DIC, and endocrine disorders. The number

one factor that contributes to the morbidity and mortality of

heat illness is the severity of underlying comorbid illnesses,

not the absolute height of the core body temperature.

DISPOSITION

..... Admission

If the patient has any serious comorbid conditions or illnesses, admission may be necessary. Patients with heat

HEAT-RELATED I LLNESS

Heat exhaustion

IV or PO

hydration with

electrolyte

containing

solutions and

ambient cooling

Discharge if no

serious comorbid il lness

Heat stroke

Rule-out 2° causes

of AMS and

hyperthermia

IVF bolus and

begin evaporative

cool ing measures

to 40°( (1 04°F)

ICU admission

.&. Figure 63-1. Heat-related ill ness diagnostic algorithm. ABCs, airway,

breathing, and circu lation; AMS, altered mental status; ICU, intensive care

unit; IV, intravenous; IVF, intravenous flu id; PO, by mouth.

stroke should be admitted to the intensive care unit for

continued monitoring of temperature and mental status.

� Discharge

Discharge home is appropriate for patients with heat

exhaustion if their symptoms resolve, vital signs normalize,

and there are no serious derangements found in laboratory

values.

SUGGESTED READING

Howe AS, Boden BP. Heat-related illness in athletes. Am J Sports

Med. 2007;35: 1384.

Smith JE. Cooling methods used in the t reatment of exertional

heat illness. Br J Sports Med. 2005;39:503.

Waters TE, Al-Salamah MA. Heat emergencies. 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: McGraw-Hill, 20 l l, pp. 1339-1344.

Drowning Incidents

Corey R. Heitz, MD

Key Points

• Drowning is defined as the process of experiencing

respiratory impairment from submersion/immersion in

liquid.

• Consider that drown ing may have resulted from a

primary medical or traumatic insult.

INTRODUCTION

The term "drowning incident" encompasses a variety of

clinical entities. A 2005 report from the World Health

Organization recommends that the term "near-drowning"

be abandoned and instead to use the term "drowning incident" with a description of the outcome (death, morbidity,

no morbidity). Drowning itself should be described as "the

process of experiencing respiratory impairment from

submersion/immersion in liquid."

Nonfatal incidents are more common than fatal incidents; in 2009, 6,5 19 nonfatal drowning incidents were

reported, whereas 4,211 incidents resulted in death. One

estimate states that there is 1 death per 13 drowning inci ­

dents, suggesting that underreporting likely occurs.

Children make up the majority of fatal incidents, with peak

ages of 1-4 years and seasonal variability. Freshwater

drowning is more common than saltwater, with bathtubs

and pool as the most common locations. Accomplished

swimmers make up 35o/o of deaths.

CLINICAL PRESENTATION

Wide variability exists in the presentation of drowningrelated injury, both in terms of time of submersion/

immersion as well as how the patient is found. Children are

often found face-down in small depths of water (bathtub,

• Treatment is largely supportive and stabilizing.

• Patients who present and remain asymptomatic for

6 hours may be discharged from the emergency

department.

5-gallon bucket, toilet).

 

New York, NY: McGraw-Hill, 201 1, pp. 1193-1 198.

Hypothermia

Michael T. Cudnik, MD

Key Points

• Intoxication with either alcohol or drugs is very common in patients with hypothermia.

• Most emergency thermometers can not accurately read

body temperatures below 34.4°( (94°F).

• Many hypothermic patients have serious underlying

ill nesses that help contribute to their presentation,

INTRODUCTION

Clinical hypothermia is defined as a core body temperature of

less than 35°C (95°F) and can be clinically stratified by the

core temperature into mild (35°-32°C/95°-89.6°F), moderate

(32°-30°C/89.S0-86°F), and severe ( <30°C/86°F) subtypes.

Hypothermia occurs as the body loses heat from 1 of 4 major

mechanisms: conduction, convection, evaporation, and radiation. Convective (windy environments) and conductive

(cold and wet exposures) mechanisms are responsible for

most cases of accidental hypothermia. Hypothermia can be

further classified as either primary or secondary. Primary

hypothermia occurs when an otherwise healthy person is

unable to compensate for an excessive exposure to cold temperatures. Secondary hypothermia occurs when a comorbid

medical condition (eg, hypothyroidism, sepsis, intoxication)

disrupts a patient's normal thermoregulatory processes.

