the pharmacokinetic features of the toxin ( eg, circulating

half-life) can be markedly prolonged secondary to

extended absorption times and the saturation of metabolizing enzymes. These toxicokinetic principles often result

in an unpredictable onset of symptoms and overall duration of toxicity.

The initial goal in managing a poisoned patient is to

provide excellent supportive care. Contact your regional

poison center ( 1 -800-222-1222) early in the management of your patient as they can provide invaluable

support. To aid in making the diagnosis, attempt to classify the patient's clinical presentation into a specific

toxidrome (a syndrome complex that characterizes

• Always focus on supportive measures first in the clin ical

management of poisoned patients.

• Consult your regional poison center (1-800-222-1 222)

to ensure the appropriate management of poisoned

patients.

certain classes of poisonings) (Table 54- 1). Only by following the preceding guidelines will certain patients be

suitable for decontamination measures and possibly

focused antidotal care.

CLINICAL PRESENTATION

� History

When possible, obtain a thorough history, including the

location of the exposure and the patient's occupation.

Pill bottles found at the scene or chemical containers

noted by emergency medical service, family, or friends

may provide the necessary clues to identify the causative

toxin. Attempt to establish the exact time of exposure,

although this is often limited to when the patient was

last seen in a "normal" condition. Try to discern the

amount that was ingested and whether it was in a regular or extended release formulation. Finally, try to establish the chronicity of the exposure, the immediate

symptoms after the exposure, a history of previous suicide attempts, a thorough past medical history, and a

history of any illicit drug abuse. If known, contacting

the patient's regular pharmacy may provide further

insight into the case.

230

THE POISONED PATIENT

Table 54-1. Common toxidromes.

Representative Additional Signs/

Toxidrome agent(s) Most Common Findings Symptoms Potential Interventions

Opioid Heroin, morphine CNS depression, miosis, respiratory Hypothermia, bradycardia, Ventilation or naloxone

depression respiratory arrest,

acute lung injury

Sympathomimetic Cocaine, amphetamine Psychomotor agitation, mydriasis, Seizures, rhabdomyolysis, Cooling, sedation with

diaphoresis, tachycardia, myocardial infarction, benzodiazepine, hydration

hypertension, hyperthermia cardiac arrest

Cholinergic Organophosphate Sal ivation, lacrimation, diaphoresis, Bradycardia, seizures, Airway protection and

insecticides, nausea, vomiting, urination, respiratory failure ventilation, atropine,

carbamate defecation, muscle fascicula- pralidoxime

insecticides tions, weakness, bronchorrhea

Anticholinergic Scopolamine, atropine AMS, mydriasis, dry /flushed skin, Seizures, dysrhythmias, Physostigmine (if applicable),

urinary retention, decreased rhabdomyolysis sedation with benzodiazepine,

bowel sounds, hyperthermia, cooling, supportive

dry mucous membranes management

Salicylates Aspirin, oil of AMS, respiratory alkalosis, Low-grade fever, MDAC, alkalinization of the urine

wintergreen metabolic acidosis, tinnitus, ketonuria, acute with K+ repletion, hemodialysis,

hyperpnea, tachycardia, lung injury hydration

diaphoresis, nausea, vomiting

Hypoglycemia Sulfonylureas, insulin AMS, diaphoresis, tachycardia, Paralysis, slurring of Glucose, octreotide

hypertension speech, seizures

Serotonin syndrome Meperidine or dextro- AMS, increased muscle tone, Intermittent whole-body Cooling, sedation with

methorphan and hyperreflexia, hyperthermia tremor benzodiazepine, supportive

MAOI; SSRI and TCA; management

SSRI/TCA/MAOI and

amphetamines; SSRI

alone

AMS, a ltered mental status; CNS, central nervous syndrome; MAOI, monoamine oxidase inhibitor; MDAC, m u lti-dose activated charcoal;

SSRI, seroton in reu ptake inhibitor; TCA, tricyclic antidepressant.

...,._ Physical Examination

Examination findings are very important to help recognize

potential toxidromes and identify to what class of agent

the patient might have been exposed. Obtain a full set of

vital signs to evaluate for evidence of hyperpyrexia,

hemodynamic instability, and tachypnea/hyperpnea (which

could indicate compensation for significant acidemia).

