The incidence of pediatric poisoning follows a biphasic curve, with 85% to 90% in children age 1 to 6 years and a second smaller peak of 10% to 15% of cases in adolescents. Most cases in children are unintentional ingestions of a single agent (frequently nontoxic household products). The most often reported pharmaceutical exposures in children <6 years of age include analgesics, cough and cold preparations, cardiovascular agents, topical preparations, sedative hypnotic agents, and antidepressants. Adolescent toxic ingestions usually involve intentional ingestion of multiple pharmaceutical agents in attempted self-harm.
The most important factor in successfully treating a patient with a toxicologic exposure is to recognize a toxicologic etiology in the undifferentiated patient. Poisoning must be considered in the differential diagnosis of multiple conditions, especially when a patient presents with cyanosis, shock, vomiting, diarrhea, hypothermia or hyperthermia, abnormal behavior, or altered mental status. A thorough history must be obtained with a focus on the identification of the toxin, timing, dosage, route, intent of ingestion, and symptom development since ingestion.
The patient, or his or her caretakers, may be able to directly identify the involved toxin because of a known exposure (eg, medications taken, intentional overdose attempt, substance abuse, exposure to occupational chemicals). Determining whether the exposure was intentional or not may aid in assessing the reliability of the history given by the patient. Regardless of intention, patients may or may not report accurate amounts, and it may be necessary to search through medication containers and count the number of remaining pills or measure approximate quantities of liquid. Comparison with the reported amount by the patient may reveal a discrepancy.
Prehospital health care workers may aid in identification of the toxin and information about dosage/route at the time of arrival in the emergency department (ED) with findings of containers or other evidence of possible toxins and can also provide information on any treatment and attempts at decontamination before hospital arrival.
It is important to also consider and investigate possible occult coingestions (eg, acetaminophen) in adolescents and multiple routes of exposure in all children, including dermal, rectal, ocular, parenteral, or transplacental. The route of exposure often affects the severity and time course of toxicity.
Determination of symptoms since ingestion will aid in recognition of toxidromes (see below) as well as determination of degree of toxicity. Attention must be paid to past medical history and comorbidities with a focus on the patient’s medications, including herbal supplements, dietary supplements, over-the-counter medications, and alternative medical therapies.
Samples of the substance may be available (eg, plants, mushrooms). For potential carbon monoxide poisoning (CO), the local fire department may also be notified to quantify the amount of CO in a building. A poison control center or product manufacturer should be contacted if the ingredients of a product are unknown. Review of drug and chemical databases (eg, Poisindex®) is also useful.
Consider child abuse in children younger than age 1 year in the setting of repeated ingestions, or if the child’s developmental level and skills preclude performance of the described events (eg, a child too young to open childproof containers).
Perform a thorough physical examination beginning with vital signs. Possible toxidromes (toxicologic syndromes that are characteristic signs and symptoms seen with certain poisons or classes of poisons) should be identified as these aid diagnosis and management of acutely ill patients, especially when a history of poisoning is lacking (see Table 17.2).
Figure 17.1 ▪ Household Products Frequently Ingested by Young Children.
Household cleaners, cosmetics, and plants are among the leading nonpharmaceutical agents ingested by children. Some of these products contain sodium hydroxide, alcohol, methyl salicylate (eg, Listerine), and sodium hypochlorite (eg, bleach). (Photo contributor: Ronak R. Shah, MD.)
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| A. Increased anion gap metabolic acidosis: | |
MUD PILES
| ACIDOSIS
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B. Anticholinergics:
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C. Cholinergics:DUMBELS
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D. Miosis: COPS
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E. Mydriasis: WASH
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F. Radiopaque substances: COCAINE
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G. Drugs or chemicals producing seizures: CAMPHOR BALLS
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TOXIDROMES (Examples of compounds categorized by their associated toxidromes):
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Laboratory studies should be performed, if clinically indicated, for diagnosis or to guide therapy (see specific chapters for agents and laboratory studies that may prove useful in management). These should include serum electrolytes, including glucose, blood urea nitrogen (BUN), and creatinine to determine renal function and calculate any anion gap. Obtaining serum osmolality will determine if substances causing an increased osmolal gap were ingested. These include ethanol, methanol, isopropyl alcohol, and ethylene glycol (osmolal gap = measured serum osmolality − calculated osmolality). Toxicology screens (either urine or serum) may occasionally help in determining occult coingestions; however, they are rarely helpful in the acute management of patients. These laboratory tests are generally used by consultants (eg, psychiatry) or admitting physicians to facilitate disposition and long-term management.
All patients with an intentional suicidal overdose should have serum acetaminophen and salicylate levels determined. All girls of childbearing age should have a pregnancy test performed.
Figure 17.2 ▪ Medications and Poisons Frequently Ingested by Adolescents.
