Lead Toxicity Clinical Presentation
- Author: Pranay Kathuria, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS more...
The clinical presentation varies widely, depending upon the age at exposure, the amount of exposure, and the duration of exposure. Organic lead, because of its higher lipid solubility, causes greater toxicity and affects the neurological system predominantly. Younger patients tend to be affected more than older children and adults, because lead is absorbed from the gastrointestinal (GI) tract of children more effectively than from that of adults.
The neurological system is most vulnerable to lead toxicity. Children are more likely to develop central nervous system toxicity while the peripheral nervous system is more often affected in adults.
The manifestations in children include temperamental lability, irritability, behavioral changes, hyperactivity or decreased activity, loss of developmental milestones and language delay. Lower IQ and ADHD like symptoms may be present. Severe toxicity can cause delirium, convulsions and encephalopathy. Depression and anxiety are more common in patients. Lead causes demyelination of the peripheral nervous system and the abnormalities mostly affect the extensor motor nerves and may result in hand and foot drop.
Anemia may develop with lead poisoning due to impaired synthesis of heme, hemolysis of red cells and shortened red cell survival. Anemia is usually mild and is more commonly seen in adults.
Patients may develop lead colic, nausea, vomiting and anorexia. Occasionally, some patients with acute poisoning can develop severe diarrhea and dehydration.
Acute nephropathy manifests with tubular defects, which may include phosphaturia, glucosuria and amino aciduria. This combination of tubular defects is referred to a Fanconi’s syndrome. Chronic lead nephropathy is characterized histologically by chronic interstitial nephritis and is frequently associated with hypertension and gout. Furthermore, lead exposure, at much lower levels than those causing lead nephropathy, acts as a cofactor with more established renal risk factors to increase the risk of chronic kidney disease and the rate of progression. Adverse renal effects have been reported at mean blood lead levels of less than 5 mcg/dL. Cumulative lead dose has also been associated with worse renal function.
Lead exposure has been associated with the development of hypertension. The development of hypertension may be secondary to oxidative stress or an association with chronic nephropathy. Studies have also documented an association between lead toxicity and cardiovascular disease and stroke.
In men, lead causes a reduction in libido, abnormal spermatogenesis, chromosomal damage and infertility. Women experience an increase in the incidence of stillbirth, miscarriage, pregnancy induced hypertension and prematurity.
No pathognomonic symptoms exist. When symptoms do occur, they are typically nonspecific. Consider lead poisoning whenever a small child presents with peculiar symptoms that do not match any particular disease entity. Common nonspecific symptoms include the following:
Temperamental lability, irritability, behavioral changes
Hyperactivity or decreased activity
Loss of developmental milestones, language delay
More significant exposure to lead may cause symptoms in children that are more likely to lead to a medical evaluation. They are as follows:
Abdominal pain, loss of appetite, vomiting, constipation
Headache, ataxia, somnolence
Lethargy, seizures, stupor, coma
The presence of fever does not rule out the diagnosis, which still must be given full consideration.
Inquiries should be made regarding possible sources of lead exposure. For example, query families about the condition of the home, the presence of peeling or cracking paint and plaster, the occupations or hobbies of the family members, and the presence of industry in the immediate vicinity.
Determine the approximate age of the home. Homes built from 1920 to 1950 are more likely to contain lead pigment-based paint than newer homes. Houses built after 1978 are unlikely to contain lead-pigmented paints. Lead contamination still may be present in plumbing fixtures, but the lead dose in plumbing fixtures is an order of magnitude less than that of paint.
Determine whether the home contains any lead-based kitchen utensils, pottery, or imported toys. In addition, inquire about other homes where the child stays, and determine whether a parent is working as a painter or renovator or in a battery factory, shooting range, or other workplace where that lead is used.
Ask about exposure to foods and additives produced outside the United States. Some spices or food coloring may also contain lead pigments, and some candies have been reported to be contaminated with lead. Also ask about the use of herbal folk remedies. Hispanic and Asian families occasionally use herbal folk remedies that may contain lead.
Investigate the patient’s past medical history, including developmental milestones or delays, hygiene, pica, and previous exposure to lead. Evidence suggests that delayed weaning is associated with excessive pica and lead poisoning. It is commonly found that lead-poisoned children are bottle-fed for protracted periods. Inquire about the patient’s siblings (eg, ages, developmental history, school performance, and blood lead levels [BLLLs] if known).