Characterize the patient's mental status and note any

neurologic deficits. Findings such as delirium, central

Table 54-2. Agents that affect pupil size.

Miosis (COPS)

Cholinergics, clonidine

Opioids, organophosphates

Phenothiazine, pilocarpine

Sedative-hypnotics

Mydriasis (AAAS)

Antihistamines

Antidepressants

Atropine (anticholinergics)

Sympathomimetics

nervous system ( CNS) hyperactivity, or frank obtundation/

coma may help to determine the responsible toxin. Perform

a careful ocular exam focusing on pupillary size and

responsiveness, the presence of nystagmus, and evidence of

abnormal lacrimation (Table 54-2). Finally, noting the

absence or presence of bowel sounds and whether the skin

is dry or wet may help differentiate anticholinergic from

sympathomimetic poisoning, respectively.

DIAGNOSTIC STUDIES

...,._ Laboratory

Obtain a basic metabolic panel looking for electrolyte

abnormalities or evidence of renal insufficiency. Check a

serum creatine phosphokinase in all patients with ongoing

seizures, prolonged down times, or renal abnormalities, as

rhabdomyolysis is a serious concern. Calculation of an

anion gap coupled to venous or arterial blood gas analysis

may help differentiate acid-base disorders. Co-oximetry

with blood gas analysis is also useful to determine

CHAPTER 54

methemoglobin and carboxyhemoglobin concentrations.

A markedly elevated serum lactate level (>8-10 mmol/L)

often indicates serious toxicity from an inhibitor of cellular

metabolism (eg, cyanide).

Quantitative blood screens for determining the serum

concentrations of multiple potential toxins including

acetaminophen, salicylates, lithium, carbamazepine,

valproic acid, lead, iron, and digoxin are usually very

helpful to guide the management of poisoned patients.

That said, qualitative urine toxicology screening rarely

changes the work-up, management, or disposition of emergency department patients. The frequent false-positive

results ( eg, positive for PCP due to dextromethorphan use)

and tests that remain persistently positive for several days

after the actual exposure ( eg, positive opiates x 7 days after

heroin use; positive cocaine x 3 days after cocaine use;

positive cannabinoids x 30 days after marijuana use) render urine toxicology screens challenging to interpret.

� Electrocardiogram

Obtain an electrocardiogram looking for any evidence of

dysrhythmias, conduction blocks, or abnormal intervals.

These findings may assist in both the diagnosis and treatment of patients poisoned by cardiotoxic agents.

� Imaging

Obtain computed tomography imaging of the brain when

either mental status changes or neurologic deficits are

present that are not consistent with the type of poisoning

being entertained (eg, focal or lateralizing signs). Order a

chest x-ray for all patients complaining of either shortness

of breath, hypoxia, toxic fume inhalation, or potential aspiration (eg, hydrocarbon ingestion). Check abdominal

x-rays,

 

 looking for radio-opaque ingestions (eg, leaded

paint chips or toys, batteries, selected drug packets) as

indicated to help complete the work-up.

MEDICAL DECISION MAKING

The first priority must always be supportive care in the management of the poisoned patient. Use all available historical

items to help identify the possible toxin. A thorough physical

exam including careful attention to the patient's mental

status, vital signs, pupillary size and responsiveness, the presence of seizures, or abnormal changes in skin color, tern ­

perature, and moisture may help classify the patient's

presentation into a specific toxidrome. Use the ancillary

studies described previously to help clarify the diagnosis and

guide further management (Figure 54-1).

