Potential complications posed by hypocalcemia in wound healing Challenging the stigma of mental health

By: Sarah, Hewady, PharmD Candidate c/o 2020

           Calcium’s fundamental importance in the early hemostasis phase of wound healing has been established through its role as a cofactor in the blood-clotting cascade, facilitator of platelet aggregation with von Willebrand factor, and activator of protein kinase C, ultimately leading to glycoprotein IIb/IIIa’s increased binding affinity for fibrinogen.^1,2 The current investigation of calcium’s role in the later proliferation stages of wound healing could further validate its importance to the wound healing process. The following case illustrates the potential complications posed by hypocalcemia in wound healing.

A twenty-seven year old female underwent a cesarean section with a low transverse abdominal incision. The patient received prophylactic antibiotics prior to her skin incision and had sutures removed five days after the procedure. She presented to the clinic eleven weeks post-surgery concerned about prolonged incision site healing. The incision, measured at twelve centimeters, presented no clinical manifestations of infection (pus, fever, inflammation, pain). Physical examination revealed a healthy periwound (the tissue surrounding the actual wound). Upon questioning, she admitted to a decreased intake of dairy products during and after her pregnancy due to intolerance. Her comprehensive metabolic panel revealed a corrected calcium level of 7.6 mg/dL (falling below the therapeutic range of 8.5 – 10.2 mg/dL) and she was initiated on 500 mg calcium supplements to be taken twice daily. A scheduled follow-up appointment seven days later revealed significant incision site healing and wound contraction. The patient exhibited continued healing in her next few follow-up appointments.

The patient’s restricted calcium intake throughout and after her pregnancy was found to be responsible for this clinically significant hypocalcemia which ultimately resulted in decelerated wound healing after her cesarean section.³ It is easy to overlook deviations in calcium levels when presented with an intricate case such as this one, yet, it is promising that the patient’s hypocalcemia was easily reversed after initiation of calcium supplements, and that the associated benefits were observed within a single week. Identifying hypocalcemia as the cause of impaired wound healing is easier in a clinical setting as lab values are readily accessible and the possibility of infection can be ruled out through examinations and lab tests. However, community pharmacists can also play a significant role in addressing such physiological abnormalities. Milder symptoms of this electrolyte’s imbalance may present on a much smaller scale, calling for community pharmacists to consider hypocalcemia as a possible cause of impaired wound healing, particularly in patients who are on antiepileptics, bisphosphonates, aminoglycosides, and proton pump inhibitors, which are classes of medications known to cause hypocalcemia.⁴ Other symptoms of hypocalcemia can also present as muscle cramps, lightheadedness, slow heartbeat, and even depression, memory loss, and hallucinations.⁴

Although further research is required to elucidate calcium’s direct role in the later stages of the wound healing process, pharmacists in all practice settings must be mindful of the risks hypocalcemia poses to all patient populations and remedy the situation through supplementation, dietary modification, and physician referral.

SOURCES:

1. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-23. doi: 10.4103/0019-5049.144643
2. Smith SA, Travers RJ, Morrissey JH. How it all starts: Initiation of the clotting cascade. Crit Rev Biochem Mol Biol. 2015;50(4):326-36. doi: 10.3109/10409238.2015.1050550
3. Moe AM, Golding AE, Bement WM. Cell healing: Calcium, repair and regeneration. Semin Cell Dev Biol. 2015;45:18-23. doi: 10.1016/j.semcdb.2015.09.026
4. Liamis G, Milionis HJ, Elisaf M. A review of drug-induced hypocalcemia. J Bone Miner Metab. 2009;27(6):635-42. doi: 10.1007/s00774-009-0119-x