Although most common in colder climates, hypothermia can occur in any environment. Case reports during

summer months and in hospitalized patients are not

uncommon. In the United States, hypothermia is responsible for approximately 700 deaths annually, with more

than half occurring in patients older than 65 years. Patients

with an initial core body temperature <23°C (73.4°) typically do not survive, and the overall mortality rate of

patients with hypothermia is approximately 40%.

and it is imperative to aggressively identify and treat

these conditions.

• Resuscitative efforts should not be terminated until

defi bri llation remains unsuccessful despite a rewarmed

core body temperature of at least 32°C.

CLINICAL PRESENTATION

..... History

The potential for hypothermia is usually obvious in

patients with significant exposures. Patients may present in

wet clothing, be found outdoors in the cold weather, or be

inappropriately dressed for the environment in which they

live. In the United States, most hypothermic patients are

either intoxicated or suffer from an underlying psychiatric

illness or dementia.

The history or presentation may be less obvious for

patients with mild hypothermia or unknown exposures.

Said patients typically present with nonspecific neurologic

findings, including dizziness, confusion, slurred speech, or

ataxia. Patients with severe hyperthermia may present

comatose or in cardiac arrest.

..... Physical Examination

As with all emergency department (ED) patients, start by

assessing and addressing the patient's airway, breathing,

and circulation (ABCs) and vital signs. Hypothermic

patients may present with unstable airways or absent

pulses. Carefully measure the patient's c ore body temperature by inserting a specialized "low-reading" probe into the

bladder, rectum, or esophagus as this will be pivotal to

259

 

, temporarily take patient off 0

2 and repeat evaluation)

History of loss of consciousness or near-syncope

History of seizure

Coma

History of hypotension during or shortly after exposure

Myocardial ischemia

History of prolonged exposure

Pregnancy with COHb >15%

DISPOSITION

...,._ Admission

Patients with any signs of hemodynamic instability warrant

admission to a critical care setting. Furthermore, admit all

patients with altered mental status or other neurologic deficits and those with indications for HBO to a critical care or

monitored setting. Well-appearing patients with no signs of

active toxicity whose poisoning was due to a suicide attempt

require psychiatric evaluation and admission.

...,._ Discharge

Patients with accidental exposures who are clinically well

with COHb levels <5% after 100% 02 treatment can be

safely discharged. Educate all discharged patients about

CO poisoning and encourage them to have their homes

examined by the fire department or gas company. Convey

the importance of a home CO detector. Provide adequate

Relative Indication

Persisting neurologic symptoms including headache and dizziness after

4 hours of 1 00% normobaric 0

2

Persisting acidosis

Concurrent thermal or chemical burns

Pregnancy with history of carbon monoxide exposure regardless of

COHb level

follow-up to assess for the development of delayed

neurological sequelae .

SUGGESTED READING

Maloney G. Carbon monoxide. In: Tintinalli JE, Kelen GD,

Stapczynski JS, eds. Tintinalli's Emergency Medicine: A

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

Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank

LR, Flomenbaum NE. Goldfrank's Toxicologic Emergencies.

9th ed. New York, NY: McGraw-Hill, 20 11.

Weaver LK. Carbon monoxide poisoning. N Engl J Med.

2009;360: 1217.

Wolf SJ, Lavonas EJ, Sloan EP, J agoda AS, American College of

Emergency Physicians. Critical issues in the management of

adult patients presenting to the emergency department with

acute carbon monoxide poisoning. Ann Emerg Med.

2008;5 1: 138-152.

Digoxin

Michael E. Nelson, MD

Key Points

• Attempt to disti nguish between acute versus chronic

ingestions, as the symptoms and treatments differ.

• Electrocardiogram changes are common and include

downward-sloping (scooped) ST-segment depressions,

premature ventricular complexes, supraventricu lar

dysrhythmias with slow ventricular rates, and

bidirectional ventricular tachycardia.

INTRODUCTION

Digoxin, a commonly prescribed agent derived from the

foxglove plant, belongs to a class of medications known as

cardiac glycosides. These agents function to increase myocardial contractility and slow AV nodal conduction and are

commonly used for the treatment of congestive heart failure

and various cardiac dysrhythmias including atrial fibrillation. Of interest, cardiac glycosides are frequently encountered in the natural world as a predatory deterrent in both

plant and animal species, including oleander, lily of the

valley, red squill, and bufo toads. The relative potency of

digoxin lends to a very narrow therapeutic window, and lifethreatening toxicity can develop with both acute overdoses

and chronic excessive exposures. Poisoned patients generally

present with variable symptoms and must be viewed in light

of acute versus chronic versus acute on chronic exposures. If

left untreated, death will invariably result secondary to cardiac instability and hemodynanlic compromise.

