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Chapter 67 PEDIATRIC AND NEONATAL RESUSCITATION468
and submandibular tissue and the larger the tongue, making any compression to these areas
during bag-valve-mask a greater risk of iatrogenic upper airway compression. The pediatric
airway is hour-glass in shape, with the cricoid cartilage composing the narrowest portion of
the airway.
In contrast, the adult airway is more conical in shape, with the inlet of the vocal cords being
the narrowest portion. Finally, the pediatric epiglottis is bigger, floppier and more omega in shape
than the adult. Due to this, for endotracheal (ET) intubation, a straight blade is placed under the
epiglottis, allowing the epiglottis to be lifted up such that the vocal cords can be viewed.
6. Does the pediatric patient require cricoid pressure during active bagging?
Yes. It is a common misconception that because the cricoid is the smallest part of the airway,
cricoid pressure is not necessary when bagging children. Just like with adults, the reasons for
cricoid pressure is to compress the esophagus in patients presenting with a presumed full
stomach. In addition, due to children’s anatomically smaller thorax, preventing gastric
insufflation is essential to prevent the pediatric stomach from distending and impeding
ventilation during bagging. Care must be taken to provide adequate pressure for esophageal
compression, yet not so much as to prevent bag-valve-mask ventilation. This can be
accomplished by gently pushing down on the cricoid ring until ventilation is impeded and then
lifting up slightly.
7. How does the approach to the B (breathing) of ABCs differ in pediatrics
relative to adults?
Children function with only 40% the functional residual capacity of adults relative to their
size. Their metabolic rate is also proportionally higher, and thus their oxygen consumption
per minute is higher. As such, they are prone to respiratory stress earlier. In addition to
this, the younger the child, the less able they are to change cardiac contractility and thus
are primarily dependent on increasing heart rate to maintain blood pressure. The result of
all of these is that children can decompensate quickly and suddenly. The practitioner
should be aware of subtle changes in mental status and work of breathing, which can
herald such an event.
8. What are alternative airway devices that can be used in the pediatric
population?
Laryngeal mask airway (LMA) is considered Class Indeterminate in the latest Pediatric
Advanced Life Support (PALS) guidelines because most of the literature comes from the adult
population. Although a rescue option, the LMA may cause an upper airway obstruction in
children under 30 kilograms, as the tip of the airway device can rest in the vallecula and fold
the larger pediatric epiglottis into the airway inlet.
Due to the slit-like cricothyroid membrane and the easily transectable airway, an open
surgical cricothyrotomy is not recommended in children younger than 8 years of age. Needle
cricothyrotomy is a rarely utilized alternative. After a 16- to 18-gauge needle is placed into the
airway via the cricothyroid membrane, the lungs are insufflated using a jet ventilation device
that allows for controlled pressures of 25 to 30 PSI.
9. What drugs and dosing should I have committed to memory in my
armamentarium for pediatric resuscitations?
Epinephrine is the most commonly used first-line medication in pediatric resuscitations. The
1:10,000 (standard dose) epinephrine should be used at 0.1 mL/kg (0.01 mg/kg). 1:1,000 can
be considered via the ET route if an intravenous/intraosseous (IV/IO) access has not been
established. However, because the ET route has not been proven of benefit, this administration
should not delay establishing IV/IO access.
10. At what point should chest compressions be initiated in children?
Chest compression should be initiated for pulseless arrest or when the heart rate is ,60 beats
per minute with evidence of poor end-organ perfusion. Chest compressions should be
Chapter 67 PEDIATRIC AND NEONATAL RESUSCITATION 469
performed at 100 per minute at a depth
1
⁄2 to
1
⁄3 of the anterior-posterior diameter of the
chest. Like advanced cardiac life support, PALS emphasizes continuous, hard, and fast chest
compressions with minimal interruptions.
11. Where should I try for vascular access in the pediatric patient?
Vascular access should be first attempted in the peripheral veins in a child with a blood
pressure. If a child presents in cardiac arrest, the provider should immediately perform IO
access placement. The anterior proximal tibia is the easiest site of entry in most
circumstances. Care should be made to angle the needle just off 90 degrees away from the
growth plate. In the young neonate, the distal femur may be a more stable and less easily
breakable bone to perform IO placement. For central venous access, the femoral vein is the
most commonly used site in children. Whatever the location for central venous access,
ultrasound guidance if available should be used to facilitate placing these lines, both in adults
and children.
