Poisonings

Chapter 39 Poisonings

Kevin C. Osterhoudt, MD, MSCE, James F. Wiley, II, MD, MPH

EPIDEMIOLOGY

1 How many poisonings occur in the united states each year? How many exposures involve children < 6 years?

Over 2 million calls are made to regional poison control centers annually. Of these, 50–60% involve toxic exposures in children younger than 6 years of age. Not all poisonings are reported to poison control centers. Estimates suggest that 4 million people are poisoned in the United States each year.

Watson WA, Litovitz TL, Rodgers Jr GC, et al: 2004 annual report of the American Association of Poison Control Centers toxic exposure surveillance system. Am J Emerg Med 23:589–666, 2005.

2 How often can poisoning be managed at home with the assistance of a regional poison control center?

Of all poison calls to a regional center, 80–90% are typically handled safely via phone advice and home observation.

Watson WA, Litovitz TL, Rodgers Jr GC, et al: 2004 annual report of the American Association of Poison Control Centers toxic exposure surveillance system. Am J Emerg Med 23:589–666, 2005.

3 When was the first poison control center established and why?

Dr. Edward Press in Chicago established the first center in 1953 in response to an American Academy of Pediatrics study published in 1952, which found that 50% of all childhood injuries were due to potentially poisonous ingestions.

Press E, Mellins RB: A poisoning control program. Am J Public Health 44:1515–1525, 1954.

4 What is the poison prevention packaging act?

Passed in 1970, this act mandated safety packaging for pharmaceuticals. It followed other important landmark legislation, including the Federal Hazardous Substances Labeling Act of 1960, which promoted product labeling, and the Child Protection Act of 1966, which required appropriate labeling of pesticides and other previously unlabeled hazardous substances.

5 What was the impact of the poison prevention packaging act?

Frequency of poisoning and death due to poisoning in children decreased significantly in 1969, one year prior to the passage of the act. This effect was due to voluntary initiation of safety packaging (childproof caps) by manufacturers in anticipation of the law.

Arena J: The pediatrician’s role in the poison control movement and poison prevention. Am J Dis Child 137:870–873, 1983.

6 What are the most common poisons to which young children are exposed?

In 2004, the top 10 exposures in young children, from most frequent to least frequent, were cosmetics, cleaning substances, topicals, foreign bodies (e.g., coins, button batteries), cough and cold preparations, plants, pesticides, vitamins, and antihistamines.

Watson WA, Litovitz TL, Rodgers GC Jr, et al: 2004 annual report of the American Association of Poison Control Centers toxic exposure surveillance system. Am J Emerg Med 23:589–666, 2005.

7 Who is more likely to ingest a poison: A 2-year-old boy or a 2-year-old girl?

The boy is more likely to ingest a poison.

8 Who is more likely to ingest a poison: A 15-year-old boy or a 15-year-old girl?

The girl is more likely to ingest a poison and usually does so intentionally.

9 What is the typical setting for a pediatric poisoning incident?

The child is usually younger than 6 years of age and is at home. The poison is typically readily available to the child. Prescription medicines that children ingest frequently belong to a grandparent or older nonparent relative. In most cases, only one poison is ingested. Social history often discloses a recent stress in the household, such as a recent move, new baby, marital discord, visiting relatives, or distracting event (holiday, wedding).

Henretig FM: Special considerations in the poisoned pediatric patient. Emerg Med Clin North Am 12:549–567, 1994.

10 What is the most common cause of death due to poisoning?

Carbon monoxide inhalation is widely felt to be the most common cause of death due to poisoning because this gas can be implicated in the numerous fire deaths that occur annually, in addition to the intentional and unintentional deaths reported to the American Association of Poison Control Centers.

Homer CD, Engelhart DA, Lavins ES, et al: Carbon monoxide-related deaths in a metropolitan county in the USA: An 11-year study. Forens Sci Int 149:159–165, 2005.