TREATMENT

The treatment of poisoned patients can be broken down

into a very systematic approach outlined by the mnemonic

ABCDEFGH. First and foremost, initiate aggressive

supportive care. The airway and breathing must be secured

and addressed without delay. Intubation may be prevented

Toxic exposure or poisoning

Supportive care: Address ABC's, IV

ccess, supplemental 02- cardiac monitor

Lab studies, ECG, identify toxidromes,

contact poison control center

consider decontamination:

• Wash patient

• Activated charcoal

• Gastric lavage

• Whole bowel irrigation

Consider enhanced elimination:

• Mu lti-dose activated charcoal

• Urinary alkalinization

• Hemodialysis

Consider focused antidotal therapy

Figure 54-1 The poisoned patient

diag nostic algorithm. ABCs, airway,

breathing, and circu lation; ECG,

electrocard iogram; IV, intravenous.

with the successful use of a focused therapy such as

naloxone in opioid toxicity or supplemental dextrose in

hypoglycemic patients. Likewise, correct any circulatory

compromise in the form of hypotension or bradycardia

with standard fluid and/or vasopressor administration. Pay

careful attention to the core temperature. Aggressively and

expeditiously correct hyperpyrexia with active cooling measures and not systemic antipyretics. These measures, rather

than the early search for specific antidotes, are the cornerstone of the initial management of the poisoned patient.

The basic goal of decontamination is to remove the poison

from the patient and the patient from the poison. Attempt

decontamination as early as possible to achieve maximal

benefit. Washing a patient's skin with soap and water to

prevent further absorption and/or prevent harm to the

emergency staff (eg, a patient covered with an organophosphate) is the simplest form of decontamination. Activated

charcoal (1 g/kg or a 10:1 ratio of charcoal to toxin) can be

given orally to bind ingested poisons and limit further gastrointestinal (GI) absorption. Although most drugs are

THE POISONED PATIENT

amenable to this, lithium, iron and other metals, hydrocarbons, caustics, and toxic alcohols are not. Consider gastric

lavage in patients who present very early (within 1 hour)

after a potentially lethal ingestion. Additionally, any potentially fatal ingestions that don't have available antidotes may

warrant lavage regardless of the timing of ingestion (eg,

massive colchicine overdose). Contraindications to gastric

lavage include the ingestion of hydrocarbons or other caustic agents, and potential complications include increased

intracranial pressure, aspiration, and esophageal rupture.

Whole-bowel irrigation with polyethylene glycol

(GoLYTELY), given at a rate between 0.5 L/hr (pediatrics)

and 2 L/hr, may help to "flush" toxins that won't bind to

charcoal (eg, leaded paint chips) out of the GI tract and

therefore limit total absorption. Contraindications to

whole-bowel irrigation include hemodynamic instability

(hypotension = lack of GI perfusion) and decreased bowel

sounds (impaired GI motility). Of note, pulmonary aspira ­

tion is the most common adverse side effect for all forms of

GI decontamination, and patients must have an intact air ­

way for these procedures to be pursued.

There are several different modalities available to

enhance the elimination of poisons. Hemodialysis is ideal

for smaller-sized poisons with small volumes of distribution

( <1 L/kg) and low degrees of protein-binding. Ideal agents

for hemodialysis include aspirin, toxic alcohols, and lithium.

Hemodialysis should also be performed in all patients with

profound acidemia regardless of the etiology. Alkalinization

of the urine is commonly initiated for ingestions of weak

acids such as aspirin and phenobarbital. The proposed

mechanism depends on increasing the urinary pH by giving

doses of intravenous (IV) sodium bicarbonate. Circulating

toxins will be preferentially converted to their conjugate

bases in the alkaline environment and consequently trapped

in the renal tubules, where they will be excreted in the urine.

Alkalinization can also benefit patients in select cases ( eg,

salicylate overdose) by keeping the poison preferentially out

of the CNS, as the ionized form cannot enter through the

blood-brain barrier. Finally, multiple doses of oral activated

charcoal (MDAC) can be administered to patients poisoned

with select agents including theophylline, phenobarbital,

carbamazepine, dapsone, or quinine. The proposed mechanism relies on the use of the GI tract wall as a dialysis membrane. The intraluminal charcoal functions to pull

circulating toxins back into the GI tract where they are

bound to the charcoal and excreted. MDAC can also be

employed to further decontaminate the gut of agents that

have erratic and prolonged absorption ( eg, salicylates, val ­

proic acid). If MDAC is entertained, ensure that the charcoal is not premixed with sorbitol, as cathartics (unlike

polyethylene glycol) can cause marked fluid and electrolyte

shifts, resulting in significant morbidity and/or mortality.

Antidotal therapy is important and necessary when

managing the poisoned patient, but should never take

priority over the supportive measures already mentioned.