12. What is the earliest gestational age that a newborn has been successfully
resuscitated after birth?
In 2006, at 21 weeks and 6 days gestational age and weighing less than 10 ounces, Amillia
Sonja Taylor was successfully resuscitated after birth.
13. What spontaneous activity should you expect in a normal newborn at the time
of birth?
Almost all infants have a grimace-like facial expression at birth and make some attempt to
move the upper and lower extremities. Infants will almost always make an effort to breathe
spontaneously and cry within 15 to 20 seconds following birth.
14. After delivery in the ED, what is the first priority in the care of the newborn?
The first priority is to prevent body heat loss. The infant must be dried immediately to
prevent evaporative heat loss and be placed under a radiant warming unit to lessen loss
of radiant heat. These initial steps take only seconds to accomplish and may prevent
serious metabolic derangements. These steps should be taken even prior to the initiation
of CPR.
15. When should central cyanosis resolve in a healthy newborn following
delivery?
Central cyanosis and cyanosis of the oral mucous membranes should clear after the first
minute of life. Peripheral cyanosis of the hands and feet may persist for several minutes in an
otherwise healthy newborn. Peripheral cyanosis restricted to the hands and feet is referred to
as acrocyanosis and usually has no clinical significance.
16. How do I approach the meconium-stained newborn?
Meconium (either thin or thick) presents a real and serious risk to the respiratory system of
the infant if it is aspirated. The material contains noxious substances such as bile acids that
can lead to pulmonary injury. The latest neonatal resuscitation guidelines call for ET intubation
and suctioning of meconium prior to bulb suctioning in newborns that are non-vigorous,
defined as weak respiratory efforts, poor muscle tone, and a heart rate ,100.
17. After the infant is dried, suctioned, and placed under the warmer, how do I
decide whether further active intervention is needed?
If the infant is active, is crying, has a heart rate of greater than 100 beats per minute, and
does not have evidence of central cyanosis, further intervention is seldom needed. If the
infant demonstrates apnea, bradycardia, or central cyanosis, then use of bag and mask
ventilation must be considered after attempts at stimulation have failed. Most of the time, if
the infant is near term gestation, the heart rate will respond quickly to a few effective
assisted breaths.
Chapter 67 PEDIATRIC AND NEONATAL RESUSCITATION470
18. For the newborn, define bradycardia and indications for intervention.
A heart rate of less than 100 beats per minute at 30 seconds following birth is considered
bradycardia in the newborn. Positive pressure ventilation and oxygenation should be initiated
if the newborn is cyanotic or has a heart rate of ,100 after 30 seconds of drying, stimulating
and giving blow by oxygen.
If the heart rate is below 60 beats per minute after providing respiratory support, the
provider should initiate chest compressions at a rate of 100 per minute using a two-finger
chest encircling technique. Avoid pressure over the liver because a liver laceration can occur.
Heart rate should be evaluated about every 30 seconds. Compressions should be performed
in between breaths. When a sustained heart rate of greater than 100 beats per minute is
achieved, compressions can be discontinued.
19. How many infants will require intubation to provide adequate ventilation?
Almost all newborn infants can be ventilated with bag-mask technique. Bag-mask ventilation
should be done only with equipment designed for newborn and premature infants. The most
effective bag for this type of assistance is an infant self-inflating unit connected to wall
oxygen. There is currently a great deal of discussion in the literature as to whether 100%
oxygen is the safest gas for this type of intervention. For the time being, in the setting of the
ED, 100% oxygen is the best choice until this debate is resolved. To avoid barotrauma,
inflation pressures should not exceed 40 cm H
2
O in the term and 25 cm H
2
O in the preterm
newborn. All neonatal bags should be equipped with pressure manometers.
20. When should I attempt vascular access? What vessel should I use?
As soon as it is fairly obvious that drugs or volume expanders may be needed, an umbilical
venous line (3.5 French for preterm and 5.0 French for term infants) should be attempted. It is
uncommon for this to be needed. For such events, an umbilical venous tray should always be
available in the ED. Remember that there is one larger umbilical vein and two umbilical
arteries (Table 67-1).
21. What drugs should be available for use in newborn resuscitation use, and
when should they be given?
