Vinas-Rios JM, Sanchez-Rodriguez JJ , Kretschmer T, Medina-Govea FA and Heinen CPG
Background: Despite an overabundance of literature the PubMed database has more than 50,000 hits for the search term “traumatic brain injury” the complex area of TBI is actually somewhat overlooked in both medical training and subsequent general medical and neuropsychiatric practice. We pretend to review the available literature on the effects of hypocalcaemia regarding prognosis in early phases after moderate- severe TBI, to identify the gaps in the literature, and to try filling these gaps by including our proposed pathophysiological schema leading to posttraumatic hypocalcaemia. Material and methods: The data from 282 patients (180 retrospective and 102 prospective) suffering moderatesevere TBI distributed in three different works was analyzed. Patients meeting the following criteria were included: Age: 16 to 87 years, Glasgow Coma Scale (GCS) from 3 to 13 points, Cranial Computed Tomography (CCT) upon admission and Calcium and/or ionized calcium measurements taken on the day of TBI, as well as on days 3 and 7. Results: The expectation that non-ionized serum calcium (serum calcium), as seen in the collective of 122 Mexican patients, would be a significant predictive factor regarding TBI was surprisingly, not the case; rather, in the retrospective and prospective German patient collectives, this factor was non-significant. Instead, a more specific calcium measure, namely ionized serum calcium, was significant as a predictor regarding mortality/morbidity in patients suffering TBI. Conclusion: Hypocalcaemia is a marker for the depth of brain damage as a result of a cascade of various pathologic mechanisms such as direct mechanical trauma, neuro-inflammation, altered vessel-autoregulation and hypoxia.
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