Experimental Study of Calcinosis Cutis after Extravasation of Calcium Gluconate.
- Author:
Kyun Tae KIM
;
Soo Jung KIM
;
Seung Hun LEE
;
Sung Ku AHN
;
Won Soo LEE
- Publication Type:Original Article
- Keywords:
Actinic Keratosis;
Bowens Disease;
Squamous Cell Carcinoma;
Keratoacanthoma;
p53;
PCNA
- MeSH:
Administration, Intravenous;
Arteries;
Bowen's Disease;
Calcinosis*;
Calcium Gluconate*;
Calcium*;
Carcinoma, Squamous Cell;
Crystallins;
Dermis;
Durapatite;
Eosine Yellowish-(YS);
Eosinophilia;
Erythema;
Formaldehyde;
Granuloma;
Humans;
Hypocalcemia;
Infant, Newborn;
Injections, Intralesional;
Injections, Subcutaneous;
Keratoacanthoma;
Keratosis, Actinic;
Mucins;
Necrosis;
Proliferating Cell Nuclear Antigen;
Rabbits;
Skin;
Subcutaneous Fat;
Transplants;
Triamcinolone;
Triamcinolone Acetonide;
Ulcer;
Veins
- From:Korean Journal of Dermatology
1994;32(4):574-582
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
