Lead Poisoning

excreted renally (80%-90%) and the remainder through the stool

S/S

• Abd pain (lead colic)
• Renal tubule toxicity (ATN)
• Anemia (sideroblastic)
• Peripheral neuropathies such as wrist drop
• CNS abnormalities such as memory loss and confusion

ABCDEFGH – Anaemia, Basophilic stripping, Colic (colicky abdominal pain), Diarrhoea, Encephalopathy, Foot and/or wrist drop, Gum deposition (lead line)/Growth retardation/Gout, Hyperuricemia/Hypertension/Hearing Loss

In children, you will see hyperacivity, aggression and learning disability (may be mistaken for ADHD)

also, impaired growth, constipation, and mental lethargy

Screening is commonly performed by capillary (fingerstick) testing, but elevated capillary results must be confirmed by venous lead levels due to the risk of contaminatino of capillary samples (eg, inadequate cleansing of the child's finger)

Venous lead level = the most accurate test <10ug/dL is considered acceptable. (<5 mcg/dL for children)

The best initial diagnostic test is an increased level of free erythrocyte protoporphyrin. (non-specific; can be elevated in iron deficiency and sickle cell anaemias)

• Lead poisoning inhibits δ-aminolevulinic acid dehydratase (ALAD) (plus other enzymes) → impaired conversion of ALA → PBG, so ALA accumulates upstream.
• AIP (acute hepatic porphyria) is characterised by accumulation of haem precursors including ALA and urinary porphobilinogen (PBG)
• Normal PBG in an unwell patient → essentially rules out acute porphyria, pushing you towards differentials like lead toxicity (then confirm with blood lead level)
• X-rays -
  • "Lead lines" in metaphyseal plates of long bones of children can be seen