As a whole, cardiac glycosides were responsible for

nearly 2,500 poisonings reported to the National Poison

Data System in the year 2010. They were the third most

common cardiovascular agent implicated in patient toxicity and were the primary agent responsible for 17 patient

deaths. Of note, clinically significant toxicity is far more

251

• Although hyperkalemia can be a marker of significant

digoxin poisoning, standard treatment with intravenous

calcium should typically be avoided.

• Empirically administer digoxin-specific antibodies (5 vials for chronic toxicity, 1 0-20 vials for acute ingestions)

to all patients with life-threatening dysrhythmias or

hemodynamic instabil ity.

common in pediatric and geriatric populations. Pediatric

overdoses arise from iatrogenic dosing errors or accidental

ingestions of adult medications, whereas geriatric t oxicity

generally results from either drug-drug interactions or

alterations in metabolic clearance. Intentional overdoses

are most common in adult patients and can be of both the

acute and chronic variety.

Orally administered digoxin begins to exhibit clinical

effects within 90 minutes of ingestion and typically reaches

maximal effect within 4-6 hours. Digoxin is primarily

eliminated by the kidneys with a usual half-life of

36-48 hours.

 

DISPOSITION

..... Admission

Admit all patients who are either suicidal, require hemodialysis, or require ADH inhibition. All patients with abnorSuspected or confirmed toxic

alcohol ingestion

Normal serum pH, osmol

gap, and anion gap

If anion gap unchanged,

toxic alcohol ingestion

ruled-out

Lab studies: Serum pH, electrolytes,

and osmolal ity. Send blood to

reference lab for STAT levels of

ethylene glycol and methanol

Initiate hemodialysis in patients with

ethylene glycol or methanol levels > so

mg/dL, severe acidemia, renal failure,

or visual impairment

• Figure 55-2. Toxic alcohols diagnostic algorithm.

CHAPTER 55

mal vital signs, systemic acidosis, or evidence of end-organ

damage require admission to an intensive care unit setting,

as do patients requiring an ethanol infusion for ADH

inhibition to follow serial ethanol levels and monitor CNS

depression. Patients receiving fomepizole can typically be

admitted to a regular hospital bed.

� Discharge

Unintentional ingestions with no evidence of acidosis or

indications for antidotal treatment or hemodialysis may be

safely discharged after appropriate poison prevention

counseling.

SUGGESTED READING

Brent J. Fomepizole for ethylene glycol and methanol poisoning.

N Engl l Med. 2009;360:2216-23.

Mycyk MB. Toxic alcohols. In: Barton C, Collings J, DeB!ieux P,

et a!., eds. Adams' Emergency Medicine. 2nd ed. Philadelphia,

PA: Elsevier, 2012, pp. 1 292-1298.

Mycyk MB, Aks SE. A visual schematic for clarifying the temporal

relationship between the anion gap and the osmol gap in cases

of toxic alcohol poisoning. Am J Emerg Med. 2003;2 1:333-335.

Smith JC, Quan D. Alcohols. In: Tintinalli JE, Stapczynski JS,

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

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

New York, NY: McGraw-Hill, 201 1:1222-1230.

Acetaminophen Toxicity

Key Points

• Acetami nophen is the most popular over-the-counter

ana lgesic in the Un ited States and is widely prescribed

in combination form with alternative pain relievers,

resulting in frequent uni ntentional overdose.

• Treatment with N-acetylcysteine detoxifies NAPQI, the

hepatotoxic byproduct of acetaminophen metabolism.

INTRODUCTION

Acetaminophen (APAP) is the most commonly used overthe-counter (OTC) analgesic in the United States. It is

found in more than 100 combination pharmaceuticals

(eg, cold and cough agents, sleep agents) and is present in

multiple prescription opioid analgesics ( eg, Vicodin,

Darvocet). Toxic exposures to analgesics as a class have

increased rapidly over the last decade. According to the

National Poison Data System (NPDS) database of expo ­

sures reported to poison centers nationwide, there were

139,780 exposures to all APAP-containing products in the

year 20 10, with 1 ,142 cases exhibiting "major" effects and

125 fatalities. APAP toxicity is the most common cause of

medication-induced liver failure in the United States and

accounts for a significant portion of liver transplants.

