydration presenting to the

ED have a benign etiology; however, there are serious

causes for dehydration that should be considered.

Consider appendicitis, intussusception, volvulus, pyloric

stenosis, urinary tract infection, hydrocephalus, brain

tumors, and diabetes mellitus as potential underlying conditions in the pediatric patient who presents with

dehydration. Other causes of dehydration include

gastrointestinal (hepatitis, liver failure, drug toxicity), endocrine (congenital adrenal hyperplasia, Addisonian crisis),

renal (pyelonephritis, renal tubular acidosis, thyrotoxicosis),

poor oral intake (pharyngitis, stomatitis), and insensible

losses (fever, burns, sweating, pulmonary processes).

CLINICAL PRESENTATION

..... History

 ondansetron in combination with oral rehydration for

patients with dehydration due to nausea and vomiting.

Ondansetron can be given as an oral dissolving tablet or

intravenously (IV; 2 mg, 4 mg). Antidiarrheal agents are not

recommended. Rapid oral rehydration has been shown to

be as effective as IV fluid therapy in restoring intravascular

Signs or symptoms of

dehydration

Fluid resuscitation

Stabil ization of vital signs

Eva luate for signs of shock

Obtain history of all intake and output

Assess severity of dehydration

Identify underlying disease or ill ness

OraljiV rehydration

ppropriate lab or radiographic studies

Correct electrolyte abnormal ities

Etiology undetermined

Admit for continued testing and

therapy

Etiology determined

Admit for further therapy OR discharge if

no clin ical signs of dehydration and no

significant ongoing losses

.6. Figure 51-1 . Dehydration diag nostic algorithm.

CHAPTER 51

Table 51-2. Calculations for maintenance fluid

in the pediatric patient.

Patient Weight

First 10 kg

Second 10 kg

Each additional 10 kg

4/2/1 Method Holiday-Segar Method

4 ml/kg/hr 1 00 mljkg/day

2 ml/kg/hr

1 ml/kg/hr

50 ml/kgfday

20 ml/kg/day

volume and correcting acidosis in patients with moderate

dehydration. For every 25 children treated with oral rehydration treatment for dehydration, 1 fails and requires

N therapy. Oral rehydration solutions for infants and toddlers should contain 45-50 mEq/L of sodium and 25-30 giL

glucose (Pedialyte, Infalyte). Give 5-10 mL of fluid every

5-10 minutes and increase as tolerated, with the goal of

30-50 mL/kg over a 4-hour period. If voruiting occurs, wait

30 minutes after last episode before reinitiating oral fluids.

An estimate for fluid replacement is 10 mL/kg body weight

for each watery stool and 2 mL!kg body weight for each

episode of vomiting.

Dehydration can be categorized according to osmolarity

and severity. Serum sodium is a good marker of osmolarity

(assuruing a normal glucose) and guides replenishment

therapy. Isotonic dehydration is the most common (80%).

Sodium and water losses are similar in intra- and extracellular compartments. Maintenance fluid requirements

plus half the fluid deficit are administered over the first

8 hours, and the remaining fluid deficit over the following

16 hours. Hypotonic dehydration (Na < 1 30 mEq/L) occurs

when more sodium than water is lost. Calculate sodium

deficit for replacement fluids. Sodium deficit (mEq) =

(135-measured Na) X (pre-illness weight in kg) x 0.6.

Sodium deficit should be replaced over a 4 -hour period

but should not exceed 1 .5-2.0 mEq/hr; 0.9 NS is an appro ­

priate solution. Hypertonic dehydration (Na >150 mEq/L)

exists when more water is lost than sodium. The free water

deficit is calculated as free water deficit (mL) = (measured

serum Na-145) x 4 mL!kg x pre-illness weight (kg).

Because of the risk of cerebral edema, correct the free water

deficit over a 48-hour period, with a goal of reducing

serum sodium by no more than 1 0-15 mEq/L!day; D5 \4

to D5 liz NS are appropriate solutions.

DISPOSITION

� Admission

Most patients with moderate-to-severe dehydration with

significant acidosis should be admitted to the hospital

(serum bicarbonate level of �13 is predictive of return to

the ED for treatment failure as outpatient). Other

indications for adruission include significant ongoing fluid

losses, inability to tolerate oral fluids, hypotonic or hypertonic dehydration, or undetermined etiology in need of

further assessment. Patients with signs of increased intracranial pressure or DKA should be adruitted to an intensive

care unit.