Drugs are rarely needed in the resuscitation of the newborn infant, especially if bag-and-mask
ventilation is started early. Usually, no more than two agents are needed.
n
Epinephrine 1:10,000 dilution is used if there has been no heart beat noted for 6 to 10
seconds at any point during the event or if heart rate remains less than 60 beats per minute
after 30 seconds of bag-and-mask ventilation and chest compressions. The standard dose
From Nadel FM: Vascular access. In Baren JM, Rothrock SG, Brennan J, et al, editors: Pediatric
emergency medicine, Philadelphia, 2008, Saunders.
TABLE 67-1. CENTRAL VENOUS CATHETER SIZE BASED ON PATIENT AGE, LENGTH/HEIGHT,
AND WEIGHT
Age Weight (kg) Length/Height (cm) French Size
Premature #2.5 ,50 2.0–2.5
Birth–30 days 3–4 50–55 3.0
.1 mo–1 yr 4.5–10 5–75 3.0–4.0
.1–7 yr 11–25 7–120 4.0–5.0
.7–15 yr 26–60 125–175 5.0–8.0
Chapter 67 PEDIATRIC AND NEONATAL RESUSCITATION 471
BIBLIOGRAPHY
1. American Academy of Pediatrics, Committee on the Fetus and Newborn: Use and abuse of the Apgar score.
Pediatrics 78:1148, 1986.
2. International Guidelines for Neonatal Resuscitation: An excerpt from the Guidelines 2000 for cardiopulmonary
resuscitation and emergency cardiovascular care: international consensus on science. Contributors and
reviewers for the Neonatal Resuscitation Guidelines. Niermeyer S. Pediatrics 106(3):E29, 2000.
3. Catlin EA, Carpenter MW, Brann BS, et al: The Apgar Score revisited; influence of gestational age. J Pediatr
109:865, 1986.
4. American College of Emergency Physicians and the American Academy of Pediatrics. Care of children in the
emergency department: guidelines for preparedness. Ann Emerg Med 37:423-427; 2001.
TABLE 67–2. APGAR SCORING SYSTEM
Sign 0 1 2
Heart rate (bpm) Absent Slow (,100) .100
Respirations Absent Slow, irregular Good, crying
Muscle tone Limp Some flexion Active motion
Reflex irritability
(catheter in nares)
No response Grimace Cough or
sneeze
Color Blue or pale Pink body with
blue extremities
Completely pink
bpm, beats per minute.
KEY POINTS: PEDIATRIC AND NEONATAL RESUSCITATION
1. For preparedness of the critical child, all caregivers should be familiar with their ED pediatric
resuscitation algorithms, equipment and support resources.
2. Due to underlying etiologies, pediatric patients in cardiac arrest have poor prognoses.
3. The highest impact intervention for a newborn or pediatric resuscitation is appropriate
respiratory support.
is 0.1 to 0.3 ml/kg (0.01 to 0.03 mg/kg), either via the umbilical vein (preferable) or via the
ET tube. The drug can be given as frequently as every 5 minutes if bradycardia persists.
n
Volume expanders may be used via the umbilical vein catheter (UVC) if there is evidence of
blood loss from the infant. Rapid volume expansion must be done with caution in infants
less than 32 weeks’ gestation because of the risk of central nervous system (CNS)
bleeding. The usual agents used are normal saline or 5% albumin in a dose of 10 mL/kg.
22. What is the best means of documentation of the results of resuscitation in the
neonate?
The Apgar score remains the standard, despite some limitations (Table 67-2). The score is
calculated at 1 minute and at 5 minutes and at every 5 minute interval thereafter.
Chapter 67 PEDIATRIC AND NEONATAL RESUSCITATION472
5. Developing a general impression: The pediatric assessment triangle. In: Susan Fuchs, Marianne Gausche-Hill, Loren
Yamamoto, editors: Advanced pediatric life support ed 4, Massachusetts, 2004, Jones and Bartlett, pp 25–34.
6. Donoghue AJ, Nadkarni V, Berg RA, et al: Out-of-hospital pediatric cardiac arrest: an epidemiologic review and
assessment of current knowledge. Ann Emerg Med 46:512–522, 2005.
7. Nadel FM: Vascular access. In Baren JM, Rothrock SG, Brennan J, et al, editors: Pediatric emergency
medicine, Philadelphia, 2008, Saunders.
