Cases reported "Fluoride Poisoning"

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1/22. Concomitant sickle cell disease and skeletal fluorosis.

    Skeletal fluorosis typically manifests as a diffuse increase in bone density, whereas avascular necrosis of the epiphyses and diaphyseal marrow are the main skeletal manifestations of sickle cell disease. The diagnostic and therapeutic challenges raised when both disorders are present are illustrated by two cases in Senegalese patients from an area characterized by high fluoride contents in the water and soil. Both had SS sickle cell disease. Skeletal fluorosis was diagnosed during evaluation for avascular necrosis in one patient and in the wake of septic arthritis in the other. Femoral head necrosis is difficult to identify in a patient with skeletal fluorosis. The bone lesions due to sickle cell disease and those due to fluorosis can mimic other bone diseases, most notably metastases. The combination of sickle cell disease and fluorosis results in significant medullary canal narrowing due to cortical thickening and to accumulation of necrotic bone. When performing hip replacement surgery, careful reaming of the medullary canal may reduce the risk of iatrogenic femoral fracture and inappropriate stem placement.
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2/22. hydrofluoric acid-induced burns and life-threatening systemic poisoning--favorable outcome after hemodialysis.

    BACKGROUND: skin contact with hydrofluoric acid (HF) may cause serious burns and life-threatening systemic poisoning. The use of hemodialysis in fluoride intoxication after severe dermal exposure to HF has been recommended but not reported. CASE REPORT: A 46-year-old previously healthy man had 7% of his body surface exposed to 71% HE Despite prompt management, with subsequent normalization of the serum electrolytes, recurrent ventricular fibrillation occurred. On clinical suspicion of fluoride-induced cardiotoxicity, acute hemodialysis was performed. The circulatory status stabilized and the patient fully recovered. High fluoride levels in the urine and serum were confirmed by the laboratory. DISCUSSION: There is no ultimate proof that the favorable outcome in this case was significantly attributable to the dialysis. However, most reported exposures of this magnitude have resulted in fatal poisoning. As our patient had normal serum electrolytes and no hypoxia or acidosis at the time of his arrhythmias, it was decided that all efforts should be focused on removing fluoride from his blood. The rationale for performing hemodialysis for this purpose is clear, even though such intervention is more obviously indicated in patients with renal failure. CONCLUSION: Hemodialysis may be an effective and potentially lifesaving additional treatment for severe exposure to HF when standard management has proven insufficient.
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3/22. Ossification of the transverse atlantal ligament associated with fluorosis: a report of two cases and review of the literature.

    STUDY DESIGN: Two cases of ossification of the transverse atlantal ligament (OTAL) are reported, and the literature is reviewed. OBJECTIVE: To report two cases of OTAL, which share fluorosis as a possible etiologic link. SUMMARY OF BACKGROUND DATA: OTAL, a rare phenomenon, may cause upper cervical canal stenosis and spastic quadriparesis. However, the incidence, etiology, and the best therapeutic options are currently unclear. methods: Two cases are reported. Included are pertinent history, physical examination, radiographic evaluation, nonsurgical interventions, and outcomes. The available literature is also reviewed. RESULTS: On systemic examination, these two cases were found to have ossification of many ligaments and interosseous membranes, i.e., the atlantal transverse ligament, posterior longitudinal ligament, and interosseous membranes of ribs, forearm, and leg. These findings were coupled with a history of high fluoride intake and dental fluorosis; the diagnosis of fluorosis was made. After 2 weeks of treatment with halo ring traction, and protection and stabilization with a hard cervical collar, the clinical symptoms significantly improved. CONCLUSION: The incidence of OTAL may be not as rare as has been thought. Although the complete etiology of OTAL is not known, fluorosis may be one of the etiologic factors related to OTAL, as well as the ossification of other ligaments and interosseous membranes. Nonsurgical treatment may be safe and effective.
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4/22. Fatality due to acute fluoride poisoning in the workplace.

    We report a case of a 65-year-old worker who suffered a third-degree skin burn to 5% of his total body surface area as a result of being splashed in the face with hydrofluoric acid (HF). He died shortly thereafter without having received adequate first aid. His serum fluoride concentration was markedly increased at 6.38 mg/dl with hypocalcemia and hyperkalemia. We concluded that he died of HF poisoning. In this case he might have managed to avoid death if he had not been working alone and if he had received adequate first aid on the scene as soon as possible. We re-emphasize the need for the immediate initiation of first aid on the scene and the distribution of information on the risks of HF to workers.
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5/22. Controlling the fluoride dosage in a patient with compromised salivary function.