Among the pharmaceutical agents that are intentionally ingested in the context of a suicide attempt by adolescents include analgesics, sedative hypnotics, tricyclic antidepressants, antihistamines, ethylene glycol, and windshield washer fluid (methanol). (Photo contributor: Ronak R. Shah, MD.)
If there is any gastric aspirate/vomitus, note appearance, pills, odor; test for occult blood in the stool.
Radiographic studies may be useful for management or confirmation of a diagnosis with a high index of suspicion, for example, iron. Chest radiographs may show pulmonary edema or aspiration pneumonitis consistent with hydrocarbon exposure. Abdominal radiographs may show radiopaque substances. However, it is important to note that absence of toxins generally considered to be radio-opaque does not exclude ingestion.
Proper external decontamination before entry into the ED is necessary to protect health care personnel and prevent contamination of the emergency department (ED). This may involve removal of all clothing and washing the skin.
All patients should have airway, breathing, and circulation (ABCs) stabilized based on abnormal vital signs before any diagnostic tests are performed. Focus on treating the patient, not the poison. Patients may have more than one type of exposure or ingestion, complicating the identification of distinct toxidromes. Consultations with the local medical toxicologist or regional poison control center may also be helpful.
Figure 17.3 ▪ Activated Charcoal Administration.
A 3-year-old child presented after accidentally drinking 4 ounces of Dimetapp liquid (grape flavor) 1 hour prior to arrival in the emergency department. He was completely asymptomatic. (A) As seen here, AC is poorly accepted by young children and often there is a battle between the hospital staff and the child over its administration. AC should not be routinely administered in the management of all poisoned patient. (B) A smiling face with a bottle full of activated charcoal given to this girl who accidentally ingested carbamazepine (sibling’s seizure medication). (Photo contributor: Binita R. Shah, MD.)
Figure 17.4 ▪ Sinus Bradycardia; Clonidine Toxicity.
A 3-year-old previously healthy child presented with lethargy and sinus bradycardia following accidental ingested his grandmother’s clonidine. His heart rate would increase to 120 bpm when stimulated, but would drop to 50 bpm when stimulation was withdrawn. (Photo contributor: Ronak R. Shah, MD.)
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Unresponsive patients may empirically be given intravenous (IV) thiamine 100 mg (in adolescents), followed by IV dextrose (1 g/kg) and IV naloxone (1–2 mg, may be repeated several times) and observed for a response. Patients with altered mental status should be evaluated for all causes of altered sensorium including nontoxicologic causes (see mnemonic COMATOSE PATIENT; Table 13-5).
Motor seizures are generally well-controlled by benzodiazepines. Anticonvulsants are rarely used in the treatment of toxin-induced seizures. If the toxic agent is known, seizures may be controlled with specific therapy (eg, pyridoxine for acute isoniazid toxicity).
GI decontamination should not routinely include syrup of ipecac or orogastric lavage. Orogastric lavage is indicated when there is a potentially life-threatening ingestion of a poison with no definitive antidote. The greatest benefit is most likely to be seen in a patient who presents within 60 minutes of ingestion. Patients presenting after 60 minutes could also benefit because of delayed gastric emptying. Contraindications include ingestion of caustics, hydrocarbons, and foreign bodies (FBs); bleeding diathesis; and an unprotected airway. Complications include aspiration pneumonia, GI perforation, laryngospasm, and emesis.
Decontamination with activated charcoal (AC) is indicated if a patient has ingested a potentially toxic amount of a poison that is known to be adsorbed by AC. AC does not adsorb acids, alkalis, lithium, iron (most metals), alcohols, or hydrocarbons. AC administration is likely to be most effective if begun within 60 minutes of ingestion, but may also be given after 60 minutes, especially if there is delayed gastric emptying, possible bezoar formation, and enterohepatic or enteroenteric circulation of the toxin. AC is given orally as a slurry in water or fruit juice (also by nasogastric or orogastric tube) and the usual single dose (children/adults) is 1 to 2 g/kg up to 50 g or 10:1 ratio of AC-drug is considered ideal. Multiple-dose AC (0.5–1 g/kg every 4–6 hours) should be considered if a patient has ingested a large quantity of agents that decreases gastric motility (eg, anticholinergics, enteric-coated preparations), theophylline, phenobarbital, carbamazepine, quinine, or dapsone. Patients should have good GI motility as evidenced by normal bowel sounds and passage of stool (ie, no evidence of GI obstruction). Contraindications include intestinal obstruction or perforation, altered sensorium (absent gag reflex/unprotected airway), and caustics (may obscure endoscopic visualization of gastroesophageal injury). Complications include pulmonary aspiration, intestinal obstruction, constipation, and development of charcoal bezoars. If desorption of ingestant from AC is a possibility, a single dose of cathartic may be given to an adolescent who has ingested a large amount of drugs. Administration of a cathartic alone has no role as a method of gut decontamination. Routine use of a cathartic with AC is not recommended. Complications include nausea, vomiting, diarrhea, abdominal pain, and dehydration with electrolyte disturbances (following multiple doses which should not be repeatedly given for >24 hours). Contraindications include absent bowel sounds, ingestion of caustics, or GI irritants.