8. Park C, Bahk JH, AhnWS, et al: The laryngeal mask airway in infants and children. Can J Anesth 48(4):413–417,
2001.
9. Roberts D, Hirschman D, Scheltema K: Adult and pediatric CPR: Attitudes and expectations of health
professionals and laypersons. Am J Emerg Med 18(4): 465–468, 2000.
10. Santillanes G, Gausche-Hill MG: Pediatric airway management. Emerg Med Clin North Am 26:961–975, 2008.
11. Saugstad OD: The role of oxygen in neonatal resuscitation. Clin Perinatol 31:3, 2004.
12. Vain NR, Szyld EG, Prudent LM, et al: Oropharyngeal and nasopharyngeal suctioning of meconium-staining
neonates before delivery of their shoulder: multicentre, randomized controlled trial. Lancet 364(9434):
597–602, 2004.
473
Note: Despite a high frequency of involvement, these substances are not the most toxic
but rather may be the most readily accessible.
Percentages total more than 100% because multiple substances are involved in some fatal
exposures. Percentages are based on the total number of human exposures rather than the
total number of substances.
2. What is the current role of syrup of ipecac in treating acute poisoning?
Although syrup of ipecac induces vomiting within 20 to 30 minutes in most people who
are given a therapeutic dose, little poison is removed; there are more effective means of
decontaminating the gastrointestinal (GI) tract. Ipecac may have a limited role in treating
children at home and who frequently can be given a dose soon after ingestion; however,
its use in the prehospital setting is rapidly declining (use of ipecac recommended in 0.07%
of all poison center cases in 2007). By the time most patients present to a hospital, too
much time has elapsed for syrup of ipecac to be of benefit. Its use also delays the
administration of activated charcoal, which needs to be given as quickly as possible for
maximal benefit.
3. What is the current role of gastric lavage in treating acute poisonings?
Gastric lavage has not been shown to alter clinical outcome in large series of patients
presenting with overdose. Although serious sequelae of gastric lavage are rare, it carries
the risk of aspiration, laryngospasm, and esophageal injury. The risk of injury appears to be
greater in uncooperative patients. Endotracheal intubation should precede gastric lavage in
patients with altered mental status or the inability to protect the airway. Although lavage
can be accomplished without prior tracheal intubation in most patients, airway equipment,
including suction, should be immediately available at the bedside. Placing the patient on
the left side in mild Trendelenburg position helps prevent aspiration if vomiting occurs.
Nasogastric tubes are too small to remove pills or large pill fragments; whenever gastric
lavage is done, a large-bore tube (36 French or 40 French in adults) should be placed through
the mouth. A bite-block with an oral airway prevents the patient from biting the tube. Proper
location of the lavage tube in the stomach must be verified clinically or radiographically
before lavage or administration of fluid or charcoal. Deaths have been reported resulting
from charcoal instillation into the trachea by nasogastric tube. Gastric lavage generally is
reserved for the small number of patients with potentially serious or life-threatening overdose
XIV. TOXICOLOGIC EMERGENCIES
GENERAL APPROACH TO POISONINGS
CHAPTER 68
Katherine M. Hurlbut, MD
1. List the 15 most common causes of death from acute poisoning reported to
poison centers.
n
Sedative/hypnotics/antipsychotics
30.4%
n
Opioids 26.7%
n
Antidepressants 17.8%
n
Acetaminophen in combination 16.8%
n
Cardiovascular drugs 16.4%
n
Stimulants and street drugs 15.2%
n
Alcohols 13.7%
n
Acetaminophen alone 11.3%
n
Anticonvulsants 8.0%
n
Fumes/gases/vapors 6.5%
n
Cyclic antidepressants 6.5%
n
Muscle relaxants 5.7%
n
Antihistamines 5.6%
n
Aspirin alone 5.1%
n
Chemicals 3.6%
Chapter 68 GENERAL APPROACH TO POISONINGS474
who present within 1 to 2 hours after ingestion. It was used in 0.36% of poison center cases
in 2007.
4. What is the current role of activated charcoal?
Activated charcoal has been shown in numerous studies to be superior to gastric emptying
procedures for the treatment of acute overdose. Gastric emptying procedures involve time and
some risk to the patient. The time involved in lavaging the patient is time during which drugs
are being actively absorbed. By giving a dose of activated charcoal immediately on patient
presentation, the most effective means of GI decontamination already has been performed.
