Patients may fall or j urnp into a

body of water and their distress is immediately noted or

alternatively may be found floating or at the bottom of a

lake or pool after a period of t ime without being seen.

Symptoms also vary. Patients may be asymptomatic or

may present with severe illness. Clinical effects of the s ubmersion/immersion event itself most often manifest as

respiratory abnormalities including hypoxia, tachypnea, or

abnormal lung sounds. Depending on the season, patients

may be hypothermic. At severe levels of illness, cardiac

dysrhythmias may occur, and mental status can change.

Most, if not all, drownings involve aspiration. "Dry drowning" (hypoxia from laryngospasm without aspiration) is

thought to be extremely rare and physiologically difficult

to explain.

� History

Drowned patients should be initially evaluated like major

trauma patients, with attention to the airway, breathing,

and circulation (ABCs) and rapid assessment of an AMPLE

history. When evaluating a patient who has experienced a

drowning incident, the following information must be

obtained:

• Events surrounding the incident (How did they end

up in the water? Did they sustain any trauma?)

• Temperature of the water and air

270

DROWNING INCIDENTS

• Length of time in the water, length of time

underwater

• Status on retrieval from the water (respiratory, mental status, cardiovascular, color)

• Was any immediate treatment needed?

• Current symptoms?

It will also be important to consider the potential of

suicide; the medical status of the patient will dictate how

urgently this assessment is needed .

..... Physical Examination

The order of the physical exam will depend on patient

stability. Assess the unstable patient like a trauma patient,

with a primary survey and management as necessary, followed by a thorough secondary survey. In the stable

patient, an examination can be conducted in a head-to-toe

fashion. Areas of focus include signs of external trauma,

especially the head and neck, lung sounds to evaluate for

water or emesis aspiration, skin color (cyanosis), core body

temperature (rectal), and a neurologic exam.

DIAGNOSTIC STUDIES

..... Laboratory

No specific laboratory testing is universally recommended

for drowned patients. If the provider feels that significant

aspiration occurred, or if the patient is unstable, useful labo ­

ratory tests to determine the severity of injury include a

blood count, serum electrolytes, and blood gases. To assess

the pH, a venous gas is sufficient. Electrolyte changes may

occur if large volumes of water are aspirated. Animal studies

have shown that 11 mL/kg of aspirated hypotonic fluid are

necessary before any effect is seen on hemoglobin, volume

status, or electrolytes. Most drowning victims aspirate less

than 4 mL/kg. In the majority of cases, hypoxia and metabolic acidosis cause the resultant morbidity and mortality.

Other laboratory studies may be indicated in certain

patients. Assessment of blood alcohol level, drug ingestions,

and medical causes for the patient's submersion (myocardial

infarction, syncope, stroke) should be considered.

..... Imaging

Patients in whom significant aspiration is suspected should

undergo chest radiography. The most common finding is

an aspiration pneumonitis (Figure 64- l). Head and cervi ­

cal spine imaging should be considered if the patient dived

into the water. Any other traumatic injuries noted on exam

or suspected by history should be imaged and evaluated as

appropriate.

MEDICAL DECISION MAKING

When a patient presents after a drowning incident, stabilization is the first priority. Once the patient is stabilized,

a detailed history of events and a thorough physical

..&. Figure 64-1. Aspiration pneumonitis. Reprinted

with permission from Heitz CR. "Drown ing Incidents."

CDEM Curricu lum, 2009. Available at: http:/ jwww

.cdemcurricu lum.orgji ndex.phpjssmjshow_ssm/

envirojdrowning.php.

exam should be obtained. The focus of the evaluation is

2-fold:

1. To determine types and extent of injury (aspiration,

exposure, trauma)

2. To determine whether this is a primary or secondary

drowning incident

Secondary drowning refers to a drowning incident that

occurred as a result of a medical event, drug or alcohol

ingestion, or preceding trauma. For instance, a boater who

drowns in a lake may have ingested a large amount of alco ­

hol, causing him to fall into the water. A diver may strike

her head on the bottom of the pool, causing prolonged

submersion. Figure 64-2 delineates a suggested algorithm

for management of the drowned patient.

TREATMENT

Initial stabilization and supportive care are the mainstays

of emergency department (ED) treatment for drowned

patients. Airway protection, management of hypoxia and

hypothermia, and urgent/emergent treatment of traumatic

injuries or medical emergencies take first priority. This

may include placement of an endotracheal t ube, high-flow

oxygen, active rewarming, and volume resuscitation.