11 What are the most dangerous substances, according to reports to the American Association of Poison Control Centers?

Investigators have devised the hazard factor, which calculates the sum of the number of deaths and major effects (patients requiring antidotes or life-saving supportive measures after exposure) for each substance divided by the total number of exposures. This number is then normalized by using a constant reflecting the overall rate of major effects and deaths for data reported between 1985 and 1989 (six major effects or deaths per 10,000 exposures). A factor of 1 suggests that the poison is no worse than the average poison on the database. A factor of 50 implies that the poison is 50 times more likely to cause major effects or death after exposure than the average poison. On the basis of this analysis, the following substances are particularly hazardous:

Substance	Hazard Factor
Rattlesnake envenomation	245
Methadone	75
Chloral hydrate	66
Cyclic antidepressant	57
Strychnine	50
Selenious acid (gun bluing)	48
Acid drain cleaner (toilet bowel cleaner)	47
Carbamazepine	33
Chloroquine (antimalarial)	32
Carbon monoxide	31
Paraquat	24

Litovitz TL, Manoguerra A: Comparison of pediatric poisoning hazards: an analysis of 3.8 million exposure incidents. A report from the American Association of Poison Control Centers. Pediatrics 89:999–1006, 1992.

12 Which medicinals are potentially life-threatening or fatal to a 10-kg toddler following ingestion of a single dose?

Benzocaine, camphor, chloroquine, clonidine, cyclic antidepressants, diphenoxylate/atropine (Lomotil), lindane, methadone (and other opioids), methyl salicylate (oil of wintergreen), oral hypoglycemics, quinidine, propranolol, theophylline, thioridazine, and verapamil.

Osterhoudt KC: The toxic toddler: Drugs that can kill in small doses. Contemp Pediatr 17:73–88, 2000.

KEY POINTS: POISONING EPIDEMIOLOGY

1 More than half of all poisoning exposures are reported among children younger than age 6 years.

2 Natural exploratory behaviors of young children put them at risk for poisoning.

3 Drug abuse, experimental risk taking, and depression put adolescents at risk for poisoning.

4 Poisoning can be prevented.

INITIAL MANAGEMENT

13 Which three antidotal drugs should be immediately considered in the resuscitation of the comatose child?

Two are often not thought of as drugs per se, but they are essential substrates for brain function: oxygen and glucose. Administration of the opioid antagonist naloxone may also be warranted.

14 What is a “toxidrome”?

The word toxidrome can be thought of as a combination of the words “toxic” and “syndrome.” Toxidromes are groupings of physical signs that may help to suggest the drug class responsible for a poisoning. These signs should be noted in the examination of every potentially poisoned patient: mental status, vital signs, pupil size and reactivity, skin color and moisture, and bowel sounds.

Osterhoudt KC: No sympathy for a boy with obtundation. Pediatr Emerg Care 20:403–406, 2004.

15 Describe the most common toxidromes

See Table 39-1.

Table 39-1 Common Toxidromes

16 How can the anticholinergic toxidrome be differentiated from the sympathomimetic toxidrome?

Anticholinergic agents and sympathomimetic agents may both produce altered mental status, tachycardia, hypertension, hyperthermia, and mydriatic pupils, so distinguishing between these drugs is not easy. Look to the skin, the bowels, and the eyes for help. Anticholinergic poisoning is likely to produce flushed skin that is surprisingly dry to the touch, diminished or absent bowel sounds, and less reactive pupils. Many people remember the characteristics of the anticholinergic toxidrome with the mnemonic: “Mad as a hatter, blind as a bat (pupils do not accommodate well), red as a beet, dry as a bone, and hot as Hades.”

17 What would be the significance of a bitter almond smell to your morning coffee?

Consider the possibility of cyanide in the coffee.

18 What other toxicants are associated with characteristic odors?

Odor	Agent
Acetone	Acetone, isopropyl alcohol, phenol
Almonds	Cyanide
Garlic	Arsenic, thallium, organophosphates, selenious acid
Pears	Chloral hydrate, paraldehyde
Rotten eggs	Hydrogen sulfide
Wintergreen	Methyl salicylate

19 List the most commonly considered methods of gastrointestinal decontamination of the poisoned patient

Gastric emptying: Induced emesis, gastric lavage

Prevention of drug absorption: Activated charcoal

Catharsis: Simple cathartics, whole-bowel irrigation

20 Elaborate the indications for ipecac-induced emesis

Induced emesis has little role in the emergency department setting. Indeed, its use as out-of-hospital first aid is now discouraged by the American Academy of Pediatrics.

American Academy of Pediatrics Committee on Injury, Violence, and Poison Prevention: Poison treatment in the home. Pediatrics 112:1182–1185, 2003.