Whole bowel irrigation (WBI) may be considered in patients who have ingested FBs, packets containing toxins, iron, and sustained-release or enteric-coated tablets. WBI should not be routinely used in the management of the poisoned patient. WBI is commonly performed by the continuous administration of a bowel-cleansing solution containing polyethylene glycol electrolyte solution (PEG ELS) via an oral or nasogastric tube. It is given at a rate of 0.5 L/h until the rectal effluent is clear. In older children and adolescents, it should be given at a rate of 1 to 2 L/h. No significant adverse effects of prolonged WBI with PEG ELS have been demonstrated.
Certain toxins can be managed with the administration of toxin-specific antidotes. Prophylactic use of antidotes is not recommended because of potentially serious side effects with inappropriate administration. Life-threatening poisonings such as opioids, cholinergics, CAs, methemoglobinemia, CO, and cyanide require simultaneous use of an antidote with the initial stabilization of vital signs.
Consider hospital admission if the patient manifests significant toxicity, suicidal intent, identification of poison is unclear, ingested substance has delayed toxicity, or patients that will require further management such as urinary alkalinization (eg, salicylates, phenobarbital), hemodialysis (eg, methanol, ethylene glycol, salicylates, lithium), or whole-bowel irrigation (eg, iron). Consider ICU admission for patients who manifest significant toxicity, or those in whom management will require rigorous nursing care.
Consider discharge to home all patients with unintentional ingestion if the patient (and/or guardians) has received appropriate counseling and social service intervention; the product or drug has been determined to be benign, the amount ingested is less than the smallest amount known to produce toxicity (note that the history is often unreliable), the patient has no signs of toxicity since the time of ingestion, the time elapsed since the ingestion is greater than the longest interval known between ingestion and peak toxicity and in cases where child abuse/neglect is not considered likely.
The most important factor in successfully treating a patient with a toxicologic exposure is to recognize that there is a toxicologic etiology of the patient’s condition.
GI decontamination has not been shown to improve patient outcome; however removal of toxin by GI decontamination before adsorption may prevent or mitigate toxicity. It is critical to ask “Has the child ingested a potentially toxic dose?” and “What is the time since ingestion?”
Gastric lavage should not be considered unless the patient has ingested a potentially life-threatening amount of a poison and toxin is expected to be remaining in the stomach.
AC should only be considered if a patient has ingested a potentially toxic amount of a poison that is known to be adsorbed by AC. A nasogastric tube should not be placed for the sole purpose of AC administration.
WBI should be considered only in patients presenting with potentially toxic ingestion of iron, lead, packets of illicit drugs, sustained-release or enteric-coated tablets.
Acetaminophen (APAP) overdose can lead to hepatic necrosis, fulminant hepatic failure, and death. The therapeutic dose is 10 to 15 mg/kg with maximum dosage of 80 mg/kg/d. Acute toxicity usually occurs at doses above >150 mg/kg.
Clinical presentation is dependent on amount of time since ingestion and patients may be completely asymptomatic initially. After 24 hours, patients may also present with Gastrointestinal (GI) symptoms of nausea, vomiting, and malaise. After 24 to 72 hours, GI symptoms may lessen, during which time hepatic damage is occurring. Patients may have right upper quadrant pain or tenderness. After 72 to 96 hours, anorexia, nausea, and vomiting worsen. Progression to fulminant hepatic failure may occur by 4 to 5 days post ingestion.
The differential diagnosis of hepatotoxicity includes viral hepatitis, other drug- or toxin-induced hepatitis (eg, isoniazid, carbamazepine, Amanita phalloides mushroom, phenytoin), alcoholic hepatitis, hepatobiliary disease, Reye’s syndrome, ischemic hepatitis (usually following a prolonged period of hypotension).
Figure 17.6 ▪ Hepatotoxicity; Acetaminophen (APAP) Overdose.
This 15-year-old female presented to emergency department 16 hours postingestion of 32.5 g of APAP (100 tablets of 325 mg each). Her serum APAP value of 62 μg/mL (plotted on nomogram; see Figure 17.7) was in “Potential for Toxicity” area. Therapy with oral N–acetylcysteine (NAC) was initiated. Her serum aspartate aminotransferase (AST) aminotransferase level (AST) was initially mildly elevated to 368 IU/L, and rose to a peak of 7600 IU/L with development of jaundice and coagulopathy (INR of 2.5) over next 72 hours. Her AST level normalized after day 5 with a full recovery. (Photo contributor: Ronak R. Shah, MD.)