Patients who have aspirated large volumes may require

positive pressure ventilation to recruit collapsed alveoli. If

intubated and large-volume aspiration occurred, consider

suctioning. Manage any cardiac dysrhythmias as recommended by Advanced Cardiac Life Support protocols.

Treatments once suggested but not currently recommended are prophylactic antibiotics or steroids. In addition,

hyperbaric chamber use has not been shown to be beneficial

unless decompression illness complicates the drowning.

CHAPTER 64

 

 Administer activated charcoal (1 g/kg) to all patients with intact airway reflexes as it

will readily bind to and decrease the absorption of cyclic

antidepressants. Orogastric lavage can be considered in

symptomatic patients who present within an hour of

ingestion after carefully weighing the benefits of removing a

highly toxic drug against the inherent risks of the procedure.

...... Sodium Bicarbonate Therapy

Because the cardiotoxicity of CA poisoning results from

the blockade of myocardial Na+ channels, treatment with

IV sodium bicarbonate (NaHC03

) remains the mainstay

of therapy. Sodium bicarbonate has been shown to improve

electrical conduction and increase myocardial contractility.

The indications for initiation of therapy are as follows:

• QRS complex > 100 msec

• Refractory hypotension

• Terminal R-wave amplitude in lead a VR >3 mm

• Ventricular dysrhythmia

Administer an initial bolus of 1-2 mEq/kg (1 ampule of

NaHC03 contains 50 mEq) and repeat as necessary until

the patient improves or the serum pH reaches 7.5-7.55.

After the initial stabilization, continue treatment with a

NaHC03 infusion at a rate of 2-3 mL!kg/hr.

...... Hypotension

Refractory hypotension is probably the most common

cause of death in cases of CA overdose. Initiate aggressive

volume resuscitation with IV boluses of normal saline, but

CHAPTER 60

Activated charcoal if airway intact

and bowel functional (1 gjkg).

Greater than 6 hours after an acute

ingestion and no evidence of

tachycardia, hemodynamic instabil ity,

CNS abnormal ities, or ECG changes

Medically clear,

consider psych iatric

consult

.A Figure 60-2. Cyclic antidepressants diag nostic algorithm. CNS, central

nervous system; ECG, electroca rd iogram; RAD, right axis deviation.

be wary of patients with underlying cardiopulmonary c onditions so as to not precipitate life-threatening pulmonary

edema. Persistent hypotension that is unresponsive to isotonic crystalloid boluses and NaHC03 therapy warrants

the initiation of vasopressor support. Norepinephrine

(1 meg/min titrated to a max of 30 meg/min) is the agent

of choice as it directly antagonizes the effects of cyclic

antidepressants on the a-adrenergic receptors.

..... Seizures

Most seizures occur within the first 3-4 hours after ingestion. Seizures are typically brief and tonic-clonic in nature.

Benzodiazepines such as diazepam or lorazepam are the

initial treatment of choice. Seizures that are refractive to

benzodiazepines require treatment with IV phenobarbital

(15 mg!kg), although careful attention must be paid to the

patient's hemodynamic status. Phenytoin should be avoided

because it is ineffective in patients with CA poisoning and

may actually exacerbate the cardiotoxicity of these agents.

DISPOSITION

..... Admission

Admit all symptomatic patients to a monitored setting.

Those with signs of moderate to severe poisoning

( eg, lethargy, hypotension, prolonged QRS duration) and

all patients who require treatment with IV NaHCO 3 require

admission to an intensive care unit. Obtain psychiatric

consultation for all patients with intentional overdoses.

..... Discharge

Patients who remain symptom-free throughout an observation period of no less than 6 hours may be safely discharged

home provided they are cleared from a psychiatric perspective .

SUGGESTED READING

Liebelt E. Cyclic antidepressants. In: Flomenbaum NE, Goldfrank

LR, Hoffman RS et al. Goldfrank's Toxicologic Emergencies.

8th ed. New York, NY: McGraw-Hill, 2006, pp. 1083-1097.

Liebelt EL, Ulrich A, Francis PD, et al. Serial electrocardiogram

changes in acute tricyclic antidepressant overdoses. Grit Care

Med. 1 997;25:1721.