Not all drugs are adsorbed to charcoal, however. Drugs that are not well adsorbed include
lithium, potassium, iron, some metals, and alcohols. Activated charcoal is contraindicated
after ingestion of hydrocarbons because toxicity from gastric absorption is generally not a
major concern with these substances, and activated charcoal may induce vomiting, which
increases the risk of aspiration pneumonitis. Activated charcoal is also not indicated after
ingestion of acids or alkalis because the primary toxicity associated with these agents is local
mucosal burns rather than systemic absorption. Patients with trivial ingestions (generally
children) do not require activated charcoal therapy.
5. What about the asymptomatic overdose patient?
It has been advocated by some that simple observation of asymptomatic overdose patients,
with treatment only if symptoms develop, is a management option. Although this approach is
safe for many patients who have ingested trivial overdoses, if a patient ingested something
quite toxic, an opportunity to prevent absorption may have been lost if nothing is done until
symptoms develop. Administering a dose of activated charcoal to all patients with a history of
deliberate drug overdose is done easily (although it is often messy) and helps to ensure safe
and timely patient disposition. If a reliable history indicates ingestion of substances with
minimal toxicity, activated charcoal may not be necessary.
6. Is there a role for cathartics in treating acute poisoning?
The theory behind cathartics is that they speed up GI transit time, allowing activated charcoal
to catch up with pills in the bowel and prevent desorption of drug from activated charcoal.
Cathartics have not been shown to reduce drug absorption or improve outcome significantly
after overdose, but they can cause vomiting, abdominal pain, and electrolyte abnormalities.
Use of cathartics is not warranted.
7. What is the current role of whole-bowel irrigation in the treatment of acute
poisoning?
Whole-bowel irrigation uses a polyethylene glycol electrolyte solution, such as GoLYTELY or
Colyte, which is not absorbed, and flushes drugs or chemicals rapidly through the GI tract.
This procedure seems to be most useful when radiopaque tablets or chemicals have been
ingested because their progress through the GI tract can be monitored by radiography. It
should also be considered when toxic amounts of substances that are not well adsorbed by
activated charcoal (i.e., iron, lithium, heavy metals) are ingested. This procedure also is
commonly used when multiple packets of street drugs, such as heroin or cocaine, have been
ingested and need to be passed through the GI tract as quickly as possible, and should be
considered after overdose of sustained-release products. The limitations of the procedure are
that, unless the patient is awake, cooperative, and able to sit on a commode, there is a risk of
vomiting and aspiration in addition to the logistical problem of having an unconscious patient
in bed with massive diarrhea.
8. What is the role of multiple-dose charcoal in the treatment of acute
poisoning?
Multiple-dose charcoal has been shown to enhance the elimination of many drugs that already
have been absorbed from the GI tract or that are given intravenously. This process has been
called gastrointestinal dialysis and has been shown to be effective for theophylline and
Chapter 68 GENERAL APPROACH TO POISONINGS 475
perhaps phenobarbital poisoning. Numerous other drugs have been shown to have their
pharmacokinetics altered by multiple-dose charcoal, but it is not clear if this makes a
difference in clinical outcome. Many of these drugs have large volumes of distribution, and
increasing elimination of the small amount present in the blood is unlikely to be of benefit.
Multiple-dose activated charcoal is used most commonly after overdose of theophylline,
phenobarbital, carbamazepine, and quinine.
9. Is forced diuresis of benefit in the treatment of acute poisoning?
Few drugs are excreted unchanged in the urine so that even increasing urine flow significantly
above baseline is unlikely to be of benefit. By manipulating the pH of the urine with infusions
of bicarbonate solution along with enhanced urine flow, however, drug elimination can be
increased in certain cases. This most commonly is used for salicylates and phenobarbital. By
placing three ampules of sodium bicarbonate in 1 L of D
5
W along with potassium chloride and
infusing this solution at rates sufficient to produce at least a normal urine flow and a urine pH
of 7.5 or greater, the elimination of salicylate and phenobarbital can be increased. Intake and
output and urine pH should be monitored hourly with a Foley catheter in place. In the
presence of pulmonary or cerebral edema, which may occur in severe salicylate intoxication,
alkaline diuresis is dangerous and should not be undertaken.
