Trousseau sign in hypocalcemia.
Ontology highlight
ABSTRACT:
SUBMITTER: Rehman HU
PROVIDER: S-EPMC3091937 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundDuring hemorrhagic shock and subsequent resuscitation, pathways reliant upon calcium such as platelet function, intrinsic and extrinsic hemostasis, and cardiac contractility are disrupted. The objective of this systematic review was to examine current literature for associations between pretransfusion, admission ionized hypocalcemia, and composite outcomes including mortality, blood transfusion requirements, and coagulopathy in adult trauma patients.MethodsThis review was reported using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist. We searched Ovid MEDLINE and grey literature from database inception till May 3, 2020. Case series and reports were excluded. Reference lists of appraised studies were also screened for articles that the aforementioned databases might not have captured. The Newcastle-Ottawa Scale was used to assess study quality.ResultsA total of 585 abstracts were screened through database searching and alternative sources. Six unique full-text studies were reviewed, of which three were excluded. Admission ionized hypocalcemia was present in up to 56.2% of the population in studies included in this review. Admission ionized hypocalcemia was also associated with increased mortality in all three studies, with increased blood transfusion requirements in two studies, and with coagulopathy in one study.ConclusionHypocalcemia is a common finding in shocked trauma patients. While an association between admission ionized hypocalcemia and mortality, blood transfusion requirements, and coagulopathy has been identified, further prospective trials are essential to corroborating this association.Level of evidenceSystematic review, level III.
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Project description:Hypocalcemia is a known risk following bariatric surgery and can contribute to the development of osteoporosis. Osteoporosis is commonly treated with denosumab, though denosumab can exacerbate underlying abnormalities in calcium homeostasis. We present the case of a 59-year-old female with severe hypocalcemia who had been treated with denosumab for osteoporosis three months before and had Billroth II gastric bypass surgery 15 years before, for bariatric purposes. Intravenous calcium supplementation was used to correct the initial electrolyte abnormality, and the patient was able to maintain appropriate calcium levels on high doses of oral calcium before discharge. Denosumab-induced hypocalcemia has been previously reported in patients with predisposing conditions including chronic kidney disease, primary sclerosing cholangitis, Crohn's disease, and a history of sleeve gastrectomy for marginal gastric ulcers. A few cases of hypocalcemia have been reported in patients with a history of bariatric surgery secondary to vitamin D deficiency, but this report is unique in demonstrating denosumab-induced hypocalcemia after bariatric surgery with normal vitamin D levels, suggesting a primary malabsorption of calcium. The risk of severe hypocalcemia should be considered before initiating denosumab to treat osteoporosis in patients with a history of bariatric surgery. If denosumab is initiated, serum calcium levels should be closely monitored, and patients should be educated about the importance of adherence to calcium supplementation.
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