A target-oriented algorithm for maintaining serum calcium stability automatically in regional citrate anticoagulation

Background: Regional citrate anticoagulation (RCA) for renal replacement therapy is widely practiced in critically ill patients. However, concern exists regarding its labor-intensiveness for monitoring and the associated hypocalcemia. In this study, we provided an algorithm for prescribing RCA and evaluated its safety in patients. Methods: During 18 hemofiltration treatments with calcium-free replacement solution, participants were randomized to receive algorithm-based or trial-and-error RCA protocol. The effluent volume, post-filter and in vivo ionized calcium (iCa), and calcium in the sera and effluents were periodically measured at an interval of 1 to 2 h. Results: For patients received algorithm-based RCA protocol, no one had a serum iCa less than 0.9 mmol/L, and none needed calcium supplement adjustment to maintain serum calcium stability. For patients accepted trial-and-error protocol, all patients had a serum iCa below 0.9 mmol/L, their serum iCa and calcium levels fluctuated dramatically, and all patients need additional calcium supplement adjustment during RCA. None of the participants showed a post-filter iCa > 0.4 mmol/L. Conclusion: We provided a safe algorithm for calculating calcium supplementation doses that could maintain serum calcium stability without additional adjustment during RCA.

EP08 Acute calcific epicondylitis associated with primary hypoparathyroidism: a paradox effect or an adverse event

Background Calcific tendonitis is characterised by the accumulation of basic calcium phosphate hydroxyapatite crystals within the tendon. It is mainly affects supraspinatus tendon and it is usually idiopathic, but can be associated with other diseases. We are describing a previously unreported case of calcific epicondylitis in a patient with primary hypoparathyroidism on a high dose of calcium supplement with a highlight on its pathogenesis. Methods We describe a previously unreported case of calcific epicondylitis in a patient with primary hypoparathyroidism on a high dose of calcium supplement with literature review highlighting the possible mechanism and pathogenesis. Results A 33-year-old male presented with acute left elbow pain and swelling. A several months earlier, presented to the Emergency Department with similar attack. The elbow x-ray showed two hyper-dense calcifications at the lateral epicondyle. His Ultrasound revealed hyperechoic deposits over the lateral epicondyle with increased Doppler activity confirming the diagnosis of lateral calcific epicondylitis. Previously, he was seen a few times because of nonspecific symptoms of irritability, generalised weakness and numbness, found to have hypocalcemia of < 1.5 mmol/l and low PTH 3 pg/ml, and diagnosed with primary hypoparathyroidism. His serum calcium was maintained by a high intake of daily calcium carbonate 1250 mg three tablets three times daily and calcitriol one mcg/day. Just prior to his presentation, he developed a foreign body sensation on swallowing, and the CT neck revealed a tiny hyper-density calcification along the posterior surface of the soft palate. We gave him Celecoxib 200 mg daily for five days with good response. All his previous calcium levels were on the low normal range, 24-hour urine calcium was elevated at 11.8 mmol/24 hours. We referred him to Endocrinologist for consideration for PTH replacement therapy. Two fundamentally different processes for calcific tendonitis have been proposed: degenerative and reactive calcification. Degenerative theory proposes that dystrophic calcification follows a necrotic phase, usually attributed to a wear-and-tear and aging. This theory is supported by an observation that calcific tendonitis seldom affects young people. While the Reactive calcification theory was described to involves four phases: pre-calcific, formative, resorptive and healing. Reactive calcification theory is supported by a variety of imaging studies demonstrating a complete resolution of the calcium deposits. Calcific tendonitis is largely idiopathic or traumatic. Metabolic causes proposed to play a role, but nothing mentioned with regards to the hypoparathyroidism. It is not clear in our case whether the cause of calcific tendonitis is primarily due to hypoparathyroidism or secondary to the high calcium replacement Conclusion In young patients with hypoparathyroidism on high dose of calcium replacement therapy, a high index of suspicion is needed to diagnose calcific tendonitis. Better understanding of the pathogenesis may help to prevent the soft tissue calcification in general Disclosures B. Awadh None. A. Al-Allaf None.

Calcium supplementation prolongs the time of hospitalization and has a double effect on mortality in septic patients: A retrospective study from MIMIC-III

Background Hypocalcemia is a common electrolyte disturbance in sepsis, calcium administration in those patients remains a controversial issue. The aim of this study was to assess the association of calcium supplementation with the time of hospitalization and mortality in septic patients. Method 5761 eligible septic patients, including 2689 with calcium supplementation and 3072 without calcium supplementation, were extracted from the MIMIC-III database. A total of 1463 pair patients were included in the analysis after propensity score matching according to the age, sex, SOFA score and lactate on first ICU admission. We compared the length of stay (LOS) in the intensive care unit (ICU) and hospital, as well as the 28-day and hospital mortality, which stratified the analysis according to the Sequential Organ Failure Assessment (SOFA) score, and the iCa on the first ICU admission between the matched groups. Results The results showed that either a too-low or a too-high iCa increased the risk for septic patients, but the minimum of the mortality curve in the non-calcium supplement group was locally in the mild hypocalcemia range. Regardless of the SOFA score and iCa, the LOS in both the ICU and hospital were higher in the calcium supplement group than in the non-calcium supplement group. Overall, the 28-day and hospital mortality were greater but not statistically significant in the calcium supplement group than in the non-calcium supplement group (14.83% vs 13.39%, p=0.416; 16.20% vs 13.88%, p=0.079, respectively). However, the survival analysis stratified by SOFA score showed that calcium supplementation reduced mortality when the patient’s SOFA score was >8 (p=0.028), while it worsen the outcome when the SOFA score was ≤4 (p<0.001) and had no significant effect with SOFA scores from 5~8 (p=0.556). Conclusion Our findings suggest that mild hypocalcemia may be protective in septic patients and that calcium supplementation may prolong hospitalization and have a double effect on mortality. The SOFA score may be a valuable clinical index for calcium administration decision making.