Case history
Case history #1
An 18-month-old girl resides in an old home that is undergoing extensive repairs. Her family has been careful to seal the rooms where the work is being done and perform an extensive post-repair clean-up. However, they choose to stay in the house throughout. The child is asymptomatic, but her aunt, a public health nurse, suggests that she be tested for lead toxicity. Laboratory investigations reveal a whole-blood lead of 3.1 micromoles/L (65 micrograms/dL). Her haemoglobin is 120 g/L (12 g/dL) and her haematocrit is 36%. Her blood smear is normal. An environmental evaluation reveals that the air conditioning ducts have been heavily contaminated with lead dust from the renovations and are the source of her severe lead poisoning.
Case history #2
A 55-year-old man presents several times to his family physician with severe crampy abdominal pain and some degree of confusion. His examination is normal, and the physician suggests that he take oral antidiarrhoeals. The patient's symptoms persist and codeine is prescribed. The pain continues to worsen and to be associated with constipation. Further history reveals that he has been extensively sanding paint in his beach house with a disc sander and no respiratory protection. A whole-blood lead is 12.1 micromoles/L (250 micrograms/dL). His haemoglobin and haematocrit are normal.
Other presentations
Most patients with lead poisoning have no specific symptoms, even with marked elevations of blood lead. However, lead toxicity should be considered in any person with acute encephalopathy and possible lead exposure. Peripheral neuropathies can also occur in adults. Although lead toxicity can cause microcytic anaemia, this is uncommon in the absence of other risk factors such as iron deficiency anaemia, and its absence does not rule out lead toxicity. Extremely severe lead poisoning has been associated with renal Fanconi's syndrome, particularly in children. Lifetime lead exposure can be expressed later in life and particularly in older people, where it may accelerate the rate of decline in cognition.
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