Evaluation should include a careful history with particular attention to comorbidities that may predispose the patient to development of hepatotoxicity and formulations that decrease GI motility (eg, combination preparations containing anticholinergic agents such as diphenhydramine or opioids such as codeine). Laboratory tests should include serum acetaminophen concentration, complete blood count (CBC), glucose, electrolytes, BUN, creatinine, phosphate, prothrombin time, International Normalized Ratio (INR), serum transaminases (ALT, AST), and serum bilirubin. Serum lactate levels can be obtained and are believed to contribute to the elevated anion gap seen early in cases of severe APAP toxicity. It has been suggested that elevated serum phosphate values can be an early predictor of outcome in severe APAP-induced hepatotoxicity. Once a serum acetaminophen level has been obtained 4 hours post ingestion, the Rumack-Matthew nomogram should be applied to determine necessity for antidotal treatment.
GI decontamination is primarily achieved through the administration of AC (1–2 g/kg orally). Antidotal therapy with N–acetylcysteine (NAC) can be empirically administered if >150 mg/kg of APAP has been ingested and the patient presents soon after ingestion via IV as three doses over 21 hours. The initial loading dose is 150 mg/kg diluted in 3 mL/kg of D5 ½ NS, infused over 60 minutes. The second dose is 50 mg/kg diluted in 7 mL of D5 ½ NS infused over then subsequent 4 hours. The third dose of 100 mg/kg diluted in 14 mL of D5 ½ NS, then infused over 16 hours. NAC dosing needs to be adjusted for young children < 20 kg because of hyperosmolarity.
Figure 17.7 ▪ Acetaminophen Toxicity Nomogram (Rumack-Matthew Nomogram).
The nomogram shows the plasma acetaminophen concentration versus time after acetaminophen ingestion. (Reprinted with permission from Management of Acetaminophen Overdose, McNeil Products 1986.)
Risk of toxicity is best evaluated by comparing serum APAP concentration to the time of ingestion.
Measure serum APAP concentrations after a single, acute overdose of an immediate-release preparation between 4 and 24 hours after ingestion, and plot results on the nomogram to determine the need for antidotal therapy.
Serum levels drawn before 4 hours may not represent peak concentrations and still should be checked at 4 hours postingestion. The optimal level is drawn at 4 hours after ingestion or as soon after 4 hours as possible. (The 4-hour level is not necessarily the peak. In fact, many people who overdose probably have much higher APAP concentrations prior to 4 hours.)
Values that fall above the “upper line or original line” in the “Potential for Toxicity” area on the nomogram, represent a 60% incidence of severe hepatotoxicity and 5% mortality, if left untreated.
“Lower line” or “broken line” that runs parallel to the upper line has been arbitrarily lowered by 25% (in order to add greater sensitivity), and represents APAP acetaminophen concentration considered to be toxic in the United States. (The “upper line” is still used in the United Kingdom and other locations.) Values that fall below the “lower line” are associated with “Toxicity Unlikely” and an absence of mortality.
There is currently insufficient evidence to support using the nomogram to assess probability of toxicity from sustained-release preparations of acetaminophen. However, if a 4-hour level is in the “Potential for Toxicity” area, treatment should be implemented. Also, this is a rare setting in which a second APAP level may be drawn 4 to 6 hours later, if the initial level is in the “Toxicity Unlikely” area. If the second level is in the “Potential for Toxicity” area, treatment should be implemented.
The nomogram is also not useful if the time of ingestion is uncertain, if ingestion occurred more than 24 hours before presentation, or if repeated ingestion has occurred.
All patients who have a toxic APAP level require a full course of NAC therapy and should be admitted. Patients with signs and/or symptoms of significant hepatotoxicity or other end organ toxicity, should be admitted to the ICU. Patients presenting after 24 hours following an overdose and with evidence of hepatotoxicity should be started on IV NAC immediately. Patients should be admitted for supportive care.
Contact the poison control center for all patients with APAP toxicity, patients who have developed signs and symptoms of hepatotoxicity, patients presenting with ingestion of extended-release preparations, or those presenting more than 24 hours post ingestion. Indications for transfer to a liver transplantation center in patients who develop hepatotoxicity include arterial pH <7.3 after fluid resuscitation, grade III or IV encephalopathy, creatinine >3.3 mg/dL, or INR >2 to 3. Psychiatry should be consulted for all cases of self-harm.
Acetaminophen is the most widely used analgesic-antipyretic in the United States and accounts for more overdoses and overdose fatalities per year than any other pharmaceutical agent.
All patients presenting with an intentional overdose of medication should have a serum APAP concentration checked.
Severe acetaminophen toxicity may produce fulminant hepatic failure 3 to 5 days post ingestion.
A 10-kg infant can be poisoned by a 15-mL bottle of 80 mg/0.8 mL preparation (15 mL contains 1500 mg of APAP, or 150 mg/kg).