21 What is the proper technique for gastric lavage?

Consider the need for airway protection with endotracheal intubation. Place the patient in left lateral decubitus position with the head slightly lower than feet if tolerated. Use a large-bore orogastric tube (24 Fr in toddlers and up to 36 Fr in adolescents). Lavage with saline aliquots until the effluent is clear of toxic materials.

22 Under what circumstances is gastric lavage indicated?

Gastric lavage, once the stalwart of emergency department management of poisonings, is falling from favor after recent investigation has questioned its efficacy. It may still have a role in the management of life-threatening overdoses presenting within the first hour. Gastric lavage may be considered more strongly for poisoning scenarios that lack dependable antidotes.

23 What is the gastrointestinal decontamination technique of choice for most poisonings?

In most cases, gastric emptying can be omitted in preference to administration of activated charcoal.

Osterhoudt KC, Durbin D, Alpern ER, et al: Activated charcoal administration in a pediatric emergency department. Pediatr Emerg Care 20:493–498, 2004.

24 What is activated charcoal?

Most would recognize charcoal as the byproduct of the pyrolysis of wood or other organic materials. “Activation” of charcoal refers to a process of further oxidizing the charcoal, either chemically or at high temperatures, to increase its surface area and adsorptive capacity.

25 List common drugs and toxicants that are poorly adsorbed by activated charcoal

Ineffective: Alcohols, iron, lithium

Poorly effective: Hydrocarbons, metals

26 What is whole-bowel irrigation?

Whole-bowel irrigation uses nonabsorbable polyethylene glycol solution (well-known as a surgical bowel prep) to wash intestinal contents through before absorption can take place. Typical administration is 500 mL/hour in a toddler and to 2 L/hour in an adolescent, continued until the rectal effluent is clear and clinical signs of continued drug absorption have subsided.

27 List the possible indications for whole-bowel irrigation

Although not yet proven to improve patient outcomes, use of whole-bowel irrigation has been advocated for the following situations:

Body packers/stuffers

Ingestion of metals, lithium

Ingestion of sustained-release preparations

Ingestion of pharmaceutical patches

Massive overdoses

Concretions of pills

28 What is a body packer or a body stuffer?

Body packers are smugglers who attempt to evade customs officials by swallowing packages (typically tied condoms) of drugs. Body stuffers are drug sellers or users who hurriedly ingest illicit substances to hide evidence from authorities. Because of the planning involved, packers are less likely to become toxic than stuffers; however, packers typically ingest more dangerous quantities of drug.

Traub SJ, Hoffman RS, Nelson LS: Body packing: The internal concealment of illicit drugs. N Engl J Med 349:2519–2526, 2003.

29 How often do poisoned patients require special therapy, such as antidote administration, elimination enhancement, or extracorporeal elimination?

Antidotes and elimination enhancement, such as urinary alkalinization or multiple-dose activated charcoal, are performed in about 1% of all reported poisonings. Extracorporeal elimination (hemodialysis or hemoperfusion) is needed in less than 0.1%.

Watson WA, Litovitz TL, Rodgers GC, et al: 2004 annual report of the American Association of Poison Control Centers toxic exposure surveillance system. Am J Emerg Med 23:589–666, 2005.

30 What are the characteristics of the ideal toxic agent that would be amenable to multiple-dose activated charcoal?

The ideal toxicant has a small volume of distribution (< 1 L/kg), has low protein binding, binds to activated charcoal, and either has an enterohepatic circulation of an active metabolite in the bowel or undergoes enteroenteric dialysis with evidence of excretion of agent from the microvillous blood circulation into the gut, where it is bound by the charcoal. Multiple-dose activated charcoal may also be of benefit after ingestion of sustained-release compounds or after a toxic gastric concretion has formed.

31 Multiple doses of activated charcoal are believed to enhance clearance of what poison(s)?

Good evidence exists to support the use of multiple-dose activated charcoal to treat certain cases of poisoning from carbamazepine, dapsone, phenobarbital, quinine, and theophylline. Elimination of amitriptyline, dextropropoxyphene, digoxin, disopyramide, nadolol, phenylbutazone, phenytoin, piroxicam, and sotalol increases with multiple-dose activated charcoal; however, improved outcomes for ingestion of these poisons with respect to morbidity and mortality have not been shown in controlled trials.