Examples of selected focused therapy along with general

indications are listed in Table 54-3. The final portion of the

Table 54-3. Specific antidotes for toxicologic agents.

Acetaminophen

Crotalidae bite

Poison

Hydrofluoric acid, calcium channel

antagonists

Cyanide

Iron

Digoxin

Ethylene glycol, methanol

Methanol, methotrexate

Calcium channel blocker, � blocker

Oxidizing chemicals (nitrites, benzocaine,

sulfonamides)

Refractory hypoglycemia after oral

hypoglycemic

Opioid, clonidine

Anticholinergic (not TCA)

Cholinergic

Heparin

Isoniazid

Anticoagulants

TCA, tricyclic antidepressant.

Antidote

N-acetylcysteine

Antivenom Fab

Calcium gluconate or

calcium chloride

Sodium nitrite, thiosulfate

Deferoxamine

Digoxin Fab

Fomepizole or ethanol

Folic acid/leucovorin

Glucagon

Methylene blue

Octreotide

Naloxone

Physostigmine

Pralidoxime (HAM)

Protamine

Pyridoxine

Vitamin K

management algorithm includes G and H. This is a

reminder for clinicians to never hesitate in calling their

regional poison center ( 1-800-222-1222) for assistance

during any point in the care of the poisoned patient.

Getting help early may facilitate a more focused work-up,

prevent unnecessary laboratory and/or diagnostic studies,

provide insight into potentially life-saving antidotal

therapy, and assist with appropriate disposition making.

 

 Approximately 20% of asymptomatic

school-aged children are chronic carriers of GABHS.

In patients with infectious mononucleosis, a complete

blood count will typically show lymphocytosis with a

preponderance of atypical lymphocytes (> 10%).

Heterophile antibody (Monospot) or EBV titers are used

to confirm the presence of infectious mononucleosis.

Monospot is very insensitive in children younger than 4

years of age. Liver enzymes may also be elevated.

..... Imaging

A soft tissue lateral neck radiograph may be helpful to visualize an aspirated foreign body or narrowing of the tracheal

air column (masses). The "thumb print'' sign is seen with

epiglottitis (Figure 53-2A). Widening of the retropharyngeal

space is seen with a retropharyngeal abscess (Figure 53-2B).

The normal retropharyngeal soft tissue space is defined as

<7 mm at C2, < 14 mm at C6 in children, and < 22 mm at

C6 in adults. Computed tomography (CT) scan of the neck

may be required for the definitive diagnosis of peritonsillar

or retropharyngeal abscess.

MEDICAL DECISION MAKING

Patients with signs and symptoms of toxicity or severe

respiratory distress need to be emergently evaluated for the

possibility of epiglottitis, retropharyngeal abscess, or

peritonsillar abscess. The history and physical examination

will help to differentiate between these conditions.

Using either the Strep score (Table 53-1) or modified

Centor criteria ( Table 53-2) can help in the decision to test

and treat patients with pharyngitis (Figure 53-3). Consider

an alternative diagnosis of viral pharyngitis or foreign

body if clinically indicated.

Table 53-1. Strep Score (each factor is worth 1 point).

• Fever > 38.3°( (1 01 °F)

• Age 5-15 years

• Season (November-May)

• Evidence of pharyngitis on exam (erythema, edema, exudates)

• Tender, enlarged > 1 em anterior cervical lymph nodes

• Absence of upper respiratory infection signs/symptoms

Scoring:

Points PPV Diagnosis/Treatment

0-1 2% Supportive care

2-4 20-40% Rapid test and treat accordingly

5-6 60-75% Consider empiric treatment

CHAPTER 53

Table 53-2. Mod ified Centor Criteria.

Criteria

Fever >38°( (101 .4°F)

Absence of cough

Tender, enlarged anterior cervical lymph

nodes

Tonsillar exudates

Age

3-14 years

1 5-44 years

45 years or older

TREATMENT

Points

0-1

2-3

4-6

Points

1

0

-1

Diagnosis/Treatment

Supportive care

Rapid test/culture and

treat accordingly

Consider empiric

treatment ± culture

Epiglottitis. Place the patient in a position of comfort

(parent's lap), avoid agitating the patient, and administer

supplemental 02" Obtain ear, nose, and throat (ENT)

consultation with the goal to secure the airway in the

operating room.

