Am Fam Physician. 2002;66(10):1839-1841
to the editor: Occult lead poisoning is a difficult diagnosis to make in a primary care setting because the symptoms of plumbism are non-specific. We would like to report a case in which unsuspected lead toxicity resulted in a delayed diagnosis and inconclusive hospital work-up.
A healthy 57-year-old man developed abdominal pain and lower back pain over the course of several days. He had no significant medical history, took no medications, and had no known allergies. He denied having any antecedent trauma and reported no other symptoms. His vital signs were normal and physical examination was unremarkable. Rapid office tests revealed a hemoglobin level of 9.7 g per dL (97 g per L) and blood on urine dipstick. The patient was admitted to the hospital for nephrolithiasis work-up and treatment. Despite an extensive three-day hospital evaluation, work-up was inconclusive.
At follow-up after discharge, the patient continued to have the same symptoms; he then revealed that he was a welder exposed to lead fumes. A whole blood lead level obtained at that time was greater than 100 mcg per dL (4.83 μmol per L), and he was re-admitted to the hospital for chelation therapy with dimer-caprol (or BAL) and edetate calcium sodium (CaNa2EDTA). Chelation was continued for five days. The patient's symptoms resolved, and the worksite evaluation was completed.
Symptoms of lead poisoning are often non-specific1 and include nausea, vomiting, abdominal pain, headache, back pain, paresthesias, limb weakness, and malaise. In severe cases, patients may present with encephalopathy. Without a history of exposure, lead poisoning has been mistaken for acute viral illness, sickle cell vasoocclusive crisis, gastro-enteritis, acute appendicitis, nephrolithiasis, and Guillain-Barré syndrome.1
Lead is primarily absorbed by the ingestion or inhalation of dust particles. Elevated lead levels greater than 10 mcg per dL (0.48 μmol per L) are associated with neurocognitive delays in children, and chronic lead intoxication in adults has resulted in hypertension, anemia, peripheral neuropathy, and nephropathy. Lead-induced nephropathy is one of the oldest described manifestations of plumbism, and it has been linked to adult-onset hypertension in several population surveys.2,3 Some centers have treated renal insufficiency and hypertension with routine chelation of body lead stores, although the long-term efficacy of such therapy still requires further evaluation.4
Since lead toxicity is so nonspecific, it should be considered in patients when diagnosis is unclear. Occupational exposure is the most common source for lead poisoning among adults. High-risk occupations include welding, batter manufacturing, mining, firing range maintenance, ship repair, glass blowing, and pottery glazing.1 The Occupational Safety and Health Administration requires removal from the worksite for a single surveillance level greater than 60 mcg per dL (2.90 μmol per L). Other common sources of lead poisoning in adults include lead-glazed dishes, food supplements contaminated with lead, herbal folk remedies, and moonshine whiskey.5,6 Unexplained anemia, basophilic stippling on the peripheral smear, and elevated creatinine are laboratory clues suggesting plumbism; the most important diagnostic maneuver is obtaining a whole blood lead level when plumbism is suspected. All patients recognized to have plumbism warrant immediate environmental intervention.