American Academy of Clinical Toxicology, European Association of Poisons Centers and Clinical Toxicologists. Position statement and practice guideline on the use of multi-dose activated charcoal in the treatment of acute poisoning. Clin Toxicol 37:731–751, 1999.

32 What is extracorporeal removal?

Extracorporeal removal refers to elimination of a poison from the blood after removing the blood or a portion of the blood from the body. The forms of extracorporeal elimination include hemodialysis, charcoal hemoperfusion, arteriovenous hemofiltration, venovenous hemofiltration, exchange transfusion, and plasmapheresis. Of these, hemodialysis is used most commonly.

33 What factors predict adequate removal of a poison by hemodialysis?

The substance should have the following characteristics: small volume of distribution, little protein binding, water solubility, low molecular weight, low endogenous clearance, and single-compartment kinetics.

34 For which toxic agents is hemodialysis most commonly considered?

Ethylene glycol

Dargan PI, Jones AL: Acute poisoning: Understanding 90% of cases in a nutshell. Postgrad Med J 81:204–216, 2005.

35 When should hemodialysis be used?

The decision to perform hemodialysis should be based on physical findings as well as drug levels. Always repeat an elevated level and check units of measurement before instituting hemodialysis.

36 What is the rationale behind urinary alkalinization?

Urinary alkalinization refers to the administration of sodium bicarbonate to raise the urine pH to 8.0. This procedure converts renally excreted toxins, which are weak acids to their ionized form within the proximal renal tubules, and thereby prevents reabsorption in the distal tubules (ion trapping). This technique is most useful for enhancing the excretion of salicylates and phenobarbital (but not other barbiturates). Urinary alkalinization is also useful to protect the kidney during rhabdomyolysis.

Proudfoot AT, Krenzelok EP, Vale JA: Position paper on urine alkalinization. J Toxicol Clin Toxicol 42:1–26, 2004.

37 What are the pitfalls of urinary alkalinization?

Urine alkalinization is inhibited by the presence of hypokalemia. Urinary alkalinization has been associated with pulmonary and cerebral edema, and fluid administration must be monitored carefully. Electrolyte and acid-base disturbances can result from sodium bicarbonate administration and merit frequent monitoring.

Proudfoot AT, Krenzelok EP, Vale JA: Position paper on urine alkalinization. J Toxicol Clin Toxicol 42:1–26, 2004.

38 List some drugs that may lead to a delayed expression of clinical toxicity

Monoamine oxidase inhibitors

Oral hypoglycemic agents

Sustained-release drug formulations

Thyroid hormones

KEY POINTS: INITIAL POISONING MANAGEMENT

1 Toxidrome analysis is more clinically useful than toxicology urine analysis.

2 In most cases, gastrointestinal decontamination with activated charcoal is preferred to gastric emptying measures.

PHARMACEUTICALS

39 Describe the pathophysiology of acetaminophen poisoning

Acetaminophen is the drug most commonly administered to children. Toxicity may occur after acute overdose of 150–200 mg/kg or after repeated supratherapeutic ingestions. Overdose of acetaminophen saturates typical hepatic metabolism pathways, and expends glutathione, resulting in the production of an intermediate metabolite, N-acetyl-p-benzoquinoneimine via cytochrome oxidase (P450) metabolism. This metabolite binds to hepatocytes and causes centrilobular liver necrosis.

40 What are the three stages of acetaminophen overdose poisoning?

Stage I (1/2–24 hours after ingestion): Often asymptomatic; occasionally nausea, vomiting, diaphoresis, and pallor are seen.

Stage II (24–48 hours after ingestion): Nausea, vomiting, right-upper-quadrant abdominal pain, elevation of hepatic aminotransferase levels.

Stage III (72–96 hours after ingestion): Fulminant hepatic failure with jaundice, thrombocytopenia, prolonged prothrombin time, and hepatic encephalopathy. Renal failure and cardiomyopathy may occur. If the patient survives, complete resolution of liver abnormalities is possible.

41 How is acetaminophen intoxication diagnosed?

The potential for acetaminophen poisoning must be thoughtfully considered since most patients are initially asymptomatic. The serum acetaminophen level should be measured in all patients with intentional drug overdose. Frequently, acetaminophen is overlooked as a coingestant with cough/cold preparations and combination analgesics such as Darvocet (propoxyphene and acetaminophen) and Percocet (oxycodone and acetaminophen). An acetaminophen level at 4–24 hours after ingestion can predict the potential for toxicity and determine the need for antidote administration based on the Rumack-Matthew nomogram.

