Low Dose Calcium Administration Increases Mortality During Septic Peritonitis

Reducing Routine Ionized Calcium Measurement

“…The consistent finding of hypocalcemia in ill patients in this and other studies indicates that hypocalcemia may be a natural response to illness, akin to the alterations in other serum analytes (fibrinogen, Alb, iron, and so forth) seen during inflammation. This finding, together with animal studies that have demonstrated possible harm from calcium administration during sepsis (16,17 ), should prompt a reevaluation of current practices regarding calcium supplementation in hospitalized patients. Standing orders and protocols that call for frequent measurement and reflexive supplementation of calcium in patients without clinically significant hypocalcemia should be scrutinized.…”

“…Mild hypocalcemia (1.00 -1.12 mmol/L) is more amenable to treatment (15 ), but treating these concentrations has not been proved to benefit patients. In fact, there is some evidence in animal models that calcium supplementation in severe sepsis is actually detrimental to survival (16,17 ), raising the question of whether hypocalcemia is an adaptive response with protective benefits.…”

An Observational Study on the Effects of Nadroparin-Based and Citrate-Based Continuous Venovenous Hemofiltration on Calcium Metabolism

“…It is unknown what the precise iCa level should be in a situation of acute renal failure and multiple organ dysfunction syndrome. A relatively low iCa level was shown to be beneficial in septic rats compared to those with higher suppletion rates but human studies are not available [8] .…”

“…Moreover, to which calcium level a critically ill patient should be replaced is in fact unknown. There is some evidence that a low calcium level in septic patients might be beneficial [8] . However, relatively low calcium levels will induce the parathyroid glands to produce parathyroid hormone (PTH) leading to an increased production of active vitamin D. In the normal situation, hypocalcemia will lead to a rapid increase in PTH levels to increase renal calcium reabsorption, to release calcium from the bone and to increase the renal production of 1,25-dihydroxycholecalciferol [9] .…”

Gadolinium blocks rat kupffer cell calcium channels: Relevance to calcium-dependent prostaglandin E2 synthesis and septic mortality

“…Nonetheless, other investigators studying the physiological derangements of septic shock have concluded that the increased [Ca ϩϩ ] i characteristic of sepsis is at least partly responsible for the poor outcome of septic shock. [54][55][56][57][58] For example, rats given systemic CaCl 2 are less able to withstand LPS administration 54 or cecal ligation and puncture. 56 The prevention of mortality with calcium antagonists in six animal studies (reviewed in Zaloga et al 56 ) further corroborates the deleterious nature of calcium in sepsis.…”