In adults, similar symptoms may develop, although cognitive changes may be discerned more easily, especially since exposures are more typically acute. In addition, adults with chronic exposure may develop other symptoms, such as the following:
Weakness of extensor muscles (eg, foot drop, wrist drop)
Adults with lead poisoning frequently have sleep disorders. They may be hypersomnolent or have difficulty falling asleep at the appropriate time.
A meticulous environmental history is necessary in patients with suspected lead exposure. Depending on whether it is tailored to children or adults, it should include the following information:
Inquire about present and recent residences, including the location, age, and condition of the building; any history of renovations, inspections, or deleading programs; and any analyses of indoor and outdoor surfaces, water, and soil (if available). Ask about practices concerning changing of clothes and the presence of any work areas in the home.
In adults, obtaining a careful occupational and hobby history is important. More than 900 occupations have been associated with cases of lead poisoning. Always ask patients not just the name of their job but also the duties the job entails. This may uncover an obvious cause of exposure.
A history of ingesting illicit liquor may be an important clue to the etiology of lead poisoning. According to a study from a large urban emergency department (ED) involving patients who reported ingesting “moonshine” sometime during the previous 5 years, 51% had elevated BLLs, and 31% had BLLS in the very elevated range (ie, ≥ 50 µg/dL).
Additionally, numerous reports document lead poisoning resulting from retained bullet or shrapnel fragments; thus, a history of military or other penetrating trauma may be important.
Subtle changes in cognitive performance are not identified easily on physical examination. Careful mental status examination may detect changes in more severe cases, while formal neuropsychological testing may be needed to detect changes in other cases.
A child with lead toxicity is frequently iron deficient and pale because of anemia. The child may be either hyperactive or lethargic.
Impaired fine-motor coordination or subtle visual-spatial impairment may be seen. In adults, chronic distal motor neuropathy (eg, foot drop or wrist drop) may be seen with decreased reflexes and weakness of extensor muscles; sensory function is relatively spared (see the image below). This is a classic, though not very common, presentation of occupational lead toxicity.
It is important to evaluate the patient for papilledema, cranial nerve abnormalities, and signs of increased intracranial pressure (ICP). Cranial nerve involvement, particularly involvement of the optic nerve, is not uncommon. Chronic lead exposure has been shown to cause optic neuritis and blindness.
Lead lines appearing on gingival tissue (see the image below) are very unusual in children. The dentition of children does not promote poor enough hygiene to produce pyorrhea and the subsequent precipitation of lead sulfide. Adults with poor dental hygiene may demonstrate this characteristic finding in any heavy metal poisoning.
A report indicates that relative hypertension is related to elevated lead levels, but this finding has never been duplicated.
Lead exposure can precipitate a gout attack. The patient should be observed for joint changes suggestive of acute arthritis. In patients with history of penetrating or military trauma, gunshot wounds must be identified.
Lead poisoning, with or without encephalopathy, may result in neurologic, renal, hepatic, or cardiac damage. All organ systems may be potentially damaged by lead. A possibility that symptoms may progress with chelation exists, and the treating physician must be prepared to manage them. Such complications may consist of syndrome of inappropriate excretion of antidiuretic hormone (SIADH), increased ICP, renal impairment from the chelated lead complex, and hypertension.
Neuropsychiatric problems, impaired cognition, learning difficulties, and antisocial behavior are described in both children and adults.
Peripherally, lead selectively affects motor axons, causing segmental demyelination and axonal degeneration. The upper extremities are affected more often than the lower extremities, and extensors are affected more often than flexors. Hand drop and foot drop are common manifestations of axonopathy.
An increased prevalence of renal adenocarcinoma is reported among lead workers. Variability in individual susceptibility may be explained by differences in lead-binding proteins.
Inhibition of enzymes in the heme synthetic pathway, including aminolevulinic acid synthase, delta-aminolevulinic acid dehydratase (ALAD), and ferrochelatase, causes anemia. With kidney disease, erythropoietin production is impaired and thus causes anemia.
Lead can interfere with bone development, leading to the formation of lead lines at bone metaphyses. These lines represent periods of growth arrest, not lead toxicity per se.
Lead interferes with the conversion of 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D and causes rickets or osteomalacia. Patients with Fanconi syndrome may develop vitamin D–resistant rickets.
Lead is a known reproductive toxin. In males, it causes reductions in sperm count and fertility. In females, it increases the risk of spontaneous abortions, stillbirths, and preterm births. Offspring may experience lead poisoning in utero and may have developmental delay. Research has demonstrated that these reproductive effects occur at relatively low levels of exposure, even those previously considered safe. Skeletal lead may be mobilized during pregnancy and lactation and can be transported to the fetus or the neonate.
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