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Hypocalcemia in trauma patients: A systematic review
Mayank Vasudeva1, Joseph K Mathew, Christopher Groombridge
1From the National Trauma Research Institute, Alfred Health (M.V., J.K.M., C.G., J.W.T., C.S.J., A.M., M.C.F.); Emergency and Trauma Centre (M.V., C.G., C.S.J., A.M.), and Trauma Service (J.K.M., C.G., J.W.T., C.S.J., A.M., M.C.F.), The Alfred Hospital; Central Clinical School (J.K.M., M.C.F.), Monash University; Software & Innovation Lab (J.K.M., M.C.F.), Deakin University; and Department of Neurosurgery (J.W.T.), The Alfred Hospital, Melbourne, Australia.
Insights
Admission ionized hypocalcemia is common in trauma patients and linked to increased mortality, transfusion needs, and coagulopathy. Further research is needed to confirm these associations.
Area of Science:
- Trauma critical care
- Calcium homeostasis
- Hemostasis and thrombosis
Background:
- Hemorrhagic shock disrupts calcium-dependent pathways like platelet function, hemostasis, and cardiac contractility.
- Ionized hypocalcemia is a significant physiological derangement during shock and resuscitation.
- Understanding calcium's role is crucial for managing trauma patients.
Purpose of the Study:
- To systematically review literature associating pretransfusion/admission ionized hypocalcemia with outcomes in adult trauma patients.
- To examine the relationship between hypocalcemia and mortality, blood transfusion needs, and coagulopathy.
- To synthesize current evidence on the clinical significance of ionized calcium levels in trauma.
Main Methods:
- Systematic review adhering to PRISMA guidelines.
- Searched Ovid MEDLINE and grey literature until May 2020; screened reference lists.
- Assessed study quality using the Newcastle-Ottawa Scale; excluded case reports/series.
Main Results:
- Six studies were included after screening 585 abstracts.
- Admission ionized hypocalcemia was observed in up to 56.2% of patients.
- Hypocalcemia correlated with increased mortality (3 studies), transfusion needs (2 studies), and coagulopathy (1 study).
Conclusions:
- Ionized hypocalcemia is prevalent in trauma patients experiencing shock.
- A significant association exists between admission hypocalcemia and adverse outcomes, including mortality, transfusion requirements, and coagulopathy.
- Prospective trials are necessary to validate these findings and guide clinical practice.
Background:
During 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.
Methods:
This 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.
Results:
A 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.
Conclusion:
Hypocalcemia 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 Evidence:
Systematic review, level III.