    BACKGROUND: High-concentration topical fluorides are used commonly to with compromised salivary function due to irradiation and chemotherapy. CASE DESCRIPTION: The authors describe a 50-year-old man with previously treated cancer who was using tray-applied topical fluoride gel. He complained of gastric symptoms, difficulty in swallowing, leg muscle soreness and knee joint soreness. A computed tomographic scan revealed thickening of the esophageal walls. An upper endoscopy revealed abnormal motility. The motility test indicated high-amplitude peristalsis and hypertensive lower esophageal sphincter, and urine testing indicated high levels of systemic fluoride. The patient's fluoride regimen was altered, and within a short period his urinary fluoride levels returned to normal and his symptoms resolved. CLINICAL IMPLICATIONS: Clinicians prescribing home-applied high-concentration fluorides need to be cognizant of the symptoms of fluoride toxicity, carefully monitor the patient's compliance with the treatment regimen, and adjust the dosage or mode of application to control the total ingested dose of fluoride.
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6/22. Endemic fluorosis with spinal cord compression. A case report and review.

    We report a case of spinal cord compression in a Mexican immigrant due to vertebral osteosclerosis from chronic fluoride intoxication. Endemic fluorosis is acquired through drinking water. groundwater sources with high fluoride content occur worldwide. The epidemiology, metabolism, and clinical features of fluorosis are reviewed. Greater physician awareness of this entity is important to identify correctly patients with this unusual and potentially devastating clinical disorder.
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7/22. Fluoride-induced chronic renal failure.

    Renal fluoride toxicity in human beings is difficult to assess in the literature. Although experimental studies and research on methoxyflurane toxicity have shown frank renal damage, observations of renal insufficiency related to chronic fluoride exposure are scarce. We report a case of fluoride intoxication related to potomania of Vichy water, a highly mineralized water containing 8.5 mg/L of fluoride. Features of fluoride osteosclerosis were prominent and end-stage renal failure was present. The young age of the patient, the long duration of high fluoride intake, and the absence of other cause of renal insufficiency suggest a causal relationship between fluoride intoxication and renal failure.
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8/22. Delayed fatal hyperkalemia in a patient with acute fluoride intoxication.

    A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of fluoride from the body by dialysis, binding fluoride with aluminum or calcium, or enhancing fluoride excretion by inducing a metabolic alkalosis. Direct treatment of the hyperkalemia with glucose, insulin, and bicarbonate is ineffective. quinidine may be an effective therapy for the hyperkalemia and ventricular irritability, but is as yet untested in human beings.
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9/22. suicide by exposure to sulfuryl fluoride.

    The insecticide fumigant, sulfuryl fluoride, was used as an instrument of self destruction in at least two of the three fatal exposures detailed in this report. The autopsy findings, while nonspecific, have a confirmatory value. Toxicologic analysis should include a plasma and a urine fluoride level, since the toxic effects of exposure are probably related to this ion. Concentrations of fluoride in our cases were: 50.42 mg/L (Case 1) and 20 mg/L (Case 3). However, the values must be interpreted in light of all known information as a result of the paucity of reported cases of fatal sulfuryl fluoride exposures. The cases described provide a model for the investigation of tent fumigation deaths. Proper investigation of fumigant deaths requires knowledge of the insecticide, the fumigation procedure, and the implementation of warning devices. Guidelines are offered along with a procedural checklist for the investigation of tent fumigation deaths.
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10/22. Reversibility of skeletal fluorosis.

    At two x ray examinations in 1957 and 1967, 17 cases of skeletal fluorosis were identified among long term cryolite workers in Copenhagen. In 1982 four of these patients were alive, eight to 15 years after exposure had ended. Radiographs were obtained, and the urinary fluoride excretion was measured. A similar picture emerged in all four cases: extensive fading of the sclerosis of trabecular bone in ribs, vertebral bodies, and pelvis, whereas cortical bone thickening and calcification of muscle insertions and ligaments remained virtually unchanged. The fluoride excretion was increased in three cases (with the shortest exposure free period). These findings indicate that with continuous remodelling of bone tissue trabecular sclerosis is slowly reversible and the excess fluoride is excreted in the urine.
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