42 What is the antidote for acetaminophen overdose? How does it work?

N-acetyl cysteine (NAC) replenishes, and substitutes for, depleted glutathione stores in the liver and detoxifies the toxic metabolite. NAC also seems to alleviate existing hepatotoxicity through antioxidant and procirculatory properties.

43 When is NAC given after acute acetaminophen overdose?

All patients with acute overdose whose acetaminophen levels fall within the potential toxicity area on the Rumack-Matthews nomogram merit administration of NAC. This therapy is most effective when initiated within 8 hours of ingestion, though it may provide benefit even if given later.

44 How is NAC administered?

Historically, within the United States, the inhalational form of NAC had been given enterally with a loading dose of 140 mg/kg, followed by 17 doses of 70 mg/kg given every 4 hours. Recently, an IV form of NAC has been approved; it is given as a continuous infusion over 21 hours. The IV route may be preferred in a pregnant patient to ensure adequate NAC delivery to the fetus via the placenta and in patients who present late with acetaminophen toxicity to augment the potential antioxidant effect.

45 Does IV NAC have any particular risks?

The IV administration of NAC may cause a life-threatening anaphylactoid reaction, which most commonly occurs during the first, higher-dose infusion. Patients with asthma may be at highest risk.

46 Can the oral NAC regimen be shortened?

Some poison centers will recommend “short-course” NAC therapy for patients who have received at least 24 hours of the antidote and have no evidence of liver toxicity by enzyme studies. Such a practice, if proven efficacious, may lead to favor of oral NAC over IV NAC in risk-benefit analysis.

Marzullo L: Update of N-acetylcysteine treatment for acute acetaminophen toxicity in children. Curr Opin Pediatr 17:239–245, 2005.

Rowken AK, Norvell J, Eldridge DL, Kirk MA: Updates on acetaminophen toxicity. Med Clin North Am 89:1145–1159, 2005.

47 Detail the pathophysiology of salicylate overdose

Salicylate overdose commonly causes gastritis and vomiting. Salicylates uncouple oxidative phosphorylation from the production of energy in the form of adenosine triphosphate. Metabolic consequences include hyperthermia, metabolic acidosis, increased glucose utilization, fatty acid catabolism, and increased free water loss. Salicylates also directly stimulate the medullary respiratory center, causing hyperpnea with respiratory alkalosis; impede platelet aggregation; and cause direct renal and hepatic impairment. Seizures and coma denote severe toxicity. Noncardiogenic pulmonary edema complicates treatment in severely affected patients.

48 Describe the treatment for acute salicylate poisoning

Activated charcoal may be considered early after overdose. Intravascular volume should be restored. Urinary alkalinization is appropriate for patients with symptoms and a peak salicylate level of > 35 mg/dL (350 mg/L). Mild alkalemia will reduce salicylate access to the brain. Patients with unremitting metabolic acidosis, pulmonary edema, severe renal impairment, coma or seizures, liver impairment, and salicylate level > 70 mg/dL meet criteria to receive hemodialysis.

Dargan P, Wallace CI, Jones AL: An evidence based flowchart to guide the management of acute salicylate (aspirin) overdose. Emerg Med J 19:206–209, 2002.

49 What hazard is associated with endotracheal intubation of salicylate-poisoned patients?

Salicylate-poisoned patients typically have profound respiratory alkalosis. This process is abruptly reversed by paralytic and sedative medications, and resulting acidemia may increase salicylate entry to the brain.

50 How does iron produce toxicity?

Iron acts as a gastrointestinal mucosal irritant and as an inhibitor of oxidative phosphorylation in the mitochondria. The body has no mode of excretion of excess iron.

51 How much iron is toxic?

Expected toxicity can be estimated by the amount of elemental iron ingested (Table 39-2).

Table 39-2 Expected Toxicity of Elemental Iron

Dose Ingested (mg/kg Elemental Iron)	Toxicity
20–60	Mild gastrointestinal symptoms
60–100	Moderate toxicity
100–200	Serious toxicity
>200	Possibly lethal

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