Alkaline diuresis also may work in a similar manner for chlorophenoxy herbicides, but
acute poisonings by these agents are rare. The use of high-volume normal saline to treat
lithium intoxication is common, and it is important to maintain adequate urine output and
serum sodium in this scenario. It is not clear, however, that forced-saline diuresis for lithium
intoxication is of extra benefit over simply ensuring normal renal flow.
10. When are extracorporeal techniques, such as hemodialysis or hemoperfusion,
indicated?
Drugs can be removed successfully by extracorporeal maneuvers only if they have relatively
small volumes of distribution and are found in significant quantities in the circulation, as
opposed to having rapid and thorough tissue distribution. This is the case for only a few
drugs. In practice, the toxins most commonly dialyzed after overdose include aspirin, lithium,
methanol, ethylene glycol, and perhaps theophylline. Dialysis has the advantage over charcoal
hemoperfusion in that it is usually easier and faster to get started, and it can correct fluid and
electrolyte abnormalities as it removes drugs. Because protein binding may be saturated in
overdose, hemodialysis may be effective for treatment of severe overdose of some drugs that
are highly protein bound at therapeutic concentrations. As protein binding is saturated,
increasing quantities of drug are present as free, unbound drug in the serum, and may be
removed by hemodialysis (one example is valproic acid).
Charcoal hemoperfusion may be more effective at removing drugs that are highly
bound to plasma proteins, because the affinity for charcoal may be higher than the affinity
for the protein carrier. The disadvantages of hemoperfusion are that it is less widely
available, it frequently causes hypocalcemia and thrombocytopenia, and it can result in
frequent canister clotting. Drugs for which charcoal hemoperfusion is frequently employed
include theophylline, phenobarbital, and a few other less common agents such as paraquat
and amatoxin.
11. How can the diagnosis of a drug overdose be made when the patient is
unconscious and history is unavailable?
The diagnosis of acute overdose is difficult to make sometimes and requires some detective
work on the part of the physician. All unconscious patients should receive a rapid bedside
serum glucose determination (or intravenous dextrose if bedside glucose measurement is
unavailable); naloxone should be administered if the presentation is consistent with opioid
overdose (central nervous system [CNS] and respiratory depression, miosis); a positive
response to either is diagnostic. Whenever possible, examine the pill bottles available to the
patient, review medical records, and interview family and friends to determine prescribed
Chapter 68 GENERAL APPROACH TO POISONINGS476
drugs. It may be useful to call the pharmacies where the prescriptions were filled to
determine if other prescriptions were filled there for different drugs. Discovering which
chemical agents were available to the patient, including street drugs, is always important. If
needle track marks are seen, consider street drugs commonly used intravenously, such as
opiates, cocaine, and amphetamine. The physical examination is useful in narrowing the
diagnosis to a class of drug or chemicals. This concept is commonly called toxic syndromes
(Table 68-1) or toxidromes.
12. How can a toxicology screen and other ancillary laboratory tests make the
diagnosis of acute poisoning?
The blood and urine toxicology screen should be done on any patient who has significant
toxicity (persistent altered mental status or abnormal vital signs) and when the diagnosis is
uncertain. Alternatives to a full toxicology screen include testing discrete serum levels of the
toxins in question, doing a urine qualitative test for drugs of abuse, or drawing specimens
but holding them until it is determined that a toxicology screen is definitely indicated. The
results of urine toxicology screens rarely alter patient management; routine use is not
warranted.
More drugs and chemicals are not found on typical toxicology screens than are found on
the screens, although most drugs that commonly are ingested are found on comprehensive
toxicology screens. It is important to communicate with the laboratory about which drugs are
suspected, which drugs the patient takes therapeutically, and the clinical condition of the
patient. Whenever there is a discrepancy between clinical suspicion and findings from the
toxicology screen, it is useful to communicate with the toxicology laboratory personnel and
determine if other tests are likely to be of benefit. Toxicology screens are expensive, frequently
are inexact, and frequently do not give all the information that is expected by the clinician. It is
important to interpret toxicology screens carefully and to know which drugs and chemicals
were not screened for.