The maximum recommended safe dose is 4 g per day

for adults and 60-90 mg/kg/day for children. Toxicity may

result after an ingestion of 7 g in adults or 140 mg/kg in a

child and is due to the conversion of APAP into toxic

byproducts. APAP is normally metabolized via multiple

pathways in healthy individuals. Sulfonation and

glucuronidation are the two primary mechanisms and

produce nontoxic metabolites that are cleared in the urine.

Approximately 10-1 5%, though, is metabolized via the

Jenny J. Lu, MD

• The Rumack-Matthew nomogram should only be used

in acute overdoses with reliable times of ingestion. Pay

careful attention to all units of measurement.

• Consider early transfer to a liver transplant center for

patients with worsening hepatic function or general

signs of deterioration before they meet criteria for liver

transplantation.

cytochrome P450 system into the toxic metabolite

N -acetyl-p-benzoq uinoneimine (NAPQ I).

After a therapeutic ingestion, endogenous stores of

hepatic glutathione will rapidly detoxify any accumulating

NAPQI. However, in cases of APAP overdose, the sulfonation and glucuronidation pathways are overwhelmed, and a

greater percentage of APAP is metabolized via cytochrome

P450 into NAPQI. Glutathione stores can become rapidly

depleted, resulting in elevated levels of intrahepatic NAPQI

with secondary toxicity. Furthermore, in overdose scenarios, a small percentage of APAP can be metabolized into

NAPQI within the kidneys, resulting in consequent renal

toxicity. Patients with lower glutathione stores (chronically

ill, malnourished, and alcoholics) and those with upregulated cytochrome P450 activity (patients on certain

medications including anticonvulsants and antituberculosis

agents, chronic alcoholics) are more likely to suffer

significant toxicity.

Clinically, APAP poisoning progresses through 4 distinct stages. Although all patients may not progress beyond

the first stage after a toxic exposure, those that do tend to

follow the following timeline. Stage 1 is generally encountered within the first 24 hours postexposure. Symptoms of

gastrointestinal ( GI) irritation predominate, including

abdominal pain and vomiting, although patients may

239

CHAPTER 56

remain asymptomatic. Stage 2 occurs between 24-48 hours

post exposure and is known as the latent stage. GI symptoms resolve, but ongoing hepatotoxicity can lead to significantly elevating serum transaminases. The third stage

occurs within 3-4 days after exposure. Abdominal symptoms return, including pain and vomiting along with jaundice and potential encephalopathy. Laboratory studies may

reveal acidemia, hypoglycemia, renal failure, and coagulopathy. Stage 4 lasts between 4 days and 2 weeks of the

exposure and involves a progression to outright liver failure

and death or complete patient recovery. The hepatic function of those patients who survive APAP poisoning will

also recover completely.

 

influenza A and B, Coxsackie, rhinovirus, coronavirus, and

Epstein-Barr virus (EBV).

Group A �-hemolytic streptococcus (GABHS) is the

most common bacterial cause of pharyngitis. It accounts

for 1 5-30% of cases of pharyngitis in children and 5-15%

in adults. The peak age group is 5-15 years old. Most cases

are seen in the winter and spring. GABHS pharyngitis is

rare in patients younger than 2 years. Antibiotics are used to

treat GABHS and to prevent suppurative andnonsuppurative

complications. Suppurative complications include abscess

formation. Nonsuppurative complications include scarlet

fever, acute rheumatic fever (ARF), poststreptococcal glomerulonephritis, and streptococcal toxic shock syndrome.

Scarlet fever, presenting with pharyngitis and a diffuse

erythematous rash, is the result of the skin's reactivity to

• Suspected group A �-hemolytic streptococcus (GABHS)

infections can be confirmed by performing a ra pid

antigen screening test or a throat culture.

• Antibiotic treatment is used to prevent suppurative and

nonsuppurative (immune-mediated) complications GABHS.

the release of pyrogenic exotoxin by GABHS. ARF is a

delayed sequela and can present with arthritis, carditis,

chorea, erythema marginatum, and subcutaneous nodules.

Poststreptococcal glomerulonephritis is caused by nephritogenic strains of GABHS. Children <7 years of age are at

the highest risk. Streptococcal toxic shock syndrome is a

severe GABHS infections presenting with shock and multisystem organ failure. The pharynx, skin, mucosa, and

vagina can be portals of entry for GABHS resulting in streptococcal toxic shock syndrome.

...... Life-Threatening Causes of Sore Throat

Epiglottitis is an infection of the epiglottis and adjacent

supraglottic structures that can result in respiratory arrest and

death if swelling is severe enough to airway occlusion. The

widespread use of Haemophilus influenzae type B (HIB) conjugate vaccine in young children has dramatically changed the

epidemiology of epiglottitis, and the incidence has decreased.

