Dr Ira Shah.
Medical Sciences Department, Pediatric Oncall, Mumbai, India. | A fifteen years old boy born of non-consanguineous marriage presented with progressive pallor since 3 months and fever, cough, hematochezia since 1 day. He had fever 3 months back that lasted for 5 days. He was diagnosed as Enteric fever at that time in view of a positive Widal test and had received a course of antibiotics for 7 days. He also had skin rash 3 months back that had now left behind hypopigmented macules all over the body. He is a known case of epilepsy and was on some ayurvedic preparations for the same since past 5 months. On examination, he had pallor with pedal edema, raised jugular venous pulsation and tachycardia (Heart rate = 130/min). He had dry and scaly skin with hypopigmented macules all over body (Figure 1). Systemic examination was normal. His hemogram revealed hemoglobin of 4.8 gm% with leucopenia (WBC count = 1,500/cumm) and thrombocytopenia (Platelet count = 9,000/cumm) with a low reticulocyte count. He was thus suspected as a case of Aplastic anemia. Bone marrow examination revealed a hypocellular marrow with reduced megakaryocytes and decreased myeloid and erythroid cell maturation. There was no granuloma, fibrosis or malignancy. A skin biopsy was suggestive of Acrokeratosis vermicuformis due to heavy metal poisoning. The ayurvedic preparation that the child was on for epilepsy was analyzed for heavy metal content by Plasma Atomic Emission Spectroscopy which showed increased levels of Arsenic and Mercury [Arsenic = 10.85 ppm, Lead = not detected, Mercury = 10.66 ppm] following which the medication was immediately stopped. His 24 hours urine Arsenic level 7.6 μg/L and 24 hrs urine mercury level were normal (< 0.5 μg/L). His liver function tests, renal function tests were also normal. In view of normal urine excretion of Arsenic and Mercury, he was just treated with packed cell transfusion. A regular hemogram was monitored and it gradually showed an improving trend with last hemogram after 20 days of presentation had hemoglobin of 10 gm%, WBC count = 3,200 cells/cumm and Platelet count of 54,000/cumm. Thus, fortunately for this child, heavy metal intoxication, which had basically involved the skin and hematopoietic system reversed on stopping the offending medication, thus requiring no antidote.
Discussion:
Arsenic Poisoning: Inorganic arsenic is found in pesticides, herbicides, dyes, homeopathic medicines and folk remedies from China, India and South East Asia and lead to toxicity in children. Occupational exposure may occur in industries such as glass manufacturing, pottery, electronic components, mining & refining. Organic form of arsenic found in seafood is non-toxic. Arsine gas is highly toxic and when inhaled, after a latent period of 2-24 hrs can lead to massive hemolysis, hepatomegaly, jaundice, hemoglobinuria and renal failure.
GI absorption of inorganic arsenic salts can lead to nausea, vomiting, abdominal pain and diarrhea within minutes to hours. Cardiovascular toxicity in form of prolonged QT interval, pulmonary edema and cardiogenic shock can occur. Neurologic symptoms such as delirium, seizures, cerebral edema, encephalopathy may also occur. Subacute toxicity is characterized by prolonged fatigue, malaise, weight loss, headache, chronic encephalopathy, peripheral neuropathy, pancytopenia and gastroenteritis. Skin manifestations such as alopecia, oral ulcers, pruritic rash, desquamation, transverse striae on nails may also be seen. Chronic exposure leads to skin diseases, hypersplenism, encephalopathy and peripheral neuropathy.
Diagnosis can be established by elevated urinary arsenic levels especially in 24 hours urine collection. Urine must be collected in a metal free container and concentrations > 50 µg/L is diagnostic. Elevated arsenic levels in hair or nails should be interpreted with caution due to possibility of external contaminations. RBCs may show basophilic stippling.
Treatment consists of prompt removal from the source of poisoning, and chelation therapy. In cases of hemoglobinuria, transfusion of RBCs, IV Fluids, sodium bicarbonate & mannitol may be required. For GI intoxication, activated charcoal is advocated. Chelation should be started as early as possible and continued until 24 hrs urinary arsenic levels return to normal or the toxic effects are irreversible. dimercaprol or bal is chelator of choice. bal may cause hemolysis in G-6-PD deficient individuals. For patients, stable enough to tolerate oral therapy. dmsa can be given.
Mercury Intoxication:
Mercury exists in 3 forms:
- Elemental Mercury (exists as silver liquid also known as quick silver).
- Inorganic Mercury (exists as mercurous salts and was used in teething powder, diaper powder in olden days. It is used in pesticides, disinfectants, antiseptics, explosives).
- Organic Mercury (is used in diuretics, antiseptics, insecticides & pesticides) and is found in fish. Methyl mercury is readily passed through the placenta and is the most toxic form of mercury).
All forms of mercury can be absorbed transcutaneously. Elemental mercury is readily absorbed as a vapor but is poorly absorbed from GI tract and can even cross placenta and blood brain barrier. The half-life of elemental mercury in tissues is about 60 days with most of the excretion in urine. Mercury salts are absorbed from the GI tract, do not cross the blood-brain barrier to that extent and their biologic half-life is about 40 days. Organic mercury is readily absorbed by inhalation and GI ingestion and distributes more in red blood cells and brain. It is excreted mainly in bile and half-life is about 70 days.
Clinical Features: CNS and kidney are the primary organs affected and can even lead to permanent brain damage. Elemental mercury leads to tremors, emotional disturbances and gingivitis. Methyl mercury effects are seen months after exposure and leads to autonomic dysfunction and peripheral neuropathy. Renal damage in form of proteinuria, nephrotic syndrome, acute tubular necrosis, renal failure can occur. Other features may be respiratory tissue damage, gastritis, intestinal necrosis, nausea, vomiting, diarrhea and even cardiovascular collapse.
Diagnosis: Blood mercury levels are used to determine acute mercury exposure because the half-life of mercury in blood is short (Normal adult mercury level < 1.5 μg/dl), 24 hours urine mercury levels provide the best estimate of current body burden of chronic mercury exposure. (concentration < 20 μg/L usually cause no signs and symptoms).
Treatment: First and foremost, the exposure to mercury from external source has to be removed and then clearance of mercury from the body must be increased by chelation with 2, 3 – Dimercaptosuccinic acid (DMSA), dimercaprol (BAL) or penicillamine. dmsa is most effective and can be given orally. If patient is unable to take oral medications, the chelator of choice is bal. | | | | Compliance with Ethical Standards | | Funding None | | | | Conflict of Interest None | | |
- Goto CS. Heavy Metal Intoxication. Eds- Behram RE, Kliegman RM, Jenson HB. In: Nelson's Textbook of Pediatrics, 17th ed. Philadelphia, W.B. Saunders, 2004:2355-2358.
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| Cite this article as: | | Shah I. APLASTIC ANEMIA DUE TO HEAVY METAL INTOXICATION. Pediatr Oncall J. 2005;2: 68. |
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