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Bismuth subsalicylate (BSS) is the active ingredient in over-the-counter antacid and antidiarrheal medications. Coagulopathy in the setting of acetylsalicylic acid toxicity is well documented but not in setting of bismuth subsalicylate overuse. We present a case report of coagulopathy from BSS poisoning in a patient with underlying cirrhosis. The patient's high prothrombin time suggests inhibition of vitamin K-dependent coagulation factors. The patient had decreased factor V activity, which is responsible for converting prothrombin to thrombin. Patients with cirrhosis often have hypoprothrombinemia which may be exacerbated by salicylate-induced coagulopathy. Given the widespread use of BSS products, physicians should recognize coagulopathy as a possible manifestation of toxicity especially in patients with underlying liver disease.

Çelebi-Tayfur A, Yaradılmış RM, Ulus F, Çaltık-Yılmaz A, Özayar E, Koşar B, Büyükkaragöz B, Horasanlı E. Bismuth intoxication resulting in acute kidney injury in a pregnant adolescent girl. Turk J Pediatr 2019; 61: 292-296. Bismuth intoxication is a rare cause of acute kidney injury (AKI) and is usually reversible by appropriate therapeutic measures. We present here a case of an adolescent pregnant girl who developed AKI due to an overdose of colloidal bismuth subcitrate (CBS, total amount of 6 g). She received parenteral chelating agent dimercaprol for 14 days. Continuous venovenous hemodiafiltration (CVVHD) with high-flux membrane was carried out in the first 3 days of chelating therapy and intermittent hemodialysis for 11 days, thereafter. The patient recovered clinically and was discharged after 21 days. She gave birth to a healthy term boy. At the last visit, the baby was 6 months old with normal growth and development as well as normal kidney functions. Neither deterioration in renal functions nor emergence of proteinuria was recorded in the patient during follow-up care after hospital discharge. In cases of AKI due to an overdose of CBS, treatment with dimercaprol combined with high flux hemodiafiltration and subsequently hemodialysis appears to be both useful and safe for bismuth elimination.

Background: Bismuth iodoform paraffin paste (BIPP) is used for the packing of wound and surgical cavities. Features of both bismuth and iodoform toxicities have been associated with the use of BIPP, but there are no previous reports of 2,3-dimercaptopropane-1-sulphonate (DMPS) chelation therapy for bismuth poisoning secondary to its use., Case Report: A 67-year-old man presented with a pelvic tumor requiring extensive surgical resection. BIPP packing was required post-operatively for surgical wound breakdown. A few days after insertion, the patient developed neurological features of bismuth toxicity (blood and urine bismuth concentrations were 340 microg/L and 2800 microg/L, respectively), which was treated with removal of the BIPP packing and DMPS chelation [27 days of intravenous DMPS (5 mg/kg 4 times daily for 5 days, 5 mg/kg three times daily for 5 days followed by 5 mg/kg twice a day for 17 days) followed by 24 days of oral DMPS (200 mg three times a day for 10 days, followed 200 mg twice daily for 14 days)]. This resulted in improvement in his symptoms and a decline in his pre-chelation bismuth concentration of 480 microg/L to 5 microg/L following chelation. There were no adverse effects during chelation., Conclusions: DMPS chelation appears to be a potentially effective chelating agent in bismuth toxicity.

A 22-year-old woman ingested 5.4 g of colloidal bismuth subcitrate (CBS) in a suicide attempt. After ingestion, she presented with Fanconi's syndrome and acute renal failure to our unit. On the third day after ingestion, she was anuric. Ulcerations of both tonsils were observed 8 days after intoxication. Sodium-2,3-dimercapto-1-propanesulfonate (DMPS) is shown to be an effective chelating agent of heavy metal intoxications, but it has only a small effect on elimination of bismuth salts in patients with renal insufficiency without hemodialysis. In our case, we initiated hemodialysis and intravenous treatment with DMPS 60 hours after intoxication. By repeated measurements of bismuth concentrations in serum and dialyzed fluid, we showed its successful elimination. Serum bismuth level decreased from 640 microg/L to 15 microg/L within 6 days. With elimination of bismuth, renal function improved, and tonsil ulcerations healed. Hemodialysis was discontinued on day 14. Follow-up examination 6 weeks later showed normal renal function. Clinicians should be aware that acute renal failure and tonsil ulcerations can occur after CBS intoxication. Generally, acute renal failure caused by CBS intoxication is reversible. Treatment with the chelating agent DMPS in combination with hemodialysis is highly effective in reducing the serum bismuth level in patients with acute renal failure., (Copyright 2002 by the National Kidney Foundation, Inc.)

Neurotoxins are an important cause of neurologic disorders. A vast number of potentially neurotoxic compounds exist, including prescription drugs, illicit substances, and exposures through the workplace, residence, hobbies, and the environment. Effects of neurotoxins can mimic neurologic illnesses; therefore, it is important to consider neurotoxins in the differential diagnosis of any patient with neurological dysfunction. Paramount to the diagnosis of a possible neurotoxic syndrome is establishing causation. This can be done by a systematic approach utilizing principles in epidemiology and applying them to the individual patient. This approach is discussed in the following article in an attempt to bring structure to solving problems in a complex area of medicine.