� Discharge

Patients with no clinical evidence of dehydration or those

with mild-to-moderate isotonic dehydration who have

received adequate fluid rehydration (oral or N) can be

discharged home.

SUGGESTED READING

Colletti JE, Brown KM, Sharieff GQ, Barata lA, Ishimine P. The

management of children with gastroenteritis and dehydration

in the emergency department. 1 Emerg Med. 2010;38:681'Hi98.

Freedman SB, Adler M Seshadri R, Powell EC. Oral ondansetron

for gastroenteritis in a pediatric e mergency department. N Eng/

1 Med. 2006;354:1698-1705.

Freedman SB and Thull-Freedman JD. Vomiting, diarrhea and

dehydration in children. In: Tintinalli JE, Stapczynski JS, Ma

OJ, Clince DM, Cydul.ka RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 20 1 1, 830-839.

Otitis Media

Suzanne M. Schmidt, MD

Key Points

• Disti nguish between acute otitis media (AOM) and otitis

media with effusion (OME), both of which present with

a middle ear effusion.

• Clinical findings most suggestive of AOM are a bulging

tympanic membrane (TM) with a purulent effusion,

whereas the TM in OME has a clear effusion with a

normal or retracted position.

INTRODUCTION

Otitis media refers to the presence of inflammation or

infection in the middle ear space. A middle ear effusion

without infection is called otitis media with effusion

( OME) or serous otitis. Infection of fluid in the middle ear

is called acute otitis media (AOM). Diagnosis of AOM

should be based on the acute onset of signs or symptoms

of middle ear inflammation (fever, ear pain, distinct

erythema of the tympanic membrane) in conjunction with

a middle ear effusion seen on physical exam.

Ear disease is common in children, with 90% of

children having at least 1 episode of a middle ear effusion

and two thirds with at least 1 episode of AOM by school

age. The peak incidence of AOM occurs between 6 and

24 months of age.

Episodes of AOM are often preceded by a viral upper

respiratory tract infection (URI). The eustachian tube in

children is shorter and more horizontal than in adults.

Eustachian tube dysfunction associated with a URI can

lead to a middle ear effusion (OME). Bacterial pathogens

in the nasopharynx ascend via the eustachian tube, leading

to infection of the fluid in the middle ear (AOM).

AOM is caused by bacteria in 50--80% of cases, most commonly Streptococcus pneumoniae or nontypable Haemophilus

221

• Erythema alone is a poor predictor of AOM and must

be combined with other TM characteristics to make a

diagnosis.

• Antibiotic treatment may be ind icated for some

episodes of AOM, but is not indicated for OME.

• Assess the patient for possible compl ications of AOM.

infl.uenzae and less commonly Moraxella catarrhalis. Purulent

otorrhea may be caused by Staphylococcus aureus or

Pseudomonas aeruginosa as well. Common complications of

AOM are persistent middle ear effusion, tympanic membrane

perforation, and tympanosclerosis. Other complications of

AOM include cholesteatoma, hearing loss, tinnitus, balance

problems, and facial nerve injury. Intracranial complications

are rare and include mastoiditis, intracranial abscess, meningitis, and venous sinus thrombosis.

CLINICAL PRESENTATION

..... History

Children with AOM usually present with acute onset of

signs and symptoms of inflammation from AOM, such as

fever and ear pain. This is often preceded by URI symp ­

toms. 

 

Sometimes, a lab result or radiograph will indicate need for

emergent directed treatment (eg, foreign body). It is

extremely important to frequently reassess the patient after

each treatment to determine response and make decisions

for further management. Clinical status can change very

quickly in patients with respiratory distress (Figure 49-5).

TREATMENT

Croup. Administer humidified oxygen, and all patients

should get dexamethasone 0.6 mg!kg/dose (max 16 mg)

intramuscular (IM) or by mouth (PO) regardless of the

RESPIRATORY DISTRESS

severity. If there is stridor at rest, give racemic epinephrine

0.5 mL of 2.25% solution in 3 mL of normal saline (NS) via

a nebulizer.

