Cases reported "Lead Poisoning"

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1/36. flour contamination as a source of lead intoxication.

    CASE REPORT: A 43-year-old man was hospitalized because of severe anemia and recurrent bouts of abdominal pain over 20 days. There was no known occupational exposure to toxins. Concomitantly, the patient's father complained of having the same symptoms. Familial lead poisoning was diagnosed when all 6 family members tested had high blood leads (31-64 micrograms/dL). RESULTS: Following detailed examination of the potential sources common to all members of the household, the cause of poisoning was determined to be corn flour containing 38.7 mg/g lead. physicians are reminded to consider lead poisoning in the differential diagnosis of individuals with unexplained symptoms, particularly those of abdominal discomfort and anemia.
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2/36. An unusual cause of recurrent abdominal pain.

    abdominal pain is a common complaint with diverse etiologies. We describe an unusual case of recurrent abdominal pain in an adult due to lead poisoning, a condition usually associated with childhood. A previously healthy 42-yr-old man presented with 2 days of severe crampy abdominal pain and a 1-month history of constipation. physical examination was remarkable for diffuse abdominal pain but peritoneal signs were not present. Blood tests were remarkable for hematocrit of 33 and mean cell volume of 78, with ovalocytes and basophilic stippling on blood smear. Abdominal x-ray showed stool throughout the colon and a nonspecific bowel gas pattern. The patient was treated with intravenous fluids and enemas, and his symptoms resolved within 2 days. Repeat history taking revealed he had been stripping paint from an old Victorian house in the preceding few months. He was discharged after a blood lead level was obtained. Before his clinic appointment he was readmitted 2 days later with recurrent abdominal pain. His blood lead level was elevated at 110 microg/dl (toxic range). After consultation with the occupational health and safety Administration and local poison control service, he was treated with intravenous calcium edetate disodium and intramuscular dimercaprol. He was asymptomatic at discharge, with a level of 56 microg/dl. Two weeks later, a repeat level was elevated at 72 microg/dl, for which he received a 3-wk course of oral dimercaptosuccimer. Subsequent levels were unremarkable, and the patient remains asymptomatic. abdominal pain secondary to lead poisoning in adults is uncommon. This case highlights the importance of taking a detailed occupational history and appropriately using "routine" blood tests to diagnose a rare condition that presented with a common complaint.
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3/36. lead poisoning after gunshot wound.

    CONTEXT: Despite the absence of symptoms in the majority of patients carrying lead bullet fragments in their bodies, there needs to be an awareness of the possible signs and symptoms of lead intoxication when bullets are lodged in large joints like knees, hips and shoulders. Such patients merit closer follow-up, and even surgical procedure for removing the fragments. OBJECTIVE: To describe a patient who developed clinical lead intoxication several years after a gunshot wound. DESIGN: Case report. CASE REPORT: A single white 23-year-old male, regular job as a bricklayer, with a history of chronic alcohol abuse, showed up at the emergency department complaining of abdominal pain with colic, weakness, vomiting and diarrhea with black feces. All the symptoms had a duration of two to three weeks, and had been recurrent for the last two years, with calming during interval periods of two to three weeks. Abdominal radiograms showed a bullet lodged in the left hip, with a neat bursogram of the whole synovial capsule. A course of chelating treatment using calcium versenate (EDTACaNa2) intravenously was started. After the chelation therapy the patient had recurrence of his symptoms and a radical solution for the chronic mobilization of lead was considered. A hip arthroplasty procedure was performed, leading to complete substitution of the left hip.
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4/36. lead poisoning from a retained bullet: a case report and review.

    A 47-year-old man with a prior gunshot wound presented with arthritis, constipation, abdominal pain, and weight loss. Arthrocentesis did not reveal the cause of the arthritic complaints, but lead poisoning was suspected and confirmed. We present this case along with a short review of the literature pertaining to this often overlooked and reversible cause of lead poisoning.
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5/36. Acute elevation of blood lead levels within hours of ingestion of large quantities of lead shot.

    BACKGROUND: Ingestion of elemental lead foreign bodies is felt to have a low risk of clinically significant lead absorption unless gastrointestinal pathology and/or prolonged transit time are present. We present a case of ingestion of a large quantity of small diameter lead shot accompanied by rapid elevation of blood lead levels. CASE REPORT: A 5 1/2-year-old previously healthy girl was found eating the pellets from an ankle weight. She vomited and complained of abdominal pain. In the emergency department, she had no complaints and normal vital signs. An abdominal X-ray showed thousands of small, round, metallic density objects in the stomach. Her white blood cell count was 14,700/mm3, and the hemoglobin, mean corpuscular volume, free erythrocyte protoporphyrin, zinc protoporphyrin, biochemistry panel 21, and urinalysis were normal. She had no prior lead level for comparison. Whole-bowel irrigation was begun and she passed over 11 stools with pellets as well as other foreign bodies (erasers, bead, etc.) in the first 24 hours. Pellets were still seen on X-ray the following day so she received a high-fiber diet and bisacodyl tablets 10 mg/d. On hospital day 2, her admission blood lead (drawn 13 hours after ingestion) was reported as 57 microg/dL (2.7 microm/L) and chelation was begun with oral 2,3-dimercaptosuccinic acid 10 mg/kg 3x/d for 5 days, then 2x/d for 14 days. Her peak measured lead level was 79 microg/dL approximately 36 hours after ingestion. She excreted 2,273 microg lead in the urine during her first 24 hours of chelation. Her blood lead dropped to 14.3 microg/dL by the end of chelation. She did not develop any apparent signs of lead poisoning. CONCLUSION: Acute elevations of blood lead concentrations may occur rapidly after ingestion of multiple small elemental lead objects.
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6/36. A presumptive case of lead poisoning in a brass-worker's child.

