D. Adam Algren
LEAD
EPIDEMIOLOGY
Lead is the most common chronic metal poisoning. Both ingestion and inhalation can result in clinical lead toxicity.
PATHOPHYSIOLOGY
Lead toxicity results in injury to multiple organ systems but primarily involves the nervous, cardiovascular, hematologic, and renal systems.
Central nervous system (CNS) neuronal injury results in cerebral edema and increased intracranial pressure. Lead toxicity may also produce peripheral neuropathies.
Lead interferes with porphyrin metabolism and heme synthesis causing anemia.
CLINICAL FEATURES
Table 116-1 lists the common signs and symptoms of lead poisoning by organ system.
TABLE 116-1 Common Manifestations of Lead Poisoning
DIAGNOSIS AND DIFFERENTIAL
Though an elevated serum lead level (>10 micrograms/dL) confirms the diagnosis, results are often not immediately available.
Radiopaque material may be present in the gastrointestinal (GI) tract following acute ingestion. With chronic exposure, children may develop horizontal metaphyseal bands in long bones, especially involving the knee (“lead lines”).
Other laboratory findings suggestive of lead poisoning include anemia with basophilic stippling of erythrocytes, hemolytic anemia, nephritis, and/or hepatitis.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Consider whole-bowel irrigation with polyethylene glycol solution for lead ingestion, especially when radiopaque material is visible on a radiograph. The adult rate of instillation is 1500 to 2000 mL/h, and the pediatric rate of instillation is 500 to 1000 mL/h.
Guidelines for chelation therapy are presented in Table 116-2.
Patients requiring parenteral chelation therapy or whose only option is to return to the environment producing the lead exposure should be admitted to the hospital.
TABLE 116-2 Guidelines for Chelation Therapy in Lead-Poisoned Patients*
ARSENIC
EPIDEMIOLOGY
Arsenic is found in agricultural chemicals, insecticides, contaminated well water, and mining/smelting operations.
Exposure to inorganic arsenic can result in significant toxicity whereas organic arsenic is minimally toxic.
PATHOPHYSIOLOGY
Arsenic inhibits multiple enzymes and uncouples oxidative phosphorylation with effects on multiple organ systems.
CLINICAL FEATURES
Clinical features of arsenic toxicity are summarized in Table 116-3.
Chronic poisoning causes stocking glove peripheral neuropathies, hyperkeratosis, peripheral vascular disease, malaise, myalgia, abdominal pain, memory loss, and personality changes.
TABLE 116-3 Clinical Features of Arsenic Toxicity
DIAGNOSIS AND DIFFERENTIAL
Consider arsenic poisoning in patients with severe vomiting and diarrhea causing hypotension.
Other diagnoses to consider include septic shock, encephalopathy, Guillain–Barre syndrome, Addison’s disease, hypo- and hyperthyroidism, porphyria, and other metal poisonings.
Acutely, the electrocardiogram (ECG) may demonstrate a prolonged QT interval; abdominal radiographs may reveal radiopaque arsenic.
Transverse white lines of the nails (Mees’ lines) may occur 4 to 6 weeks following ingestion.
Definitive diagnosis depends on 24-hour urine arsenic levels.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Treat hypotension with aggressive volume resuscitation with isotonic crystalloid, and vasopressors for fluid-refractory shock.
Manage dysrhythmias according to Advanced Cardiac Life Support (ACLS) protocols, but avoid drugs that prolong the QT interval (class IA, IC, and III agents).
Consider gastric lavage if the patient presents early following acute ingestion. Whole-bowel irrigation with polyethylene glycol solution is indicated for patients in whom abdominal radiographs demonstrate radiopaque material.
Guidelines for inpatient chelation therapy with dimercaprol and outpatient treatment of stable patients with succimer are presented in Table 116-4.
Hospitalization is recommended for patients with severe symptoms, those requiring parenteral chelation, and those with suicidal or homicidal intent.
TABLE 116-4 Guidelines for Chelation Therapy in Arsenic-Poisoned Patients
MERCURY
EPIDEMIOLOGY
Elemental mercury is present in older thermometers and exposures occur via inhalation, especially when vacuumed or heated. Ingestion of elemental mercury typically does not result in toxicity.
Organic mercury is used in wood preservatives, fungicides, pesticides, and is also found in contaminated seafood. Absorption primarily occurs via the GI tract.
PATHOPHYSIOLOGY
Similar to other heavy metals, mercury binds to sulfhydryl groups and affects multiple enzymes and organ systems.
CLINICAL FEATURES
Inhalation of elemental mercury can result in fever, cough, dyspnea, vomiting, and headache that can progress to acute respiratory failure.
Ingestion of inorganic mercury salts results in corrosive injury to the GI tract: vomiting, diarrhea, abdominal pain, and GI bleeding may occur. Acute renal failure often accompanies significant toxicity.
Chronic inorganic mercury toxicity is associated with multiple neurologic effects including tremor, fatigue, depression, and headaches. Erethism refers the constellation of emotional lability, shyness, irritability, insomnia, and blushing. Acrodynia (“pink disease”) is characterized by a generalized rash, edema/erythema of the palms/soles, excessive sweating, fever, irritability, and muscle weakness.
Organic mercury poisoning is usually seen with chronic ingestion and is associated with headache, tremor, fatigue, ataxia, blindness, muscle spasticity, and dementia.
DIAGNOSIS AND DIFFERENTIAL
A history of exposure or physical findings of erethism or acrodynia may suggest the diagnosis.
An elevated 24-hour urine mercury level confirms the diagnosis in cases of elemental and inorganic mercury exposures. An elevated whole blood mercury level is necessary to confirm poisoning from organic mercury compounds.
The differential diagnosis of symptoms caused by mercury poisoning is extensive and includes other causes of encephalopathy, tremor, gastroenteritis, and acute renal failure.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Supportive care and removal from exposure are the most important aspects in managing mercury poisoning. Intubation may be necessary in cases of respiratory failure associated with elemental mercury vapor exposure.
Chelation is most effective in cases of elemental and inorganic mercury poisoning and should be considered in cases with significant symptoms (Table 116-5). Parenteral chelation is contraindicated in cases of organic mercury poisoning due to the potential to exacerbate CNS symptoms.
TABLE 116-5 Guidelines for Chelation Therapy in Mercury-Poisoned Patients
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 197, “Metals and Metalloids,” by Heather Long and Lewis S. Nelson.