The most common salicylate therapeutically used is acetylsalicylic acid (ASA; aspirin). Many over-the-counter products contain salicylates, including Ben-Gay® and Pepto-Bismol®, as well as the highly concentrated salicylate product, oil of wintergreen. Toxicity generally occurs at doses of >150 mg/kg, with >300 mg/kg considered as potentially lethal. Ingested ASA tablets may occasionally form concretions (bezoars) or cause pylorospasm, resulting in delayed and prolonged absorption. Enteric-coated preparations may also result in delayed or prolonged absorption.
Clinical findings of salicylate toxicity include nausea, vomiting, epigastric pain, and possible hematemesis. Hyperpnea and tachypnea may lead to respiratory alkalosis and noncardiogenic pulmonary edema. Also known as acute lung injury (ALI). Patients may complain of tinnitus, deafness, delirium, seizures, or coma. Anion gap metabolic acidosis may develop. Increased sweating, vomiting, and tachypnea may lead to dehydration, hypernatremia, hypokalemia, or hypocalcemia. Hypoglycemia may also occur.
Differential diagnosis of other causes of increased anion gap metabolic acidosis should be considered (see Table 17.2). Other etiologies must also be considered for hypoglycemia, gastroenteritis, and acute respiratory distress syndrome (ARDS).
Take a careful history with attention to amount, time of ingestion, intent, possibility of coingestants, and type of preparation (ie, immediate-release vs enteric-coated). Laboratory tests should include CBC, serum electrolytes, glucose, BUN, creatinine, arterial blood gases (ABG), liver transaminases, coagulation studies, serum calcium, and ketone concentrations.
Figure 17.9 ▪ Oil of Wintergreen.
This sweet-smelling product contains 100% methyl salicylate. One teaspoon of contains 7000 mg of methyl salicylate (equivalent to 21.5 tablets of aspirin, each containing 325 mg). In a 10-kg child, the minimum toxic salicylate dose of about 150 mg/kg body weight can almost be achieved with ingestion of 1 mL (1 mL = 1400 mg of methyl salicylate = 140 mg/kg for a 10-kg child). As little as 1.5 mL (2100 mg) can kill a small child; thus, ingestion of this preparation is potentially very dangerous. (Photo contributor: Robert J. Hoffman, MD.)
A serum salicylate level should be obtained on presentation and every 2 hours thereafter for the first 4 to 8 hours. If the salicylate level is >30 mg/dL, obtain serial concentrations hourly until a consistent decrease is noted. Determine urinary pH in all patients and obtain a urine pregnancy test in girls of reproductive age. Abdominal radiographs may demonstrate enteric-coated tablets, concretions, or bezoars. A chest radiograph may show acute lung injury.
All patients should be fluid resuscitated with IV crystalloid solution and electrolyte abnormalities corrected (eg, add potassium supplementation to IV fluids after urine output is established). In the case of GI bleeding, administer blood products such as packed red blood cells.
Treat patients with large ingestions, metabolic acidosis, symptoms of severe toxicity, or serum salicylate level >70 mg/dL with an initial sodium bicarbonate bolus of 1 to 2 mEq/kg followed by a continuous infusion made from 3 ampules (44–50 mEq each) of NaHCO3 in 1 L D5W and infused at 1.5 to 2 times maintenance fluid rate to alkalinize the urine (goal of urinary pH of 7.5–8.0) unless there is encephalopathy, cerebral edema, pulmonary edema, blood pH >7.55, renal failure, or serum sodium >150 mEq/L. Measure urinary pH hourly and titrate the NaHCO3 infusion accordingly. Serum potassium must be closely monitored and replaced as necessary.
Consider emergent hemodialysis for patients who are severely poisoned, that is, hemodynamically unstable, comatose, or seizing; have pulmonary edema, cerebral edema, or oliguric renal failure; or who have rising salicylate levels despite GI decontamination and proper urinary alkalinization.
Consider GI decontamination with AC after ingestion >150 mg/kg. Multiple-dose AC (0.5–1 g/kg) may be given for an additional 1 to 2 doses. Consider whole bowel irrigation if concretions are seen on abdominal x-ray or ingestion of enteric-coated preparations. Gastric endoscopy may rarely be required for bezoar removal.
Asymptomatic patients observed for 4 to 6 hours, with nontoxic serum salicylate levels, and no significant acid-base abnormalities may be medically cleared. Consult the local medical toxicologist, regional poison control center, nephrology (hemodialysis), psychiatry (suicidal intent), and rarely gastroenterology (possible endoscopic removal of aspirin bezoars) as indicated.
Admit symptomatic patients for repeat doses of AC, urinary alkalinization, observation, hemodialysis, and supportive care.
Treat based on clinical and metabolic abnormalities not absolute serum salicylate concentration (unless very high [>100 mg/dL]).