Graudins A, Dowsett RP, Liddle C. The toxicity of antidepressant

poisoning: Is it changing? A comparative study of cyclic and

new serotonin-specific antidepressants. EmergMed (Fremantle).

2002; 14:440-446.

Mills KC. Cyclic antidepressants. In: Tintinalli JE, Stapczynski JS,

Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli's

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

 

MEDICAL DECISION MAKING

CO poisoning presents similar to many other conditions,

including migraine headaches, influenza-like illnesses,

acute gastroenteritis, vasovagal syncope, and cerebrovascular accident. Question patients about any possible expo ­

sures. Start supplemental 02 while obtaining confirmatory

studies. Send co-oximetry to measure the COHb level in

patients with concerning presentations and those with an

unexplained high anion gap metabolic acidosis. Consider

concurrent cyanide toxicity in the unconscious and hypotensive patient who was rescued from a house or industrial

fire. Rapidly exclude pregnancy with bedside urine testing,

as this will significantly impact management. Use the absolute COHb in combination with the patient's symptoms

to dictate further care including possible hyperbaric

oxygen (HBO) therapy (Figure 58-2).

TREATMENT

Treat concomitant injuries such as smoke inhalation, trauma,

myocardial injury, seizures, or neurologic deficits as you

would in any other setting. Supportive care in the form of

airway management, oxygen therapy, and intravenous fluids

remains the most important intervention. Normobaric 0 2 via

a nonrebreather facemask should be administered until the

COHb level is <5% and the patient is clinically stable. The

circulating half-life of CO is approximately 4--6 hours in

patients breathing room air, 90 minutes for those on 100% 02,

and approximately 20 minutes for those undergoing HBO

therapy. The absolute indications for HBO therapy are debatable, but it is generally indicated for those patients with significant exposures (Table 58-1). The true benefit of treatment

with HBO is most likely to limit the prevalence of delayed

neurologic symptoms. The only absolute contraindication to

HBO is an untreated pneumothorax. Because most hospitals

do not have hyperbaric chambers, contacting your regional

poison control center can be very helpful in the management

and disposition of these patients.

Check COHb level

Neurologic abnormal ity, loss 02 therapy via nonrebreather, consult poison

control center and/or

transfer for HBO chamber

No neurologic abnormal ity

Discharge home after

oxygen therapy and

asymptomatic

of consciousness, coma,

cardiovascular dysfunction,

severe acidosis, pregnancy,

intermittent exposure > 24 H

• Figure 58-2. Carbon monoxide poisoning diag nostic algorithm.

CHAPTER 58

Table 58-1 . Ind ications for hyperbaric 02 treatment in acute co poisoning.

Definite Indication

AMS and/or abnormal neurologic examination (if patient has normal

evaluation while on supplemental 0

2

 

 Ocular examination may reveal blurred

vision, decreased visual acuity, retinal edema, optic atrophy,

or hyperemia of the optic disc in methanol poisoning.

Abdominal tenderness or blood on rectal examination

may indicate isopropanol ingestion as it is classically

associated with hemorrhagic gastritis.

DIAGNOSTIC STUDIES

..... Laboratory

A basic metabolic panel is indicated to determine renal

function, acid-base status, and calculate an anion gap (the

normal range is 8-12 mEq/L). Obtain an arterial blood gas

to ascertain the degree of acidosis. A serum ethanol level is

required in all cases of suspected toxic alcohol poisoning,

as this result impacts the osmol gap equation and helps

determine the timing of ADH inhibition.

An osmol gap can be a useful screening test for toxic

alcohol poisoning if calculated early after the ingestion.

Send a serum sample to the laboratory to measure

osmolality. The osmol gap is equal to this value minus the

0

s

M

0

L

A

L

I

T

y

Time course

calculated osmolality (2*Na + glucose/18 + blood urea

nitrogen/2.8 + ethanol/4.6). Traditionally a normal osmol

gap is < 10 mEq/L, but in actuality will normally range

between -7 to + 14. It is the toxic alcohol parent compound that contributes to the osmol gap, and elevated

gaps occur early after ingestion before the metabolism of

the toxic alcohols into their poisonous byproducts. Later,

as the toxic organic acid metabolites build up and the

parent compound levels decrease, an anion gap metabolic

acidosis becomes the predominant finding, with the

osmol gap becoming less significant (Figure 55- 1).

