S. Asaadi1, R. Rojas1, S. Lee1, M.B. Tabrizi1, K. Mukherjee1, M.G. Rosenthal1 1Loma Linda University, Acute Care Surgery, Loma Linda, CALIFORNIA, USA
Introduction:
Calcium is vital for the clotting cascade, and trauma patients are frequently hypocalcemic, which can lead to coagulopathy and worsened outcomes. For traumatic brain injury (TBI) patients coagulopathy can be especially detrimental. This study evaluates the relationship between hypocalcemia, the progression of intracranial hemorrhage (ICH in traumatic brain injury (TBI) patients.
Methods:
This retrospective study at a level I trauma center included adult trauma patients with an AIS head score > 3 and initial CT findings of ICH, followed by a repeat CT within 12 hours and documented ionized calcium (iCa) levels. Exclusions included, craniectomy/craniotomy before the repeat CT, those on pre-hospital antiplatelet/anticoagulation medications, transfers from outside facilities, or those receiving blood before iCa lab draws.
Results:
A total of 331 TBI patients were included. Median serum iCa was 1.13 mmol/L, 16 (4.8%) patients had severe hypocalcemia (iCa<0.9), and 169 had mild to moderate hypocalcemia( 0.9<iCa<1.6). The median age of patients in the ICH progression (ICHP) group was higher (39.5 vs. 33 years, P=0.046). The ICHP group had higher partial thromboplastin time (PTT) (25.6s vs. 24.3s, P=0.015). Intraparenchymal hemorrhage was more common in the worsening group (62.2% vs. 56.9%, P=0.046), and they required more packed red blood cells (4 units vs. 3 units, P=0.017), fresh frozen plasma (4 units vs. 2 units, P=0.024), and cryoprecipitate (1 unit vs. 0.5 units, P=0.016). Tranexamic acid administration was higher in the ICHP group (50% vs. 26.7%, P=0.002). iCa levels did not show a significant difference between the two groups (1.14 [1.08-1.19] mmol/L vs. 1,13 [1.08-1.2] mmol/L, P=0.583). In-hospital mortality was higher in the ICHP group (67.9% vs. 32.1%, P=0.016). Binary logistic regression showed no significant association between ICHP and ionized calcium level (OR 3.520, P=0.487) after adjustment for age, PTT, intraparenchymal hemorrhage, FFP, cryoprecipitate, and AIS head.
iCa levels were not significantly different between survivors and non-survivors (1.15 [1.08-1.19] vs. 1.13 [1.05-1.19] mmol/L, P=0.449). Binary logistic regression showed no significant association between mortality rate and iCa (OR 0.442, P=0.621) after adjustment for age, PTT, intraparenchymal hemorrhage, FFP, cryoprecipitate, AIS head, ISS, worsening CT findings, and GCS.
Conclusion:
Hypocalcemia was not associated with the progression of intracranial hemorrhage or increased mortality in TBI patients. Further controlled studies are warranted to explore the impact of different cutoffs of serum calcium in TBI management.