Salicylate toxicity initially causes a respiratory alkalosis that progresses to a metabolic acidosis with increased anion gap.
Young children may initially present without apparent respiratory alkalosis. Adolescents and adults develop respiratory alkalosis early after an overdose.
Endotracheal intubation may be potentially harmful because of transient apnea and respiratory acidosis. Adjust ventilator settings to account for the patient’s increased minute ventilation prior to intubation as well. Failure to manage this aspect of a patient’s care may result in abrupt and rapid demise.
Figure 17.10 ▪ Positive Ferric Chloride Reaction with Salicylate-Containing Topical Cream.
(A) A 14-month-old Chinese boy was found unconscious with vomitus on floor of his grandmother’s bedroom. An open tube of a topical rubefacient was also in the room, and the parents reported that the vomitus smelled like the rubefacient (a very strong, pleasant smell of wintergreen or mint). A sample of the rubefacient balm was available (most of the package label was worn off, and the remaining label, printed in Chinese, did not identify the ingredients). (B) Positive ferric chloride reaction. Application of ferric chloride to the product yielded a purple color (positive ferric chloride test). In its natural state, ferric chloride is translucent brown, and upon reaction with salicylate it produces a purple hue. (Photo contributor: Robert J. Hoffman, MD.)
Iron is commonly available as ferrous fumarate, ferrous gluconate, and ferrous sulfate, each containing 33%, 12%, and 20% elemental iron, respectively. Children’s multivitamin tablets contain 10 to 18 mg elemental iron per tablet; adult multivitamins contain up to 65 mg elemental iron per tablet. To determine if the amount ingested is potentially toxic, determine the elemental iron ingested. Signs of toxicity usually begin with ingestions >20 mg/kg.
There are 5 stages of iron toxicity commonly described. In stage I, the first 12 hours after exposure, profuse GI symptoms occur including abdominal pain, nausea, vomiting, and diarrhea (occasionally bloody). In stage II, 6 to 24 hours after ingestion, GI symptoms improve, though patients may still be ill and develop metabolic acidosis and/or hypovolemia. In stage III, 1 to 3 days post ingestion, multiorgan failure develops. Patients may develop altered mental status, renal failure, respiratory failure, and cardiovascular collapse. During stage IV, 2 to 5 days post ingestion, hepatic failure is characterized by coagulopathy, and elevations in serum transaminases, ammonia and bilirubin, as well as hypoglycemia. In stage V, some patients develop gastric outlet and small bowel obstruction 1 to 2 weeks later after overdose.
Figure 17.11 ▪ Radiopaque Tablets in Iron Poisoning.
A flat plate of abdomen shows presence of radiopaque tablets (left panel) in a 2-year-old child presenting about 1 hour after ingestion of a number of ferrous sulfate tablets. Gastric lavage was performed (whole-bowel irrigation was not used for GI decontamination of such cases in past). The right panel, radiograph taken shortly after lavage, shows removal of almost all of the tablets. Currently, whole-bowel irrigation would be the method of choice for GI decontamination in such patients. Identification of radiopaque tablets confirms diagnosis in a patient with a suspected iron overdose, and helps guide gastric decontamination. (Photo contributor: James G. Linakis, MD.)
Figure 17.12 ▪ Radiopaque Tablets in Iron Poisoning.
Single frontal view of the abdomen shows multiple ingested radio-opaque iron pills. This 17-year-old female with altered mental status was found by her family with a bottle of vodka and mumbling “pills.” The patient was prescribed iron supplements after a spontaneous miscarriage 2 months ago. The patient was obtunded and intubated for airway protection. After this kidney, ureters, and bladder (KUB) radiograph, whole bowel irrigation was initiated via nasogastric tube. The patient’s serum iron rose as high as 350 μg/dL, but chelation therapy was initiated with deferoxamine because of an anion gap of 24, with a serum pH of 7.1 and her altered mental status. (Photo contributor: Ronak R. Shah, MD.)
Differential diagnosis includes acute GI injury (eg, poisoning by acetaminophen, salicylates, mushrooms, heavy metals, theophylline, and nonsteroidal anti-inflammatory drugs [NSAIDs]) and acute gastroenteritis (eg, Salmonella, Shigella, viral). Increased anion gap metabolic acidosis from other etiologies should be considered (see Table 17.2). Consider other causes of acute hepatitis or acute surgical abdomen.
Obtain a thorough history with careful attention to amount, time of ingestion, intent, possibility of coingestants, and specific type of preparation (eg, ferrous sulfate, fumarate). Laboratory analysis should include CBC (may show anemia or leukocytosis), ABG (metabolic acidosis), electrolytes (increased anion gap, hyperglycemia or hypoglycemia), prothrombin time (PT)/partial thromboplastin time (PTT) (coagulopathy), liver function tests, serum lactate, and a type and screen in the event of GI hemorrhage. Obtain serum iron levels. Use abdominal x-rays to check for presence of radio-opaque pills and GI perforation.