Retropharyngeal abscess. Start intravenous (N) antibiotics (ampicillin-sulbactam 50 mg/kg or clindamycin

13 mg/kg). Obtain ENT consultation for surgical drainage

if the CT reveals an abscess.

Peritonsillar abscess. Start N antibiotics (ampicillinsulbactam or clindamycin). Needle aspiration and/or incision and drainage in ED can be done in older children.

Surgical drainage of the abscess in the operating room will

be necessary for children requiring significant sedation.

Pharyngitis. Advise symptomatic treatment with warm

salt water gargles (not for young children who will swallow

the salt water) and acetaminophen (15 mg/kg every

4-6 hours) or ibuprofen (10 mg/kg every 6-8 hours).

Antibiotics are prescribed in patients with suspected or

confirmed GABHS. Oral choices of antibiotics include

penicillin (25-50 mg/kg day PO TID or QID for 10 days),

amoxicillin (50 mg/kg!day PO BID-TID for 10 days), or a

first-generation cephalosporin. Benzathine penicillin ( <27 kg:

600,000 units; >27 kg: 1 .2 million units) can be given intramuscularly to ensure compliance. Patients with penicillin

or cephalosporin allergies can be given either erythromycin ethyl succinate ( 40 mg/kg/ day PO BID or TID for

10 days), azithromycin (children: 12 mg/kg/day PO, maximum dose 500 mg/day PO for 5 days; adolescents and

adults 500 mg tablet on day 1 followed by 250 mg tablet on

days 2-5), or clindamycin (20 mg/kg!day PO TID for 10

days, maximum 1.8 g/day).

DISPOSITION

..... Admission

Admit patients with epiglottitis and retropharyngeal

abscess with potential airway compromise to an intensive

care unit. Young patients with peritonsillar abscess who

cannot be drained in the ED or are unable to tolerate

liquids also require admission. When Kawasaki disease is

suspected or pharyngitis causes severe dysphagia preventing adequate oral intake, admission may be necessary.

..... Discharge

Patients with a peritonsillar abscess drained either by

needle aspiration or incision and drainage who are

tolerating oral fluid adequately can be discharged from the

ED. The first dose of antibiotics should be given N.

Uncomplicated pharyngitis in patients tolerating oral fluids can also be discharged from the ED.

SUGGESTED READING

Caglar D, Kwun R. The mouth and throat. In Tintinalli JE,

Stapczynski JS, Cline DM, Ma OJ, Cydulka R.K, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 20 11, pp. 774-782.

Fleischer GR. Sore throat. In: Fleisher GR, Ludwig S. Textbook of

Pediatric Emergency Medicine. 6th ed. Philadelphia, PA:

Lippincott Williams & Wilkins, 20 1 0, pp. 579-583.

Gunn JD Ill. Stridor and drooling. In Tintinalli JE, Stapczynski

JS, Cline DM, Ma OJ, Cydulka R.K, Meckler GD. Tintinalli's

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

New York, NY: McGraw-Hill, 201 1, pp. 788-796.

PHARYNGITIS

Throat pain

Assess for signs of toxicity

or respiratory distress

2. Supportive care

.&. Figure 53-3. Pharyngitis diag nostic algorithm.

The Poisoned Patient

Sean M. Bryant, MD

Key Points

• A thorough history of present ill ness including information gathered from available friends, family, and

emergency medical service personnel can be invaluable

in the management of poisoned patients.

• Perform a comprehensive physical exam including a fu ll

set of vital signs t o h e l p classify the patient's clinical

presentation into a particu lar toxidrome.

INTRODUCTION

More than 2 million toxic exposures and poisonings are

reported to U.S. regional poison centers annually.

Consequently, all emergency physicians should possess a

basic fundamental comprehension of emergency

toxicology and a sound clinical approach for managing

the poisoned patient. Depending on the absolute dose

and/or duration of exposure, all substances have the

potential for harm. Factors including the absorption,

distribution, and elimination rate of the inciting agent

help determine its overall toxicity. In poisoned patients,

 

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.