Ionized Calcium, Parathormone, and Mortality in Critically 111 Surgical Patients

Abstract

A prospective study measured ionized calcium and parathormone sequentially at 48- to 72-hour intervals in 25 surgical intensive care unit patients. Twelve patients (48%) died at mean day 40 and median day 26. Levels of ionized calcium, parathormone, blood urea nitrogen, creatinine, albumin, magnesium, and phosphate for patients who lived were compared with levels for patients who died. The incidence of hypotension, renal failure (creatinine greater than or equal to 3.0), and bacteremia, as well as the amount of red cell, crystalloid, and colloid administration for the two groups was compared. Hypotension, bacteremia, red cells, crystalloid, and colloid were no different. On days 1 and 2 ionized calcium levels were significantly lower and parathormone levels significantly higher in nonsurviving patients; this difference persisted through days 3 and 4. Blood urea nitrogen and creatinine levels increased early in nonsurviving patients but renal failure, which occurred in nine nonsurviving patients, did not develop until mean day 14, median day 18. The phosphate level was slightly higher but still within normal range in nonsurviving patients. By days 5 and 6 ionized calcium and parathormone levels were no different in nonsurviving patients, despite there being no improvement in renal function. Magnesium and albumin levels were no different between groups. Ionized calcium levels are lower and parathormone levels higher early in nonsurviving patients. This difference is not readily explained by associated clinical conditions, including renal dysfunction. Although etiology remains unclear, low ionized calcium and elevated parathormone are early predictors of mortality in critically ill surgical patients.

Sequential vitamin D and parathyroid hormone measurement in patients with septic shock: Could they be prognostic marker in septic shock

“…It has been suggested that hypocalcemia in critically ill patients might be caused by the resistance to the action of PTH in the kidney and bone. There are many previous studies which are demonstrated elevation of PTH is associated with disease severity and mortality [23,[30][31][32]. Our results support previous studies.…”

Vitamin D Deficiency as an Ignored Cause of Hypocalcemia in Acute Illness: Report of 2 Cases and Review of Literature

“…It can lead to serious conditions [13,14]; it has been suggested that hypocalcemia is associated with the severity of disease and fairly predicts mortality in critically ill patients [15][16][17]19]. Hypocalcemia in critical illness is presumably multifactorial.…”

“…In addition to the common causes of hypocalcemia ( PTH is one of the major regulators of extracellular calcium lying in a negative feedback way responding to changes in ionized calcium levels and vitamin D. PTH reportedly affects vascular smooth cells and ventricular myocytes [29], and impairs cardiac energy production, transfer, and utilization by enhanced entry and the accumulation of calcium in the myocardium [30] leading to development of cardiovascular disease [20,[31][32][33]. There have been several reports of elevated PTH value in patients with acute disease, which was associated with disease severity and poor outcome [17][18][19][20]. In most cases with acute illness, hypocalcemia was not restored by elevated concentration of PTH.…”

“…This points to the possibility that secretion or action of PTH is relatively impaired in addition to vitamin D deficiency [15,25,34]. It is also conceivable that PTH might affect cytokine link [19,27] and immune system [35], resulting in refractory hypocalcemia.…”

“…Hypocalcemia and consequent hyperparathyroidism are common in acute illness such as sepsis, acute pancreatitis, or major surgery, and they have been reported to predict mortality in these settings [15][16][17][18][19][20][21][22]. Although vitamin D deficiency is frequent and it has been described as a cause of hypocalcemia, it has received little attention and only few reports scrutinized vitamin D status and response in acute disease [23][24][25][26].…”