Figure 17.13 ▪ Vin Rose Urine; Iron Poisoning.
An example of the progression of coloration of vin rose urine (from excreted ferrioxamine complex) over 15 hours of chelation with deferoxamine is shown. Deferoxamine chelates free iron (but not iron present in transferrin, hemoglobin, hemosiderin or ferritin). (Reproduced with permission from Strange GR, Ahrens WR, Schafermeyer RW et al: Pediatric Emergency Medicine, 3rd ed. Mc-Graw-Hill Co., New York, 2009.)
Consider gastric lavage if pill fragments are visualized on the kidney, ureters, and bladder (KUB) radiograph. AC does not adsorb iron and should not be used. If pills are seen on radiography, whole bowel irrigation with Go-Lytely® (25 mL/kg/h up to maximum 1–2 L/h) should be initiated. Consider endoscopic removal of adherent particles or bezoars.
For severely ill patients, initiate chelation therapy with deferoxamine mesylate as soon as possible. Indications for chelation therapy include severe GI symptoms, hypotension, shock, metabolic acidosis, or serum iron concentration >500 μg/dL. Deferoxamine should be slowly infused over 20 minutes at a dose of up to 15 mg/kg/h via continuous infusion. Infusion should be started at lower doses and titrated up if patient’s clinical course does not improve or titrated down if patient develops hypotension or ARDS. Monitor blood pressure; if hypotension occurs, decrease the infusion rate or temporarily stop the infusion.
Consult with the local medical toxicologist or regional poison control center, psychiatry and with gastroenterology as needed.
Asymptomatic patients may be discharged 6 hours postingestion provided there are no tablets seen on abdominal radiography, the serum iron level is <500 μg/mL, and psychiatry consultation has been provided, if indicated.
All other patients should be admitted to the hospital. Consider ICU admission for those with shock, lethargy, GI bleed, or metabolic acidosis.
Do not induce emesis; iron toxicity-induced GI irritation may result.
Do not use declining serum iron concentrations as a sign of clinical improvement or response to therapy as this may reflect iron uptake into cells.
Serum iron concentration is unreliable in patients receiving deferoxamine.
Antidotal treatment should not be delayed while awaiting serum iron concentrations or other laboratory tests in patients who are severely ill.
Opioids are found in many forms including morphine, meperidine, codeine, oxycodone, methadone, hydromorphone, propoxyphene, and fentanyl as well as street drugs such as heroin. Opioid use is ubiquitous, thus, opioid toxicity is a common occurrence in the emergency department. Less common scenarios are “body packing” and “body stuffing.” “Body packing” is intentional transport of opioids inside a body cavity and is accomplished via ingestion of drug packets wrapped in condoms, latex, or tape. Generally, packets have multiple layers to prevent leakage. “Body stuffing” implies haphazard ingestion of contraband and is usually without layers or intent to prevent leakage.
Therapeutic and toxic doses vary, as does individual tolerance. Toxicity may be affected by coingestants, especially those that cause central nervous system (CNS) depression (eg, alcohol, benzodiazepines etc).
Opioid toxicity is characterized by CNS depression, miosis, and respiratory depression. Other CNS signs may include seizures and coma. GI involvement includes nausea, vomiting, and constipation. Patients may present with hypotension or bradycardia. In addition to respiratory depression, patients may develop pulmonary edema (acute lung injury).
Differential diagnosis includes altered mental status (see mnemonic COMATOSE PATIENT, Table 13.5) and miosis from other etiologies.
Obtain a thorough history with careful attention to amount, time of ingestion, intent, and possibility of coingestants. Laboratory analysis is not typically needed unless there is concern for other coingestants. ABG may be useful in patients with hypoxia or hypoventilation. Chest x-ray may be performed to evaluate for aspiration or acute lung injury.
AC adsorbs orally ingested opioids and can be used for GI decontamination. Consider multidose AC for body packers. Use whole bowel irrigation with Go-Lytely® (25 mL/kg/h up to maximum 1–2 L/h) for asymptomatic body packers.
| Opioids | Sedative-hypnotics | |
| Vital signs | Bradypnea, bradycardia, hypotension, hypothermia | Bradypnea, bradycardia, hypotension, hypothermia |
| Pupils | Miosis (except meperidine) | Mydriasis, miosis (early) |
| CNS | Lethargy to coma | Coma, nystagmus, ataxia |
| Other | Acute lung injury, track marks | Bullae |
| Antidote | Naloxone | Flumazenil (for benzodiazepine only) |
Airway and respiratory support are essential. Naloxone causes immediate reversal of CNS and cardiopulmonary depression and can be given IV, intramuscularly (IM), subcutaneously (SC), and sublingually. In children, the initial dose of naloxone is 0.01 mg/kg IV and may be repeated, up to a total of 10 mg. Failure to respond to 10 mg of naloxone excludes opioids as the sole cause of respiratory depression. Judicious use of naloxone is not associated with significant side effects except acute opioid withdrawal, which is generally not acutely life-threatening. However, in opioid-dependent neonates, acute opioid withdrawal may be associated with significant toxicity including seizures.