Ethylene glycol and methanol can result in a simultane ­

ous anion gap metabolic acidosis and elevated osmol gap.

Because isopropanol is not metabolized into an organic

acid, ingestion typically results in an elevated osmol gap

in the absence of an elevated anion gap. Because isopropanol is rapidly converted to acetone, a serum acetone

level can help identify isopropanol poisoning in this

setting.

Calcium oxalate crystals on urine microscopy or urine

fluorescence under ultraviolet light (due to the addition of

fluorescein to most commercial antifreeze) may be clues

for ethylene glycol poisoning, but the absence of either

should not be used to rule out exposure.

Most importantly, serum toxic alcohol levels

(quantitative ethylene glycol, methanol, and isopropanol)

should be ordered STAT in cases of suspected toxic alcohol

poisoning to confirm ingestion and guide management. It

is important to recognize that toxic alcohol tests are rarely

performed in hospital laboratories and must be sent to an

off-site reference lab in most cases, so results may not be

available for several hours.

..... Imaging Studies

Although imaging studies do not help diagnose toxic

alcohol poisoning, methanol exposure has been

reported to cause basal ganglia hemorrhage or infarct.

Computed tomography imaging of the head should

also be considered when the mental status does not cor ­

relate with the presumed exposure or associated trauma

is a concern.

A

c

I

D

E

M

I

A

.A. Figure 55-1 . Relationship of degree of osmolal ity and acidosis

during the course of ethylene g lycol or methanol poisoning. Used

with permission from Mark B. Mycyk, MD.

TOXIC ALCOHOLS

MEDICAL DECISION MAKING

History alone may be sufficient to prompt a work-up for

toxic alcohol poisoning. In the absence of a reported ingestion, an unexplained anion gap acidosis or elevated osmol

gap should prompt further evaluation for a toxic alcohol.

Order STAT serum tests for all toxic alcohols (ethylene

glycol, methanol, and isopropanol). Initiate care based on

the presumptive clinical diagnosis and do not delay ED

treatment awaiting laboratory confirmation, as even in

ideal scenarios these levels will often take several hours to

measure. The initiation of antidotal therapy to inhibit

ADH should be the management priority early after an

ingestion before the onset of acidosis, whereas hemodialysis should be the priority in cases with a delayed presenta ­

tion when severe acidosis is already present (Figure 55 -2).

TREATMENT

Attention to the airway in cases of CNS depression

should take precedence. IV fluids should be administered

to treat hypotension and maintain renal perfusion in all

cases of toxic alcohol poisoning. In cases of isopropanol

ingestion, no additional treatment is necessary. In cases

of ethylene glycol or methanol poisoning, initiate ADH

inhibition until the ethylene glycol or methanol level is

<20 mg/dL and no acidosis is present. ADH may be inhibited with either IV fomepizole (load = 15 mglkg) or an IV

ethanol infusion (to achieve a serum ethanol level between

100-150 mg/dL).

Obtain early nephrology consultation to facilitate

emergent hemodialysis if the ethylene glycol or methanol

level is >50 mg/dL to filter out the parent compound and

any accumulated toxic metabolites. Emergent dialysis is

also indicated in cases of renal failure or severe acidosis

irrespective of the ethylene glycol or methanol level to

remove any remaining toxic metabolites and improve the

systemic acid-base status. In cases of ethylene glycol

poisoning, both thiamine 10 mg IV and pyridoxine

50 mg IV every 6 hours may help convert glyoxylic acid to

nontoxic metabolites. In cases of methanol poisoning,

folic acid 50 mg IV every 4 hours may help convert formic acid to C02 and Hp.

 

OTITIS MEDIA

TREATMENT

Antibiotics are not recommended in OME. Analgesics

should be given if the child has pain associated with the

middle ear effusion.

In children <2 years of age, oral antibiotic therapy is

indicated in AOM because ear infections in this age group

are less likely to resolve without antibiotic therapy. For

children �2 years of age with uncomplicated AOM, a

"wait-and-see" approach to treatment is an option. Because

many cases of AOM will resolve without antibiotic therapy,

the parent is given a prescription for antibiotics to be given

to the patient if symptoms worsen or do not improve in

48-72 hours. Ear pain should always be managed with

analgesics as needed, regardless of the therapeutic approach

taken. Analgesics for ear pain include oral ibuprofen and

acetaminophen as well as topical benzocaine/antipyrine

drops. Topical analgesics should not be given if there is

concern for a perforated TM.

