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Year : 2005  |  Volume : 15  |  Issue : 2  |  Page : 247-249
Lead poisoning

Department of Radiodiagnosis, M.G.M. Medical College and Associated M.Y Hospitals, Indore, MP, India

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Keywords: Lead poisoning, Metaphyseal bands, Encephalopathy

How to cite this article:
Singhal M, Tiwari O P. Lead poisoning. Indian J Radiol Imaging 2005;15:247-9

How to cite this URL:
Singhal M, Tiwari O P. Lead poisoning. Indian J Radiol Imaging [serial online] 2005 [cited 2020 May 28];15:247-9. Available from:

   Introduction Top

Lead poisoning or plumbism in children can be traced to pica (eg, dirt eating), acute ingestion of lead-based paints or consumption of home remedies [1],[2].

Lead poisoning in children presents with non-specific and vague symptomatology, however in serious conditions it may present with encephalopathic features [1],[3].

Radiologically it is characterized by presence of dense transverse bands in the growing metaphyseal regions [2],[3],[4].

Here we report a case of chronic lead poisoning in a child of 18 months, which presented with encephalopathy.

   Case report Top

A 18 months male child born in lower socio-economic strata presented with an episode of generalized tonic-clonic seizure lasting for half an hour not associated with fever, the history of projectile vomitings since 3 days, passage of watery stools 3-4 times a day and drowsiness. There was history of recurrent admissions in the past 4 months in some peripheral hospital for near similar complaints and empirically was on anti-tubercular therapy but no significant improvement was noted. His developmental milestones were normal. There was no history to suggest birth asphyxia and peri-natal history was non-contributory.

On examination child was drowsy and irritable but arousable. General examination revealed pallor of mucosal membranes and gums, otherwise normal. Detailed neurological examination revealed the following: child was drowsy and irritable, normal cranial nerves, motor system examination showed hypotonia, grade 3 power in all limbs with absent deep tendon jerks and equivocal planter reflexes, co-ordination could not be tested, was responding to prick. He had no signs of meningeal irritation. Fundus examination revealed no significant abnormality. Other systemic examination showed hepatomegaly of 4 cms.

Investigations revealed: Hb-9.4 gm%, TLC-12650, DLC- N62L31M3E4B0, ESR-38 mm/hr, platelet count-3.79 lacs, random blood sugar-93 gm%, SGOT-310 IU/dl, serum calcium-8.7 mg%, routine urine examination- showed traces of albumin, blood urea- 39 mg%, serum creatinine- 1.2mg%, CSF analysis revealed no significant abnormality.

Ultrasound of the abdomen showed mild hepatosplenomegaly. Contrast enhanced CT of head showed mild prominence of lateral ventricles and subtle hypodensities in left hippocampal region, which did not explain patient's symptoms. Chest X-ray revealed prominent costochondral junctions and more strikingly dense proximal metaphysis of humerus on left side [Figure - 1]. This prompted us to take radiographs of extremities for further evaluation. Radiographs of wrist with hands and both the lower extremities were taken which showed thick metaphyseal bands in the distil ends of radius and ulna,

both femurs, bases of metacarpals and phalanges [Figure - 2][Figure - 3]. Considering the clinical presentation and radiological features a probable diagnosis of heavy metal poisoning was thought. On further interrogation of the parents, they came out with the history that child used to ingest the lead of the batteries which his father used to bring home for repairs. To confirm the diagnosis blood lead levels was done which showed very high lead levels of 97 gm/dl (Normal level-10 gm/dl). Erythrocyte protoporphyrin levels were raised to 144 gm/dl. Peripheral smear showed basophilic stippling and reticulocyte count was 12%.

Since whole of the family was exposed to lead X-rays of other sibling were also done which too showed evidence of lead poisoning.

After confirmation of diagnosis anti tubercular treatment was stopped and chelation therapy was started. Patient responded to treatment and regained consciousnesses, muscle power, and there was no episode of convulsion.

   Discussion Top

The natural blood level of lead is 0 g/dl but practically levels upto 10 g/dl are considered normal. Any level above this is considered abnormal and lead lines (metaphyseal band sign) appear at levels of 50 g/dl while encephalopathic features are usually seen when lead levels are more than 100 g/dl [1],[5].