Figure 17.16 ▪ Skin Popping.
This habitual drug user bears the scars of his trade. The large erosions in his arm are due to “skin popping,” which is typically used for cocaine or heroine. It is when the user injects the drug directly under the skin instead of into a vein. This way it lasts longer and the user does not have to find a vein which often is difficult. (Photo contributor: Mark Silverberg, MD.)
Patients with prolonged duration of symptoms or severe symptoms should be admitted. Consider admission to an ICU for continuous monitoring and additional doses of naloxone as indicated for patients with persistent altered mental status, recurrent respiratory depression, hypoxia, or hypotension. Consider admission for children under 12 years old. Older patients may be discharged from the ED if they are asymptomatic after 6 hours of observation and have been evaluated by psychiatry (if indicated).
Consult medical toxicology, poison control center, psychiatry (intentional ingestion), and, for body packers, gastroenterologist and/or surgery.
Naloxone is generally effective for 30 to 60 minutes; most ingested opioids exert their effects for a longer time. Patients should be observed for more than 90 minutes; in case of relapse, naloxone may need to be readministered.
Children may have unusual sensitivity to opioids and can display signs of toxicity at therapeutic doses.
Maintain a high index of suspicion for aspirin and acetaminophen, which are often present in combination with opioids.
For chronic opioid users, start with small doses of naloxone for diagnostic and therapeutic purposes to decrease the likelihood of acute withdrawal. Excessive naloxone administration may result in withdrawal symptoms refractory to supportive care.
Body packers may place packets containing contraband in the ears, vagina, or rectum. Careful inspection of all body cavities is warranted.
Opioid toxicity due to synthetic opioids (eg, fentanyl) may require higher doses of naloxone.
Cocaine is most often used via nasal insufflation and intravenously or in its “freebase” or “crack” form smoked and inhaled through the lungs. Inhalational and IV routes have peak effect within 5 minutes, while insufflation produces a peak in 20 minutes. Although short-lived, rapid, intense euphoria is the usual impetus for recreational cocaine use.
Cocaine causes multisystem symptomats including tachycardia, hyperthermia, and hypertension. Head/neck examination may reveal mydriasis or nasal septal perforation. Cardiac effects include acute myocardial ischemia, aortic dissection, fatal dysrhythmias, or cardiac arrest. Chronic use may lead to congestive heart failure, myocarditis, or dilated cardiomyopathy. Pulmonary signs include wheezing pneumothorax, pneumomediastinum, or pulmonary edema. Bowel ischemia and infarction may be caused by splanchnic vasospasm. Patients may develop acute renal failure because of renal infarction or rhabdomyolysis. Neurologic effects include agitation, seizures, intracerebral hemorrhage, or infarction. Acute cocaine toxicity can be indistinguishable from acute psychiatric diseases because of the appearance of euphoria, agitation, or mania.
Cocaine washout syndrome refers to persistent lethargy and altered mental status following repeated use over a short period caused by depletion of CNS catecholamines. This may manifest as coma. The patient’s condition usually improves over several hours with supportive care.
Differential includes other stimulants including amphetamines, oral decongestants, thyroid hormone, β-adrenergic agents, ergot alkaloids, and monoamine oxidase (MAO) inhibitor toxicity. Neuroleptic malignant syndrome, malignant hyperthermia, and serotonin syndrome may present similarly with muscular rigidity, hyperthermia, and altered mental status. Nontoxicologic etiologies in the differential include hypoglycemia, pheochromocytoma, hyperthyroidism, alcohol or sedative-hypnotic withdrawal, or acute psychosis.
Obtain a thorough history with careful attention to amount, time of ingestion, intent, and possibility of coingestants. CBC may demonstrate a leukocytosis. Use serum chemistries, BUN, Cr, and glucose to evaluate for alternative causes of altered mental status or seizures and to assess for dehydration and renal function. Obtain an ECG and chest x-ray in any patient with chest pain. Abdominal radiographs may help evaluate for body packing/stuffing. Brain CT may demonstrate intracerebral hemorrhage or infarction. Exclude subarachnoid hemorrhage by lumbar puncture. Creatine kinase may be elevated with rhabdomyolysis. Serum transaminases may be elevated and patients may develop a coagulopathy in the setting of hyperthermia. Serum troponin may be elevated if patient develops myocardial ischemia or infarction. Obtain serum aspirin, acetaminophen, and urine drug screens to evaluate for coingestants.
Figure 17.17 ▪ Pulmonary Complication Related to Crack Cocaine Inhalation.
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