If antibiotic therapy is chosen, high-dose amoxicillin

(80-90 mg/kg/day divided BID) is recommended as firstline treatment for uncomplicated AOM. Treatment duration is 10 days in children <2 years of age and can be

shortened to a 5-7 day course in children >2 years of age

with uncomplicated infections. Amoxicillin-clavulanate

(90/6.4 mg/kg!day divided BID) may be needed to treat

�-lactamase producing H. influenzae and M. catarrhalis

and should be used for AOM not responsive to amoxicillin. In addition, it may be considered as initial therapy in

Ear pain, fever, otorrhea, irritabil ity

Age > 2 years,

uncompl icated

AOM

"Wait-and-see"

prescription

No antibiotics

Consider

alternative

diagnosis

Figure 52-3. Otitis media diag nostic algorithm. AOM, acute otitis media; CT, computed

tomography; OME, otitis media with effusion; TM, tympanic membrane.

CHAPTER 52

children with severe disease (fever >39°C or severe ear

pain). Cephalosporins ( cefdinir 14 mg/kg/day in 1-2 doses,

cefuroxime 30 mg/kg/day divided bid, cefpodoxime

10 mg/kg/day once daily) may also be used for treatment

failures. Ceftriaxone (50 mg/kg intramuscularly or intravenously) may be used to treat AOM in a patient with

vomiting and an inability to tolerate oral medications. A

single dose is adequate for initial treatment; 3 doses over

3 days are recommended for treatment failures. For patients

with a penicillin allergy, a third-generation cephalosporin

should be given if it is a non-type I hypersensitivity. With

a type I hypersensitivity to penicillins, options include

clindamycin, macrolides, erythromycin-sulfisoxazole, and

trimethoprim-sulfisoxazole, but all provide suboptimal

coverage.

DISPOSITION

..... Admission

Only children with complications of AOM, such as

mastoiditis or other intracranial complications, require

hospitalization.

..... Discharge

Non-toxic-appearing children without complications of

AOM may be discharged home. Discharge instructions

should be clear, especially if using a "wait-and-see"

prescription for antibiotics, and should always include

treatment of ear pain with analgesics as needed. Patients

should be instructed to follow up with the primary care

provider if symptoms do not improve in 48-72 hours or

earlier if symptoms worsen or there are signs or symptoms

of complications of AOM.

SUGGESTED READING

AAP Clinical Practice Guideline. Diagnosis and management of

acute otitis media. Pediatrics. 2004;1 13:1451-1465.

AAP Clinical Practice Guideline. Otitis media with effusion.

Pediatrics. 2004;1 13:1412-1429.

Spiro DM, Arnold DH. Ear and mastoid disorders in infants and

children. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM,

Cydulka RK, Meckler GD. Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawHill, 201 1.

Pharyngitis

S. Margaret Pa i k, MD

Key Points

• Disti nguish potentially life-threatening (epiglottitis,

peritonsillar, and retropharyngeal abscess) and benign

(uncompl icated pharyngitis) conditions.

• Use a scoring system to guide management of

pharyngitis.

INTRODUCTION

Sore throat is a common complaint seen in the emergency

department (ED). Pharyngitis is inflammation of the throat

and is usually the cause of sore throat. Inflammation of the

tonsils (ie, tonsillitis) may also be present. The goal of the initial evaluation of patients with a complaint of sore throat is to

exclude the most serious conditions (eg, abscess, epiglottitis).

Infectious pharyngitis involves direct invasion of the

pharyngeal mucosa by bacteria or viruses leading to a local

inflammatory response. Viruses are the most common

cause of pharyngitis and include adenovirus, parainfluenza,

 

• Nonabdominal conditions including strep pharyngitis

and pneumonia often present with abdominal pain.

