The Acute Calcification of Traumatized Muscle, With Particular Reference to Acute Post-Traumatic Renal Insufficiency 1

Abstract

Previous studies of acute post-traumatic renal insufficiency in man have shown that plasma concentrations of inorganic phosphate and calcium were inversely related (2), and that those patients with extensive devitalization of muscle had the most acute and extreme hyperphosphatemia and hypocalcemia (3). When calcium was injected intravenously into such patients, the elevation of plasma concentration was very transient, and the rate at which the injected calcium escaped from the plasma appeared to be proportional to the degree of the pre-injection hypocalcemia and hyperphosphatemia, which, in turn, was roughly proportional to the degree of muscle damage. In order to maintain plasma calcium at a desired level, it was necessary to infuse calcium continuously. The purpose of the maintenance of a near-normal calcium level was to antagonize the toxic effects of hyperpotassemia, and in this respect prolonged infusions were quite effective; however, the desirability of the procedure was questioned because the fate of the infused calcium was unknown, and the quantities employed might be harmful if deposited in certain viscera.At first consideration it might be assumed that the calcium which escaped from the plasma was deposited in bones. However, this would not explain the difference in the rate of disappearance of calcium from the plasma of patients with and without muscle injury, since the bones were similar in both. An alternate possibility is that some of the calcium was deposited in the damaged tissue, a phenomenon well recognized in chronic states but not known to occur acutely. It is to test this possibility that the present experiments are designed. The procedure for dogs 6 and 7 was the same as for dogs 1 and 2 except that nephrectomy was not performed.The procedure for dog 8 was the same as for 6 and 7 except that the initial, normal biopsy was omitted and the biopsies of the hind limbs were performed on day 4, 24 hours following injury. Dogs 9 to 13 were not nephrectomized, the initial biopsies were omitted, and radioactive calcium was not given. Dog 9 received intravenously 1050 ml. of an aqueous solution containing 2.95 Gm. NaH.PO4 and 11.7 Gm. Na,HPO, per liter (3.2 mgm. phosphorus per ml., pH 7.4) during the six hours following the trauma and preceding the biopsies. Dog 10 received 1200 ml. of this solution during the six hours following the trauma and an additional 1150 ml. over a six-hour period prior to biopsies the following day. Dog 11 received 600 ml. 0.4 molar NaHCO, in water during the six hours following the trauma and preceding the biopsies. Dog 12 received 600 ml. 0.1 molar HCI in five per cent glucose during the six hours following the trauma and preceding the biopsies. Dog 13 received 300,u parathyroid extract (from a lot of known potency) intramuscularly immediately following trauma, and three doses of 200,u each at twohour intervals prior to biopsies six hours following trauma.The tissues from the initial, normal biopsies were weighed, frozen, and saved to be processed with the specimens of t...

Acute Kidney Injury Facilitates Hypocalcemia by Exacerbating the Hyperphosphatemic Effect of Muscle Damage in Rhabdomyolysis

“…Several factors have been proposed to underlie the pathogenesis of hypocalcemia in rhabdomyolysis [3,4,5,8,9,10,16]. Among them, evidence supports calcium deposition in damaged muscle as a dominant factor, and the volume of damaged muscle is expected to affect the amount of calcium deposited [5,16].…”

“…Among them, evidence supports calcium deposition in damaged muscle as a dominant factor, and the volume of damaged muscle is expected to affect the amount of calcium deposited [5,16]. In several studies of eccentric exercise, CK reached its peak in approximately 3 days and decreased to its basal level in 7-14 days [17,18].…”

“…Phosphate retention can enhance calcium deposition and, consequently, is a factor associated with hypocalcemia in rhabdomyolysis [5,19,20]. By reducing urinary phosphate excretion, AKI can contribute to phosphate retention [6,7].…”

“…When released into circulation, these constituents have toxic effects on several organs and complicate the clinical manifestation of rhabdomyolysis. Hypocalcemia is an important complication of rhabdomyolysis, and several pathogenic factors have been proposed, including (a) calcium deposition in damaged muscle, (b) hyperphosphatemia and (c) skeletal resistance to calcemic hormones [3,4,5]. …”

Crush injury and rhabdomyolysis

“…The hypocalcemia that accompanies rhabdomyolysis should not be corrected unless there is danger of a hyperkalemic arrhythmia [92], for most of the infused calcium is deposited in injured muscles and may aggravate the pathogenesis of rhabdomyolysis and lead to metastatic calcification [93].…”