13. What other studies are useful in the evaluation of a poisoned patient?
n
An acetaminophen level should be obtained in patients with deliberate overdose because
this substance is widely available, frequently involved in overdoses, and causes little in the
way of initial symptoms; and treatment with N-acetylcysteine is most effective if begun
within 8 hours of ingestion.
n
Nontoxicologic laboratory tests that are frequently useful include an electrocardiogram
(ECG), which can help diagnose overdose of tricyclic antidepressants or cardiac
medications; a chest radiograph in patients with pulmonary symptoms or hypoxia, which if
demonstrative of acute lung injury would make one think of salicylates or opiates; and,
rarely, a kidneys-ureters-bladder (KUB) screen, looking for radiopaque material, which
would make one suspicious of ingestion of a heavy metal, iron, phenothiazines, chloral
hydrate, or chlorinated hydrocarbon solvents.
n
Liver enzymes may help to diagnose ingestion of hepatotoxins, such as acetaminophen or
carbon tetrachloride late in the course of poisoning.
n
A urinalysis may show the presence of calcium oxalate crystals, suggesting the diagnosis
of ethylene glycol poisoning.
n
The acid-base status of the patient is important and should be evaluated in all patients
with deliberate overdose. Persistent unexplained metabolic acidosis always should
prompt the search for other diagnostic clues to aspirin, iron, methanol, or ethylene glycol
poisoning. Many other drugs can cause a persistent, unexplained metabolic acidosis,
including the ingestion of acids themselves, cyanide, carbon monoxide, theophylline,
and others.
n
In the work-up of persistent acidosis, a serum osmolality done by freezing point
depression can be useful if it is elevated. A difference between the measured osmolality and
the calculated osmolality of greater than 10 is always significant, although a normal
osmolal gap does not rule out toxic alcohol ingestion.
Chapter 68 GENERAL APPROACH TO POISONINGS 477
GI, gastrointestinal; MDA, methylenedioxyamphetamine; MDEA, methyl diethanolamine; MDMA,
3,4-methylenedioxymethamphetamine.
Syndrome Common Signs Common Causes
Anticholinergic Agitated delirium, often with visual
hallucinations and mumbling
speech, tachycardia, dry flushed
skin, dilated pupils, myoclonus,
temperature slightly elevated, uri-
nary retention, decreased bowel
sounds. Seizures and dysrhyth-
mias may occur in severe cases.
Antihistamines, antiparkinsonism
medication, atropine, scopolamine,
amantadine, antipsychotics,
antidepressants, antispasmodics,
mydriatics, skeletal muscle relax-
ants, many plants (most notably
jimson weed)
Sympathomimetic Delusions, agitation, paranoia,
tachycardia, hypertension, hyper-
pyrexia, diaphoresis, piloerection,
slight mydriasis, hyperreflexia. Sei-
zures and dysrhythmias may occur
in severe cases.
Cocaine, amphetamine, metham-
phetamine (and derivatives MDA,
MDMA, MDEA), over-the-counter
decongestants (phenylpropanol-
amine, ephedrine, pseudoephed-
rine). Caffeine and theophylline
overdoses cause similar findings
secondary to catecholamine
release, except for the organic
psychiatric signs.
Opiate/sedative Coma, respiratory depression,
miosis, hypotension, bradycardia,
hypothermia, acute lung injury,
decreased bowel sounds, hypore-
flexia, needle marks
Narcotics, barbiturates, benzodiaz-
epines, ethchlorvynol, glutethi-
mide, methyprylon, methaqualone,
meprobamate
Cholinergic Confusion/central nervous system
depression, weakness, salivation,
lacrimation, urinary and fecal
incontinence, GI cramping, emesis,
diaphoresis, muscle fasciculations,
pulmonary edema, miosis, brady-
cardia (or tachycardia), seizures
Organophosphate and carbamate
insecticides, physostigmine, edro-
phonium, some mushrooms (Ama-
nita muscaria, Amanita pantherina,
Inocybe, Clitocybe)
Serotonin Fever, tremor, incoordination,
agitation, mental status changes,
diaphoresis, myoclonus, diarrhea,
rigidity
Fluoxetine, sertraline, paroxetine,
venlafaxine, clomipramine; the pre-
ceding drugs in combination with
monoamine oxidase inhibitors
TABLE 68-1. MOST COMMON TOXIC SYNDROMES