Introduction:
For centuries, lead toxicity has been one of the important preventable causes of morbidity. It interferes with a number of body functions primarily affecting the central nervous, hematopoietic, hepatic and renal system causing serious disorders. Uncommon etiology of acute toxicity because of occupational exposure. The ongoing emphasis on abatement of lead environments places added emphasis on occupational exposure to lead (e.g among workers at smelters or battery recycling plants).1 Early suspicion, desensitization and chelation therapy may prevent the patients from long term associated consequences. Here, we report a case of lead toxicity and acute kidney injury in occupational exposure.
Methods:
Case Report
Results:
A 28-year-old male with no known comorbidity presented to our OPD with renal dysfunction on routine evaluation. He complained of having generalized weakness, fatigue since last 4 months and tremors and weakness in all four limbs without any apparent paresis since last 1 month. Later 2 days prior to admission he developed constipation with generalized pain abdomen. There is history of similar illness in past for which he sought many gastroenterologists’ opinion and was treated with laxatives. He doesn't give any history of fever, joint pain, rash, decreased urine output or urinary retention. There is no history of any illicit drug intake.
On clinical evaluation he was anemic, icteric. Abdominal examination revealed soft abdomen with generalized pain and increased intensity of bowel sounds. On neurological examination power was 4/5 in all four limbs, brisk deep tendon reflex without any sensory or autonomic deficit.
On further evaluation there was normocytic normochromic anaemia, indirect hyperbilirubinemia, high retic counts with rise in creatinine (2.1 mg/dl) without any dyselectrolytemia. ANA and other autoimmune markers for connective tissue disorder were negative.
MRI brain was normal and MRI spine was suggestive of early degenerative changes in the lumbar spine. NCS revealed early demyelination in all four limbs. X - Ray abdomen showed dilated bowel loops with faecal loading and multiple air fluid levels. CT enteroclysis featured faecal loading in the left side of the colon from splenic flexure to the sigmoid colon with fluid filled large bowel dilation up to caecum. Porphyria panel was sent which came out to be negative. Serum levels were sent in view of multi system involvement and history of working in battery factory which came out to be high (93 mcg /dl) Patient was treated conservatively with intravenous fluid resuscitation, laxatives and other supportive care and advised for abstinence from the current job. Patient improved symptomatically and discharged with a creatinine of 1.6 mg/dl. He was followed up on outpatient basis and serum lead levels were monitored after abstinence from the job. Later serum lead levels came down to normal level and there was improvement in renal function as well (Serum Creatinine 1.2 mg/d)
Conclusions:
Lead toxicity is a life-threatening condition because of its severe acute and chronic complications. Even though the diagnosis represents a challenge physician must always include this possibility in the differential diagnosis for cases with suggestive symptoms with multisystem involvement. A blood lead level remains the mainstay for assessing an individual’s exposure to lead. All patients with elevated blood lead levels or exposure to lead should undergo education, exposure reduction and chelation therapy whenever necessary.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.