The toxicity of lead results from its avidity for the sulfhydryl (SH) group of proteins and various enzymes which leads to jeopardization of their function [1],[3]. In bones lead inhibits osteoclastic remodeling preferentially in the zone of provisional calcification which results in an increase in the thickness and number of trabeculae at the metaphysis. And exuberant calcium deposition in the zone of provisional calcification yields dense metaphyseal bands [2],[6].

The most serious manifestation of lead poisoning is acute encephalopathy. This is usually preceded by behavioral changes and/or vomitings, intermittent abdominal pain and constipation. Encephalopathy includes persistent vomtings, ataxia, seizures, altered behavior, impaired consciousness and coma. In absence of encephalopathy symptomatology is non specific and vague, and difficult to diagnose [1],[3].

Diagnosis is established by definitive history of exposure of lead in any form, raised blood levels of lead and erythrocyte protoporphyrin levels. Radiological examination is supportive and can give a clue to clinch the diagnostic possibility. Features to suggest are dense transverse metaphyseal bands at ends of growing bones particularly around the knee [2],[4]. On review of literature in one study presence of dense metaphyseal band especially in proximal fibula was highly suggestive of plumbism [5]. With treatment or cessation of lead exposure, the lead band will demonstrate an apparent migration into the metadiaphysis because of normal new bone growth. Accordingly, when the lead level returns to normal, the metaphyseal band will gradually decrease in radiopacity and disappear in approximately 4 years [2]. On imaging calcifications in basal ganglia region can be appreciated in some cases [7].

The dense metaphyseal band sign enables a lengthy differential diagnosis. In order of decreasing frequency, the causes of a dense metaphysis include normal variance, plumbism, treated leukemia, healing rickets, other heavy metal (arsenic, bismuth, mercury) poisoning, recovery from scurvy, vitamin D hypervitaminosis, congenital hypothyroidism, hypoparathyroidism, and transplacental infections (eg, toxoplasmosis, rubella, cytomegalovirus, and herpes) [7],[8],[9],[10].

In conclusion, as laboratory analysis of lead levels cannot always be readily performed in infants with unexplained encephalopathy, in such cases radiography of the knees can be of great help. The presence of dense metaphyseal bands strongly supports the diagnosis of lead toxicity which can be confirmed by relevant investigations [11].

   References Top

1.Sachev HPS, Puri RK, Bagga A, Choudhary P; Principles of pediatric and neonatal emergencies, Jaypee brothers, New Delhi;1996: 284-287.  Back to cited text no. 1    
2.Scott A. Raber, Signs in Imaging; Radiology.1999; 211:773-774.)  Back to cited text no. 2    
3.Nelson textbook of Pediatrics, Saunders; vol. I, Edi.16th  Back to cited text no. 3    
4.Sutton D; Textbook of Radiology and Imaging, Churchill Livingstone; vol. I, Edi.6th: 252.  Back to cited text no. 4    
5.Blickman JG, Wilkinson RH, Graef JW. The radiologic "lead band" revisited. AJR 1986; 146:245-247.  Back to cited text no. 5  [PUBMED]  
6.Leone AJ. On lead lines. AJR 1968; 103:165-167.  Back to cited text no. 6    
7.Marchiori DM; Clinical imaging, Mosby; 1999: 228, 326-327, 747.  Back to cited text no. 7    
8.Swischuk L. Metaphyseal abnormalities. In: Tracy TM, eds. Differential diagnosis in pediatric radiology. Baltimore, Md: Williams & Wilkins, 1984; 226-229.  Back to cited text no. 8    
9.Eisenberg R. Skeletal patterns. In: Berk RN, eds. Clinical imaging: an atlas of differential diagnosis. 3rd ed. Philadelphia, Pa: Lippincott-Raven, 1997; 808-811.  Back to cited text no. 9    
10.Resnick D. Heavy metal poisoning and deficiency. In: Resnick D, eds. Bone and joint imaging. 2nd ed. Philadelphia, Pa: Saunders, 1996; 912-915.  Back to cited text no. 10    
11.Woolf DA, Riach IC, Derweesh A, Vyas H. Lead lines in young infants with acute lead encephalopathy: a reliable diagnostic test. J Trop Pediatr 1990; 36:90-94.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]

Correspondence Address:
M Singhal
14002/11, Ganesha Basti, Bathinda (Punjab) - 151001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-3026.28814

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[Figure - 1], [Figure - 2], [Figure - 3]


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