Case of bismuth subsalicylate poisoning in 70-year-old patient
A 70-year-old female patient with depression and irritable bowel syndrome arrived at the emergency department after experiencing changed mental status, shortness of breath, nausea, and vomiting for three days. She had lately increased her daily intake of liquid bismuth subsalicylate, which she had previously used to manage irritable bowel symptoms, to treat severe diarrhoea and abdominal pain. A respiration rate of 22 breaths per minute, disorientation, and mild, diffuse abdominal pain were all noted during the physical examination. Primary anion-gap metabolic acidosis, primary respiratory alkalosis, and a salicylate level of 76 mg per deciliter (5.50 mmol per litre; normal value, 5 mg per deciliter [0.35 mmol per litre]) were discovered in laboratory tests. Based on the findings, the patient was diagnosed with bismuth subsalicylate poisoning.
An abdominal radiograph with no oral contrast material revealed intraluminal radiopaque material throughout the bowel. Bismuth subsalicylate toxicity was diagnosed. In the gastrointestinal tract, bismuth subsalicylate is converted to bismuth and salicylic acid. Because of its high density, which approaches that of lead, large quantities of bismuth seem radiopaque. The patient’s symptoms improved after therapy with sodium bicarbonate infusion and hemodialysis for salicylate poisoning; a repeat salicylate level was 0.
Bismuth subsalicylate (BSS) has been around for over a century and was initially approved by the FDA in 1939. It was developed prior to the use of hygiene and sanitation to treat cholera infections. BSS has given healthcare practitioners an alternative to antimicrobials for treating nausea and diarrhoea. The most common symptoms of BSS are gastrointestinal problems and traveler’s diarrhoea.
Clinical findings
Many of the features of bismuth subsalicylate (BSS) are related to its formulation as an insoluble salt of salicylic acid and trivalent bismuth. The method of action by which BSS operates is complex. BSS hydrolyzes in the stomach into two compounds: bismuth and salicylic acid. The salicylate molecule is almost entirely absorbed into the bloodstream, but the bismuth salt is absorbed only marginally. Bismuth salts are formed when bismuth stays in the gastrointestinal tract. Bactericidal and antibacterial activity of these bismuth salts prevents bacteria from binding and developing on stomach mucosal cells. This is the method by which BSS aids in the eradication of H. pylori. Furthermore, blocking bacterial attachment to mucosal cells has numerous advantages, including reducing intestinal secretion and boosting fluid absorption.
BSS appears to have no effect on the natural flora of the stomach; nonetheless, its antibacterial and antisecretory effects are important in the treatment of diarrhoea. BSS’s antidiarrheal action is most likely attributable to:
- Prostaglandin formation is reduced because BSS inhibits cyclooxygenase. Prostaglandins are known to cause inflammation and hypermotility.
- The stimulation of fluid, sodium, and chloride reabsorption – this activity aids in the reduction of fluid loss.
- Intestinal secretion suppression.
- While the likely mechanism of BSS in peptic ulcer disease involves its cytoprotective and demulcent activities. BSS, in particular, inhibits the bacteria’s adherence to stomach epithelial cells in H. pylori. Furthermore, BSS inhibits H. pylori enzyme activity such as phospholipase, protease, and urease.
Administration
Bismuth subsalicylate is taken orally and should be stored at room temperature. BSS is offered as a pill or a suspension. Patients (including adults and children) should be instructed to thoroughly shake the suspension before using the accompanying dosing cup. Chewable pills can be eaten whole or dissolved in the mouth. Non-chewable tablets, on the other hand, should be ingested whole and with water. The appropriate dosage is determined on the indication and the patient’s age. It should be noted that there is a scarcity of evidence on the usage of BSS in paediatric patients under the age of 12.
Source: NEJM
