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Radiological Case of the Month
Hassib Narchi, MD, FRCP, FRCPCH
From the Al-Hasa Specialty Services Division, Saudi Aramco-Al-Hasa Health Center, Saudi Aramco Medical Services Organization, Mubarraz, Kingdom of Saudi Arabia.
Arch Pediatr Adolesc Med. 2000;154:83-84.
A 2-MONTH-OLD boy presented with a history of 6 episodes of generalized 5-minute tonicoclonic seizures. Previously, he was well. His birth weight was 2780 g, and Apgar scores were 9 and 10 at 1 and 5 minutes, respectively. On hospital admission, he weighed 3540 g with a head circumference of 37 cm. He was afebrile, hypotonic, drowsy, and pale. His blood pressure was 95/55 mm Hg; pulse rate, 100/min; and respirations, 30/min. The anterior fontanelle was soft, the pupils were equal and reactive to light, and no retinal hemorrhages were present at funduscopy. Findings from pulmonary and cardiac auscultation and abdominal examination were normal. Blood serum values from laboratory test results were as follows: glucose, 6.8 mmol/L (122 mg/dL); calcium, 0.78 mmol/L (3.1 mg/dL); phosphorus, 0.16 mmol/L; magnesium, 0.78 mmol/L (1.9 mg/dL); sodium, 143 mmol/L; potassium, 5.3 mmol/L; chloride, 113 mmol/L; and bicarbonate, 17 mmol/L. The hemoglobin value was 76 g/L; mean corpuscular volume, 74 fL/L; total white blood cell count, 11.5 x 109/L with 0.22 neutrophils; and platelet count, 150 x 109/L. Arterial blood gas showed a pH of 7.34; PaCO2, 29 mm Hg; PaO2, 90 mm Hg; and a base deficit of 6 mEq/L. The corrected QTc interval on electrocardiogram was 0.49 seconds, and the rhythm was regular. Findings from urinalysis and antigen studies were normal, and cerebrospinal fluid showed no white cells. Levels for protein and cerebrospinal fluid glucose were 24 g/L and 4.2 mmol/L (76 mg/dL), respectively. No organisms were present on the Gram stain and none were found in blood and urine culture samples. Findings from an electroencephalogram showed mild discharge in the left posterior temporal area. A skull radiograph was requested (Figure 1), followed by radiography of the hands (Figure 2).
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Figure 1.
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Figure 2.
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Denouement and Discussion: Lead Poisoning
Figure 1 Anteroposterior radiograph of the skull shows wide sutures.
Figure 2. Radiograph of the hands in which radiodense lines are seen in the metaphyses.
Basophilic stippling was seen on the blood smear. Levels of serum lead (Pb) and free erythrocyte protoporphyrin were 9.66 µmol/L (200 µg/dL) and 2.78 µmol/L, respectively. A cranial computed tomogram showed no abnormalities. At hospital admission, no cosmetic products were seen on the face; however, the mother did note regularly applying kohl, a Pb-containing eye cosmetic, to the infant's eyelids. Hypocalcemia was corrected with intravenous calcium gluconate, and chelation therapy with intravenous calcium sodium edetate was given for 5 days. The infant rapidly improved, and the serum Pb value dropped to reference levels over the next few weeks. The family was educated to avoid using Pb-containing products.
Lead is a neurotoxic metal, and acute encephalopathy may be the first sign of Pb poisoning.1 The fatality rate is high, and survivors often suffer permanent neurological sequelae.2 Several cases of Pb poisoning from traditional Pb-containing medicine or cosmetics have been reported in developing countries.3 Kohl, or surma, is an eye cosmetic applied to the conjunctival margins of the eyes or, medicinally, to the umbilical stumps of infants in Middle Eastern countries. The Pb content is variable and may reach 91.8%. Lead ingestion from kohl may result from hand-to-mouth activities in children whose fingers are contaminated or from absorption from the nasolacrimal mucosa. The presence of kohl on an infant's eyelids suggests Pb exposure.4-9 Although washing off the product removes the characteristic dark staining, the product may remain on the conjunctival margins. The heavy metal coating of the palpebral edges is seen on radiographs of the skull.
Lead poisoning should always be considered in children who present with acute encephalopathy. A history of Pb exposure or the visualization of kohl on the eyelids are helpful evidence. Microcytic anemia and basophilic stippling of the red blood cells suggest Pb poisoning, and elevated levels of serum Pb and erythrocyte protoporphyrin confirm the diagnosis. Heavy metal poisoning as metaphyseal bands on bone radiographs is a helpful finding that may aid in dating Pb exposure onset time.10-11
Specific treatment of Pb encephalopathy is by chelation therapy with dimercaprol and calcium sodium edetate.
AUTHOR INFORMATION
Accepted for publication September 9, 1998.
Corresponding author: Hassib Narchi, MD, FRCP, FRCPCH, Al-Hasa Specialty Services Division, Saudi Aramco Al-Hasa Health Center, Saudi Aramco Medical Services Organization, Box 6030, Mubarraz 31311, Kingdom of Saudi Arabia (e-mail: hassibnarchi{at}hotmail.com).
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2. Abdullah MA. Lead poisoning among children in Saudi Arabia. J Trop Med Hyg. 1984;87:67-70.
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4. Ali AR, Smales OR, Aslam M. Surma and lead poisoning. BMJ. 1978;2:915-916.
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8. Sprinkle RV. Leaded eye cosmetics: a cultural cause of elevated lead levels in children. J Fam Pract. 1995;40:358-362.
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9. Fernando N-P, Healy MA, Aslam M, Davis SS, Hussein A. Lead poisoning and traditional practices: the consequences for world health: a study in Kuwait. Public Health. 1981;95:250-260.
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10. Pearl M, Boxt LM. Radiographic findings in congenital lead poisoning. Radiology. 1980;136:83-84.
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11. Sachs HK. The evolution of the radiologic lead line. Radiology. 1981;139:81-85.
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