For decades, drugs containing bismuth have been used to treat gastrointestinal disorders. Although a variety of adverse effects, including neurological syndromes, have been recorded, the biological/toxicological effects of bismuth ions are far from disclosed. Until recently, only quantitative assessments were possible, but resent research has made histochemical tracing of bismuth possible. The technique involves silver enhancement of bismuth crystallites by autometallography (AMG). In the present study, the localization of bismuth was traced by AMG in sections of paraffin-embedded brain tissue obtained by autopsy from 6 patients suffering from bismuth intoxication in a period ranging from 1975 through 1977. Tissue was analyzed at light and electron microscopical levels, and the presence of bismuth further confirmed by proton-induced x-ray emission (PIXE). Clinical data and bismuth concentrations in blood, cerebellum, and thalamus were measured by atomic absorption spectrophotometry (AAS) and are reported here. Histochemical analyses demonstrate that bismuth accumulated in neurons and glia cells in the brain regions examined (neocortex, cerebellum, thalamus, hippocampus). Cerebellar blood vessels stained most intensely. The PIXE and AAS data correlated with the histochemical staining patterns and intensities. At the ultrastructural level, bismuth was found to accumulate intracellularly in lysosomes and extracellularly in the basement membranes of some vessels.

The paper presents the clinical description of the masticatory organ and biochemical assessment of dental tissue in a patient employed in a glassworks for 20 years. During 12 years the patient has suffered baldness ("Alopecia areata") and atypical extensive and non-healing cutaneous lesions. Dental examination revealed changes typical of chronic poisoning by cadmium and bismuth compounds.

A 58-year-old woman developed severe progressive dementia. Markedly impaired memory, apraxia and abnormal behaviour with psychotic components suggested Alzheimer's syndrome. But there were atypical signs, namely abnormal coordination, occasional tremors and dysarthria. A search for a possible toxic cause was at first unsuccessful, but by chance a "gastric power" containing 0.1 g of bismuth gallate per gram of powder, was found in her night-table. The patient had taken it regularly over years, at a dosage of up to 1.5 g daily, to combat gastric acidity. Six days after stopping the drug the blood bismuth level was 70 micrograms/l, which within 1-2 months fell to 9 micrograms/l. After 4 1/2 months in hospital the patient was discharged in a good general condition and with normal intellectual function.

In the recent literature, only a few reports deal with generalized pigmentation caused by bismuth treatment. We report a patient developing generalized pigmentation of the skin and mucous membranes without further signs of chronic bismuth poisoning following long-term administration of bismuth for pneumatosis cystoides intestinalis. Bismuth deposits were documented in a skin biopsy.

We present four cases of heavy metal poisoning (mercury, lead, bismuth and arsenic) in which plain chest and/or abdominal assisted in the differential diagnosis of the clinical picture manifested upon admission at our Emergency Department. The patients suffering from mercury, lead, and bismuth poisoning recovered some weeks after treatment was started. However, the patient with arsenic trioxide poisoning developed cardio-circulatory collapse leading to death three days after admission.

Twenty-four urinary bismuth excretion was measured in five patients who had been treated with tripotassium dicitrato bismuthate, before and after single 1 g oral dose of D-penicillamine. Before dosing with D-penicillamine, the median 24 h urinary bismuth output was 55 micrograms 24 h-1 (range 17-156 micrograms 24 h-1) and following dosing with D-penicillamine the median 24 h urinary bismuth output was 53 micrograms 24 h-1 (range 12-156 micrograms 24 h-1). D-penicillamine does not facilitate the urinary excretion of bismuth, hence it is unsuitable for use as an oral chelator in patients with bismuth intoxication.

The central metabolism of dopamine, serotonin, cyclic AMP and cyclic GMP was studied by use of the probenecid test in three patients with bismuth encephalopathy and in one patient with mercury encephalopathy. The accumulation of HVA and of cGMP in the cerebrospinal fluid was depressed during the acute phase of bismuth encephalopathy with severe hyposomnia, while it was increased in a patient with regression of clinical symptoms and normal in a patient with more advanced recovery. The patient with chronic mercury poisoning showing a severe cerebellar ataxia and rigidity had an almost complete suppression of HVA accumulation and an increase of cGMP accumulation. No pronounced differences of 5-HIAA and cAMP behavior were found. It is concluded that the central metabolism of dopamine and of cGMP is severely affected in bismuth and mercury encephalopathies.

Seventy patients admitted to hospital with bismuth encephalopathy had repeated clinical and EEG examinations. All the patients exhibited myoclonic jerks, but no paroxysmal features ever appeared on EEG. Computed tomography showed cortical hyperdensities. Seizures were observed in 22 patients, but epileptic EEG patterns appeared only when the bismuth blood level was below 1500 microgram/1. It is suggested that a high cortical intracellular bismuth concentration induces a "cortical inhibition" which causes suppression of physiological electrical brain activity, the absence of EEG paroxysmal phenomena during myoclonic jerks, and explains the rarity of epileptic seizures.

Neuropathological study of 3 patients dying from bismuth encephalopathy showed the absence of specific lesions and the probably secondary nature of the abnormalities found. Multiple samples taken from various areas of the brain were used for the purpose of the analysis of the topographical distribution of bismuth. Levels were invariably very high and to toxic agent diffusely distributed. The concentration was nevertheless higher in the grey matter than in the white matter. They hypothesis of a liposoluble compound which would explain the affinity of bismuth for cerebral tissue is probable.

Experimental intoxications of pigs were performed. It seems to be confirmed that bismuth crosses the blood-brain barrier. An organic derivative, trivinyl-bismuth, is more active than the inorganic salt of bismuth. In the brain, bismuth is preferentially found in synaptosomes. Bismuth is found in brain lipids of control pigs at very low levels. In intoxicated pigs, the level of bismuth is increased mainly in cerebellum and then in thalamus. Bismuth is partly associated to lipids. There is not a correlation between the level of bismuth in blood and in brain lipids. However, in the trivinyl intoxicated pig, a high level of blood bismuth is concomittant to a high level of brain lipid bismuth. The high content of this metal in cerebellum lipid extract may be of functional significance.