Intussusception. This is a telescoping of bowel into a

proximal segment. In young children 2 months to 2 years

old, the condition is usually idiopathic, and the most

common location is ileocolic. Over the age of 3 years, a

lead point such as a polyp or Meckel diverticulum may be

the culprit. The typical presentation is intermittent

colicky abdominal pain of a few minutes' duration associated with vomiting. These episodes of pain are followed

by periods of lethargy. Unfortunately, the classic triad of

symptoms-currant jelly stools, vomiting, and colicky

abdominal pain-occurs in only 20% of patients. Physical

exam may reveal an empty right lower quadrant and nontender mass in the right upper quadrant. Prolonged

duration leads to bowel ischemia and necrosis. HenochSchonlein purpura is associated with ileo-ileal intussusception. Because of this unusual location, it is neither

visualizable nor reducible by standard methods and

requires computed tomography (CT) scan and surgical

reduction.

Meckel diverticulum. The most common congenital

abnormality of the gastrointestinal tract, Meckel diverticulum is the remnant of the vitelline duct. In half of all cases

there is ectopic tissue (usually gastric). Painless rectal

bleeding is the most common presentation of Meckel, but

other symptoms include abdominal pain, nausea, and

vomiting. The rules of 2s is a good way to classify the condition (Table 50-1).

212

ABDOMINAL PAIN

Table 50-1 . Meckel diverticu lum and rule of 2s.

2% of the population

2 years old most common age of presentation

2 inches long

2 feet from the ileocecal valve

2 types of ectopic tissue (gastric and pancreatic)

Malrotation and volvulus. This entity refers to abnormal intrauterine rotation and fixation of bowel within the

abdomen. This abnormal development around a narrow

mesenteric pedicle puts the bowel at risk of twisting

around these vessels and subsequent bowel necrosis.

Classic symptoms include bilious vomiting, abdominal

pain, distention, and bloody diarrhea.

Appendicitis. Although uncommon in young children, more than 80% present after the appendix has

ruptured. Their presentation is often atypical, with a

high rate of diarrhea and absence of typical migration

of pain.

� Medical Causes of Abdominal Pain

Constipation. Constipation is particularly common in

toddlers around potty training age. Symptoms include

diffuse colicky abdominal pain, anorexia, hard stools,

and straining. Constipation can be confused with intussusception because of the intermittent nature of the

pain.

Gastroenteritis. This entity is prevalent in childhood,

particularly in those children in daycare. The most likely

agents are viral; bacterial should be considered in those

with bloody diarrhea. Pain is associated with abdominal

cramping. Fever, vomiting, diarrhea, and pain are all

symptoms of the condition. Appendicitis particularly

early in the course of illness is often mistaken for acute

gastroenteritis.

CLINICAL PRESENTATION

� History

A careful, detailed history is essential in the evaluation of

the pediatric patient with abdominal pain. Questions

should be asked of both the caregiver and child. Most preschoolers over the age of 3 or 4 years old can provide reliable information. Inquire about the location of pain

(diffuse vs. localized) and whether it has remained consistent or migrated (as in the case of appendicitis from peri ­

umbilical to right lower quadrant). The duration of the

pain is essential to distinguish between acute and chronic

conditions. Ask about associated symptoms such as vomiting (bloody, bilious, projectile, post prandial), diarrhea

(bloody, currant jelly), anorexia, dysuria, and fever (height

and duration).

� Physical Examination

Before focusing on the abdomen, a thorough physical

examination is necessary to rule out extraabdominal

conditions, which can present with abdominal pain.

Assess the pharynx for exudate and skin for the stereotypical sandpaper rash, as strep pharyngitis and scarlet fever

can produce diffuse abdominal pain. Carefully examine the

lower extremities and buttocks for the characteristic

purpuric lesions of Henoch-SchOnlein purpura, which can

produce abdominal pain and ileo-ileal intussusception.

Auscultate the lungs, as lower lobe pneumonia will irritate

the diaphragm, resulting in pain that may even overshadow the cough. A thorough genitourinary evaluation is

necessary to rule out genitourinary causes, including

testicular torsion and hernias.

Delicate palpation of the abdomen to assess for focal

tenderness and masses will often narrow the differential

diagnosis. A firm mass in the left lower quadrant or mid

abdomen supports the clinical picture of constipation, as

does hard stool on rectal exam. An olive-shaped mass in

the epigastrium of a newborn with postprandial vomiting

is pathognomonic of pyloric stenosis. Examination

should include abdominal auscultation and assessment of

tenderness, rebound, and guarding. Asking the child

"where does it hurt the most?" and "can you show me

with one finger?" enlists assistance and allows accurate

identification of the most distressing location of pain.