More on poisonings...

The following information was condensed from:

  • The University of Chicago Pritzker School of Medicine, Poisoning in Childhood
  • McGuigan ME. Poisoning Potpourri. Pediatrics in Review. 2001;22:295-302.
  • Markowitz M. Lead Poisoning. Pediatrics in Review. 2000;21:327-335.
  • Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright 2002 Mosby, Inc, 36t.


Iron poisoning is the leading cause of pediatric poisoning death in the United States.

Nearly 60% of iron ingestions occur in children under six years of age.

Iron is dangerous because small amounts can cause serious toxicity, it is readily available, many adults are not aware of the danger, and available treatments are not adequate.

In overdose Iron is well absorbed and very slowly excreted. Less than 10-20mg/kg is rarely toxic; 20-60mg/kg can be mildly toxic; over 60 mg/kg is severely toxic.

Phase 1: 30 minutes - 2 hours - mild acidosis, CNS depression, corrosive effect on GI tract (nausea/vomiting).
Phase 2: May see a period of apparent recovery; often not when large overdose taken.
Phase 3: 2-12 hours - hypotension and metabolic acidosis.
Phase 4: 2-4 days - end organ failure, ARDS, hepatic necrosis
Phase 5: 2-4 weeks - gastric scarring and stricture formation

GI decontamination is critical, activated charcoal does not bind Iron. Need abdominal X-ray to look for pill fragments, then give whole bowel lavage with electrolyte solution and recheck X-ray to be sure all fragments are gone.

Check serum iron level 2-6 hours after ingestion. Level >350mcg/dl causes mild to moderate toxicity; >500mcg/dl is severely toxic.

Treat with IV deferoxamine which binds iron to make desferioxamine. The highest dose can only remove about 500mg of iron/day.


On the kitchen counter they might find a bottle of Acetaminophen (Tylenol, but we shouldn't use the trade name).

Toxic doses: Children are prescribed 10-15 mg/kg for fever or pain, toxic doses are 150mg/kg or ten times the usual dose and lethal doses are approximately 250mg/kg or 16 times the usual dose. In children over 12 and adults the usual dose is 1 gram; 7.5 grams, or 15 extra strength tablets, is toxic. The toxicity from acetaminophen overdose arises from metabolism of the drug. During hepatic metabolism by glutathione of large quantities of acetaminophen, as in an overdose, a toxic metabolite accumulates in the hepatocyte and binds to intracellular molecules, causing damage to the liver cells..

Symptoms follow a predictable pattern:
Stage 1: First 24 hours - either asymptomatic or nausea/vomiting. Glutathione stores in the liver are mobilizing; liver function tests are normal. Treatment during this phase will lesson the toxicity.
Stage 2: 24-48 hours - Alanine Transaminase (ALT), Aspartate Transaminase (AST), and bilirubin levels as well as the Prothrombin time (PT) will be increased. Patient usually feels better.
Stage 3: 48-96 hours - The patient becomes icteric, hypoglycemic, and can have renal changes and encephalopathy.
Stage 4: Episode may resolve with lab tests returning to normal.

Treatment: Clear stomach via emesis or gastric lavage then give activated charcoal. Acetaminophen level should be drawn at 4 hours after ingestion and nomogram used to determine the patient's likelihood of having liver damage. Give acetylcysteine (Mucomyst) within 16 hours after ingestion by gavage (through a nasogastric tube) and continue every 4 hours for 17 doses. Starting mucomyst after 32 hours may not prevent hepatic damage.

Nomogram of Acetominophen level and risk of hepatic toxicity

(click graph to see a larger image)


Seventy-five percent of hydrocarbon ingestions involve petroleum distillates such as gasoline, kerosene, lighter fluid, and mineral spirits. Gasoline is most common, kerosene has the highest morbidity (11% of ingestions have moderate or major clinical effects), and lighter fluid is the only one that has reportedly caused death.

Petroleum distillate hydrocarbons irritate the gastrointestinal and respiratory tracts. The primary clinical effect of concern is chemical pneumonitis, and the major determinants of the degree of chemical pneumonitis are the volume of liquid aspirated and the product's viscosity. Pneumonitis does not result from gastrointestinal absorption of the liquid or from inhalation of the fumes or vapors. Asymptomatic patients who remain so during 4 to 6 hours of observation and have normal chest radiographic findings may be discharged home. Patients who are symptomatic should be admitted for observation and supportive care.

The majority of hydrocarbon ingestions result in either no or only minor clinical effects, and most patients who have petroleum distillate hydrocarbon aspiration chemical pneumonitis recover completely. Rarely, cases of pneumonitis have been associated with prolonged bronchospastic tendencies or pneumatoceles.


The prevalence of lead poisoning has dramatically decreased over the past several decades in the United States, largely due to regulations on the amount of lead that can be used in paint (current maximum is 0.06% by weight while some paints were up to 50% lead in the past) and gasoline (less than 0.1g/L, down from 1.5g/L). The other large source of lead contamination in the past was the soldering of cans of food, a practice that is no longer followed. Unfortunately, lead is very stable and does not decay for millions of years, so lead can remain in the environment and pose a risk to those who are exposed. Those at highest risk live in housing built before 1960 or those who are rehabilitating older housing. Inner city children living in older, poorly kept buildings, are at high risk of lead poisoning.

Most lead is absorbed through the GI tract. Children ingest lead dust from their environments. Iron or calcium deficiency increases lead absorption from the gut.

Most children with elevated lead levels (>10 mcg/dl) are asymptomatic. There is a correlation, however, between elevated lead levels and decreased IQ. At approximately 50 mcg/dl patients may present with gastrointestinal symptoms. Higher levels lead to encaphalopathy.

Most pediatric offices use screening questions to decide whom to screen for lead. A history of living in older housing or having a close relative with lead poisoning indicates a need to screen. In areas where more than 11% of the children have elevated lead levels or more than 26% of the housing was built before 1959 all children are screened. Screening is done at one year of age and then at least once more at age two. In Cleveland, the Head Start programs required yearly screening to age 5.

Treatment consists of chelation therapy. Most protocols don't recommend treatment for levels less than 45mcg/dl. For more specific information see The Harriet Lane Handbook, available through MDConsult (search for lead chelation).