    A one-year-old male child was admitted with the complaints of vomiting and irritability for 4 days, haematemesis and melaena for one day and had generalised tonic convulsions on the day of admission. Examination revealed exaggerated reflexes with group II coma. Blood film showed basophilic shippling. Straight x-ray showed lead lines in the metaphyses of ribs, humerii, scapulae, iliac crests and upper ends of femurs. The boy's father was an employee of brass industry where brass alloys used cotained lead in substantial amount. A presumptive case of lead poisoning (as diagnosed) was treated symptomatically. Chelating agent was called for but the patient left. In the present case the hands of the child were contaminated with lead dust brought home by his father either in person or in clothings. The child used his hands constantly in his mouth to get poisoned by lead.
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7/36. Peripheral neuropathy in chronic occupational inorganic lead exposure: a clinical and electrophysiological study.

    BACKGROUND AND OBJECTIVES: Traditionally the neuromuscular disorder associated with lead poisoning has been purely motor. This study assessed peripheral nerve function clinically and electrophysiologically in 46 patients with neuropathic features out of a total population of 151 workers with raised blood and/or urinary lead concentrations. RESULTS: Average duration of occupational exposure for the neuropathic group ranged from 8-47 years (mean 21.7). Their mean blood lead concentration (SD) was 63.9 (18.3) microg/dl (normal <40), urinary lead 8.6 (3.3) microg/dl (normal<5.0), urinary coproporphyrins 66.7 (38.4) microg/g creatinine (20-80), urinary aminolaevulinic acid 1.54 (0.39) mg/g creatinine (0.5-2.5). All 46 had distal paraesthesiae, pain, impaired pin prick sensation, diminished or absent ankle jerks, and autonomic vasomotor or sudomotor disturbances. Reduced vibration sensation and postural hypotension were present in all 20 studied. None of these 46 patients had motor abnormalities. Motor conduction velocity and compound muscle action potential amplitudes were normal, with marginally prolonged distal motor latencies. Sensory nerve action potential amplitudes lay at the lower end of the normal range, and the distal sensory latencies were prolonged. No direct correlation was found between the biochemical variables, and the clinical or electrophysiological data. CONCLUSIONS: One additional patient was seen with shorter term exposure to lead fumes with subacute development of colicky abdominal pain, severe limb weakness, and only minor sensory symptoms. Unlike the patients chronically exposed to lead, he had massively raised porphyrins (aminolaevulinic acid 21 mg/g creatinine, coproporphyrins 2102 microg/g creatinine). patients with unusually long term inorganic lead exposure showed mild sensory and autonomic neuropathic features rather than the motor neuropathy classically attributed to lead toxicity. It is proposed that the traditional motor syndrome associated with subacute lead poisoning is more likely to be a form of lead induced porphyria rather than a direct neurotoxic effect of lead.
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8/36. Bite the bullet: lead poisoning after ingestion of 206 lead bullets.

    A 45-y-o male with a history of schizophrenia was admitted to a local VA psychiatric unit. Five days later, endoscopy due to abdominal pain, gastrointestinal bleeding and blood hemoglobin of 5.6 g/dL revealed bullets in the stomach. On subsequent radiograph, > 50 bullets were visualized in the stomach and intestines. Poison Center recommendations included whole bowel irrigation and a blood lead level. After poor results with gastrointestinal decontamination and a repeat radiograph showing > 100 cartridges, surgical intervention was considered but not performed due to perceived risk of bullet detonation from electrocautery. The blood lead was reported as 391 mcg/dL. calcium EDTA therapy was initiated, followed by aggressive gastrointestinal decontamination. Four days of whole bowel irrigation facilitated passage of 206 cartridges over the next 10 days. The patient was discharged on a 14-day course of 600 mg succimer tid to treat the bone lead deposits and blood lead level of 49 mcg/dl. An outpatient visit 6 w later showed the blood lead level had dropped to 24 mcg/dl. Aggressive gastrointestinal decontamination and calcium EDTA and succimer administration successfully treated an ingestion lead bullets and the resulting lead poisoning.
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9/36. adult lead poisoning from a herbal medicine.

    A 56-year-old Indian lady presented with one week history of abdominal pain, jaundice and chronic polyarthralgia. She had evidence of hemolytic anemia and hepatitis. Her blood lead level was high and a peripheral blood film showed dense basophilic stippling. It is believed that the lead toxicity was due to the use of Indian herbal medicine.
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10/36. Maternal-fetal lead poisoning from a 15-year-old bullet.

    Blood lead was mildly elevated (31 microg/dl, where 25 microg/dl is the upper limit of the normal range) in a woman with lumbar bullet fragments who was evaluated for anemia in the 23rd week of pregnancy. She required cesarean section at term for pre-eclampsia and fetal distress. The infant had multiple congenital abnormalities. Postpartum maternal blood lead level was 75-85 microg/dl. The infant's blood lead level was also elevated. Chelation lowered the infant's blood lead level, but not the mother's. Surgical debulking of the lumbar lead deposits was followed by a fall in blood lead level from 65 to 52 microg/dl. This case demonstrates a remarkable gestational rise in maternal blood lead level. The infant's congenital abnormalities could be causally related to lead.
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