Epiglottitis is currently more often seen in adolescents and

adults. Common organisms include Streptococcus pneumoniae, Staphylococcus aureus, nontypeable H. influenza, and

�-hemolytic streptococcus.

Retropharyngeal abscess is a deep space neck infection

involving the lymph nodes that drain the nasopharynx,

adenoids, posterior paranasal sinuses, and middle ear. The

disease can start as an infection in these nodes (adenitis)

225

CHAPTER 53

leading to a suppurative adenitis, phlegmon formation, and

finally, a retropharyngeal abscess. Incidence peaks between

2 and 4 years of age, as the retropharyngeal lymph nodes are

prominent in young children but atrophy before puberty.

Peritonsillar abscess (PTA) is a collection of pus between

the tonsillar capsule and the palatopharyngeal muscle. It is

usually preceded by pharyngitis or tonsillitis with progression

from cellulitis to phlegmon, and then abscess. It is the most

common deep neck infection in children and adolescents.

Infections are polymicrobial and include anaerobic and a erobic organisms (GABHS, S. aureus, fusiform, and bacteroides).

CLINICAL PRESENTATION

Most patients with pharyngitis will complain of sore throat

and fever. Symptoms are acute in onset with GABHS

pharyngitis. There is also pain on swallowing (odynophagia)

or difficulty swallowing (dysphagia). Young children may

not localize the pain to the throat and will complain of headache and/or abdominal pain instead of sore throat. Nausea

and vomiting may also be present. Toddlers can present with

fever, fussiness, or refusal to take liquids and solids.

Coryza, conjunctivitis, and hoarseness are symptoms

suggestive of viral illness. Pharyngitis with fever, red

eyes, and rash prompts concern for Kawasaki disease

(mucocutaneous lymph node syndrome). Fatigue and

anorexia are associated with infectious mononucleosis.

Drooling and the inability to handle oral secretions are

seen is patients with epiglottitis, peritonsillar, or retropharyngeal abscess. Increased work of breathing (tachypnea, r etractions, and stridor) is seen in patients with e piglottitis. Severe

unilateral throat pain and inability to open the mouth ( trismus) is seen in patients with a peritonsillar abscess. A muffled

or "hot potato" voice can be heard in patients with a peri ton ­

sillar abscess, but is also present with epiglottitis and retropharyngeal abscess. Children with a retropharyngeal abscess may

also have neck stiffness and pain with extension of the neck.

� Physical Examination

Airway patency must be assured, and impending airway

compromise needs to be rapidly identified. Evaluate the

hydration status, focusing on findings that have been correlated with dehydration in children. Signs and symptoms

include a general "ill" appearance, the absence of tears with

crying, dry mucous membranes, decreased skin turgor,

tachycardia, and delayed capillary refill (>2 seconds).

Auscultate the heart and document murmurs that might

suggest the presence of acute rheumatic fever.

Patients with epiglottitis will be "toxic" appearing,

showing signs of respiratory distress with stridor. The

patient may prefer to sit in the "sniffing position" with the

neck extended. Drooling, respiratory distress, and

hyperextension of the neck are seen in patients with

retropharyngeal abscess. Anterior bulging of the posterior

pharyngeal wall may be visualized on examination. Those

with a peritonsillar abscess may have trismus, "hot potato"

muffled voice, and drooling with a fluctuant bulge in the

posterior aspect of soft palate with contralateral deviation

of the uvula (Figure 53-lA). Classic findings in GABHS

pharyngitis are fever, tender cervical adenopathy, tonsillar

erythema, exudates, and hypertrophy (Figure 53- lB).

Those with scarlet fever may have a fine, erythematous,

"sandpaper-like" rash. Palatal petechiae (Figure 53- lC), a

A

B

(

Figure 53-1. A. Peritonsillar abscess. B. Tonsill itis.

C. Pa latal petechiae. (a rrows)

PHARYNG ITIS

B

Figure 53-2. A. Epiglottitis. The epiglottis is located by tracing the base of the tongue inferiorly until it reaches

the va llecula. The structure immediately posterior is the epiglottis. If the epiglottis is enlarged (th umb print) and

the va llecula is sha llow, epiglottitis is present. B. Retropharyngeal abscess. The normal retropharyngeal soft tissue

space is <7 mm at C2, <14 mm at C6 in children, and <22 mm at C6 in adu lts.

white or red "strawberry tongue" (inflamed tongue

papillae), desquamating rash, and Pastia lines (accentuation

of rash in flexor creases) are also suggestive of GABHS

infection and scarlet fever.