Foreign body aspiration. Definitive management is to

remove in the operating room by laryngoscopy or bronchoscopy. In the setting of critical airway obstruction or

impending/actual respiratory arrest, attempt to force the

foreign body out with back blows or chest or abdominal

thrusts depending on the age and size of the patient. These

are all safer methods than the blind finger sweep, which can

convert a partial obstruction to a complete obstruction.

Other life-saving measures include laryngoscopy and direct

retrieval with Magill forceps, passing the endotracheal tube

beyond the obstruction and forcing the foreign body into

either mainstem bronchus, or needle cricothyrotomy.

Epiglottitis or bacterial tracheitis. It is particularly

important to allow the patient to assume a position of comfort, and if they are in the sniffing position, this is an omi ­

no us sign for severe obstruction. Ideally these patients should

have a definitive airway placed in the operating r oom by the

most skilled physician in difficult airway techniques, but if

there is respiratory arrest, then immediate endotracheal intubation or needle cricothyrotomy should be performed.

Anaphylaxis and severe angioedema. Treat with epinephrine, steroids, H1 and H2 blockers.

Asthma. Treat with �-adrenergic agonists: albuterol

2.5 mg every 20 minutes as needed or 15 mg in NS nebulized

over 1 hour continuously. For moderate to severe exacerbations, add anticholinergics (ipratropium bromide 500 meg

every 20 minutes for 3 doses) and steroids. If tolerating oral

intake with no impending respiratory failure, administer

prednisone 1-2 mg/kglday; otherwise use N steroids (SoluMedrol 2 mglkg, max 125 mg). If the patient's respiratory

effort is poor and respiratory failure is imminent, administer

IM epinephrine 0.0 1 mg/kgldose (max 0.5 mg) 1:1,000,

which can be repeated every 20 minutes for 2 more doses.

Terbutaline 2-10 meg N loading dose then 0.1-0.6 meg/kg/

min can also be used. Magnesium sulfate (50 mg/kg over

20 minutes to max 2 g) should be considered in patients

with moderate to severe exacerbations or those who do not

improve after initial therapy. Heliox, a mixture of helium

and oxygen, improves laminar flow through the bronchioles,

resulting in decreased work of breathing. There is some

evidence showing it improves pulmonary function in

patients with severe obstruction. The maximum amount of

oxygen in the mixture is 30%, so if the patient is hypoxic and

requires more than 30% FlO 2, then Heliox is not an option.

Bronchiolitis. Attempt a trial with �-agonists and/or

nebulized epinephrine. Clinical trials demonstrate that

corticosteroids are of no benefit in the treatment of bronchiolitis, but they may be useful in patients with a history

of reactive airway disease. High-flow humidified oxygen

via nasal cannula is a more novel treatment that is showing

some promising utility, especially in patients with RSV

and hypoventilation. The proposed mechanisms are

improvement of respiratory mechanics, washout of naso ­

pharyngeal dead space, and decreased work of breathing.

Some recent studies showed that it may decrease need for

endotracheal intubation. Hypertonic saline (3-5%) with

or without bronchodilators is another new therapy being

studied, with minimal side effects.

Pneumonia. Administer antibiotics early and oxygen as

needed.

DISPOSITION

..... Admission

Admission is indicated in respiratory failure requiring

mechanical ventilation, respiratory distress not reversible

with definitive therapy or requiring intensive monitoring,

pneumonia in patients <6 months, foreign body aspirations

with respiratory symptoms, or new oxygen requirements.

..... Discharge

The decision to discharge a patient is dependent on several

factors: clinical response to treatment, work of breathing,

hypoxia, hydration status, preexisting medical conditions,

and social factors. Keep in mind that respiratory status can

change quickly, and it is crucial to monitor a patient for a

significant amount of time after treatment to make sure

their clinical status does not deteriorate again. If the

patient continues to have increased work of breathing and

there is concern for impending respiratory failure, these

patients should not go home. Ensure the patient is well

hydrated and can tolerate oral intake before discharge.

Make sure the patient has reliable caregivers who can

administer treatments and medications and will bring the

patient back if they worsen again. Lastly, arrange secure

follow-up for the patient with his or her pediatrician or

specialist.