Patients with infectious mononucleosis will have

pharyngeal injection with exudates, posterior cervical

adenopathy, and hepatosplenomegaly. A maculopapular

rash is often seen in patients who are treated with amoxicillin or ampicillin.

DIAGNOSTIC STUDIES

..... Laboratory

Rapid antigen detection of GABHS is 70-90% sensitive

and 95-100% specific when performed correctly. GABHS

diagnosis based solely on clinical grounds is accurate 50%

of the time. A negative rapid strep test should be confirmed

with a throat culture. Throat culture is the gold standard

for diagnosis of GABHS pharyngitis, but results can take

up to 48 hours.

 

 A

general assessment of hydration status is essential, as

decreased oral intake and vomiting often accompany

pediatric abdominal pain.

DIAGNOSTIC STUDIES

� Laboratory

General laboratory studies (complete blood count,

electrolytes) do not often add significant information in

the evaluation of children with abdominal pain. The total

white blood cell count in children with appendicitis is

often normal. With the correct clinical picture, an elevated

absolute neutrophil count is strongly supportive of the

condition. A prolonged case of pyloric stenosis will show

the stereotypical hypochloremic, hypokalemic, metabolic

alkalosis.

� Imaging

Flat and upright abdominal radiographs are useful to look

for obstruction, seen as a dilated stomach or bowel with

paucity of air distally. Free air under the diaphragm is seen

in the case of a ruptured viscus. In intussusception, a standard x-ray may reveal a paucity of bowel gas in the right

lower quadrant (Figure 50- 1).

Ultrasound is the preferred modality to diagnose

appendicitis in children, intussusception, and pyloric

stenosis. Classic ultrasound findings include target, hull's

eye, and pseudokidney signs (Figure 50-2). Reduction of

CHAPTER 50

.&. Figure 50-1 . Pa ucity of dista l bowel gas in child

with malrotation.

.&. Figure 50-2. U ltrasound showing classic target

sign in intussusception.

.&. Figure 50-3. Fl uoroscopy of malrotation with

corkscrew sign.

intussusception is routinely accomplished under fluoroscopy with air or barium. CT should be reserved for

equivocal cases of appendicitis or when the appendix is

not visualized on ultrasound. Upper GI series reveals

duodenal obstruction with an abnormal course and

"corkscrew" appearance in malrotation (Figure 50-3 ).

Meckel diverticulum with ectopic gastric tissue is diagnosed

with a technetium-99m pertechnetate study, commonly

referred to as a Meckel scan. It can also be visualized on

ultrasound or CT scan when it acts as a lead point in

intussusception.

MEDICAL DECISION MAKING

Age of patient, history, and physical exam are often sufficient

to narrow a differential diagnosis. Consider the following

extra abdominal causes of abdominal pain in the

investigation: urinary tract infection, inguinal hernia, testicular torsion, ovarian torsion and ovarian cysts, strep pharyngitis, and pneumonia. Children with bilious vomiting or

peritoneal findings require immediate surgical evaluation

(Figure 50-4).

ABDOMINAL PAIN

Abdominal pain/distress

or vomiting

Note vita l signs; observe chi ld's activity level

and interaction with parent(s)

Cobta in history to differentiat cute vs chronic condi�

Perform physica l exam. Note specifical ly presence of

· Mass

• Distention (obstruction)

• Periton itis

( Consider age of patient J

-...

La b studies and imaging (CT, ultrasound, upper

Gl, barium enema), as indicated

Surgical condition identified

Send appropriate pre-op labs

Consult pediatric surgery

Pursue identification of

medical diagnosis

Figure 50-4. Abdominal pain diagnostic algorithm.

TREATMENT

Pain control is essential in the care of patients. Analgesia

does not interfere with the examination; on the contrary,

it may even improve one's diagnostic accuracy by facilitating patient cooperation and removing less severe

aspects of the pain. The treatment of the distress should

proceed in parallel with the investigation of the etiology

of the pain. In addition, nausea and vomiting often

accompany abdominal pain and should be appropriately

managed.

Intussusception. For ileo-colic intussusception, emergent

radiologic reduction is necessary. In cases of unsuccessful

radiologic reduction and with ileo-ileal intussusceptions, surgical reduction is indicated to prevent bowel

necrosis.

CHAPTER 50

Pyloric stenosis. Correction of electrolytes is a prerequisite

for surgical repair. Pylorotomy is the treatment of cure.