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PubMed1983

Calcium gluconate pretreatment for prevention of succinylcholine-induced myalgia.

The effects of calcium gluconate pretreatment on succinylcholine-induced postoperative muscle pain and on the changes in serum potassium and calcium levels were studied in 80 patients undergoing elective surgery who were to become ambulatory on the same evening. A test group of 40 patients was given 10 ml of 10% calcium gluconate intravenously immediately before induction of anesthesia with thiopental followed by succinylcholine for tracheal intubation. A control group of 40 patients was given thiopental and succinylcholine without calcium gluconate. Muscle pains were graded according to severity as nil, mild, moderate, and severe. The incidence of postoperative muscle pains was significantly less (5%) in the test group than in the control group (45%). In control patients who subsequently developed muscle pain, serum levels of potassium were significantly increased above preinduction levels 2 min after succinylcholine was administered and serum calcium levels were significantly decreased. In control patients who did not develop postoperative myalgia, there were no significant changes in serum levels of either calcium or potassium. This was also true for patients pretreated with calcium gluconate. Therefore, calcium gluconate pretreatment reduces both the increase in serum potassium and the decrease in serum calcium associated with succinylcholine, and decreases the incidence and severity of postoperative myalgia.

Adolescent↗
PubMed1990

Ionization and hemodynamic effects of calcium chloride and calcium gluconate in the absence of hepatic function.

Serial serum ionized calcium concentrations were measured before and after administration of either calcium chloride or calcium gluconate during the anhepatic stage of liver transplantation in 15 patients to determine the release of ionized calcium in the absence of hepatic function. When hypocalcemia (Ca++ less than 0.8 mM) occurred during the anhepatic stage, patients were randomly assigned to treatment with chemically equivalent doses of either calcium chloride (10 mg/kg, n = 8) or calcium gluconate (30 mg/kg, n = 7). Serum concentrations of ionized calcium and citrate, hematocrit, arterial blood gas tensions, acid-base state, and hemodynamic profiles were determined before and up to 10 min after calcium therapy. In both groups of patients initial similar and rapid increases in Ca++ (0.98 +/- 0.14 mM in the calcium chloride group and 1.05 +/- 0.10 mM in the calcium gluconate group) were followed by gradual decreases over the next 10 min. Measured hemodynamic values were similar in the two groups, and neither group showed improvement in cardiovascular function after calcium therapy, possibly because of the decrease in preload that occurred during the anhepatic stage. Equally rapid increases in Ca++ after administration of calcium chloride and gluconate in the anhepatic state suggest that calcium gluconate does not require hepatic metabolism for the release of Ca++ and is as effective as calcium chloride in treating ionic hypocalcemia in the absence of hepatic function.

Adult↗
PubMedDate not supplied

Treatment of hydrofluoric acid burn to the face by carotid artery infusion of calcium gluconate.

Hydrofluoric acid (HF) is highly corrosive substance often used in industrial processes. HF burns to the skin cause local tissue injury. Systemic hypocalcemia may ensue, with the potential to produce life-threatening arrhythmias. Medical treatment consists of local application of topical calcium gels, subcutaneous injection of calcium gluconate, and intravenous or intra-arterial infusion of calcium gluconate. Calcium gluconate infusions have been used for HF burns on distal extremities and digits. We report a case of HF burn to the face that was treated by the use of calcium gluconate infusion via the external carotid artery.

Accidents, Occupational↗
PubMed1987

Calcium chloride versus calcium gluconate: comparison of ionization and cardiovascular effects in children and dogs.

A randomized prospective study in both children and dogs compared ionization of calcium chloride and calcium gluconate. Five conditioned dogs under halothane anesthesia received calcium chloride (4, 8, 12 mg/kg) and calcium gluconate (14, 28, 42 mg/kg) intravenously. Ten children scheduled for burn wound excision and grafting received both calcium chloride (2.5 mg/kg) and calcium gluconate (7.5 mg/kg) injected through a central venous cannula. Ionized calcium was measured at 0, 0.5, 1, 3, 5, and 10 min in the children, and 0, 0.5, 1, 2, 3, 4, 5, 10, 20, and 45 min in the dogs. The authors conclude that equal elemental calcium doses of calcium gluconate (10%) and calcium chloride (10%) (approximately 3:1), injected over the same period of time, are equivalent in their ability to raise [Ca++] during normocalcemic states in children and dogs; the changes in [Ca++] following calcium administration are short-lived (minutes); rapidity of ionization seems to exclude hepatic metabolism as an important factor in the dissociation of calcium gluconate; and equivalent rises in [Ca++] produced by calcium gluconate or calcium chloride resulted in equivalent cardiovascular effects. The authors feel that either form of calcium salt would be satisfactory if indicated during cardiopulmonary resuscitation or for the treatment of ionized hypocalcemia due to massive blood transfusion.

Adolescent↗
PubMed1999

[Effect of calcium gluconate on the toxicity and antitumor of doxorubicin in mice].

The effect of calcium gluconate on the toxicity and specific activity of the anthracycline antibiotic doxorubicin was studied on mice with transplanted hemoblastosis La or plasmocytoma MOPS-406. In both cases after the animal exposure to nontoxic therapeutic doses of doxorubicin no influence of calcium gluconate on the antibiotic antitumor activity was observed. When doxorubicin was used in toxic (and even lethal) doses the antitoxic effect of calcium gluconate and an increase of the antibiotic therapeutic activity were stated. The combination of calcium gluconate and doxorubicin made it possible to significantly increase the maximum therapeutic effect of doxorubicin (higher levels of the animal survival and some cures) and to widen the ranges of the drug therapeutic doses at the account of decreasing the toxicity of the antibiotic and increasing its dose. The results suggested that the antitoxic modifier calcium gluconate could be used for increasing anticancer efficacy of doxorubicin which is given now at the total dose limit of 550 mg/m2 even in cases with preserved tumor sensitivity to the drug.

Animals↗
PubMed1981

Gluconate calcium therapy and neonatal hypercalciuria.

Nephrolithiasis was present in a 2-month-old premature infant with bronchopulmonary dysplasia who had been receiving furosemide and intravenous (IV) gluconate calcium therapy. This infant was found to be hypercalciuric. Furosemide therapy is known to increase calcium excretion. In the present study, we examined sick infants who were receiving gluconate calcium without furosemide to evaluate the effect of gluconate calcium therapy on urinary calcium excretion. The sick infants receiving gluconate calcium had higher values of urinary calcium than did the well infants taking regular formula feedings. Moreover, the calciuria appeared to increase progressively with continued gluconate calcium therapy. It appears that prolonged use of either furosemide or IV gluconate calcium leads to hypercalciuria, which, in turn, may predispose the premature infant to nephrolithiasis.

Calcium↗
PubMedDate not supplied

The efficacy of treatment with triamcinolone acetonide in calcinosis cutis following extravasation of calcium gluconate: a preliminary study.

Neonatal hypocalcemia is not an uncommon condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intravenous infusion include localized calcification and occasionally necrosis. When this occurs, however, there is no specific mode of treatment except supportive management and skin graft. This experiment was designed to evaluate the efficacy and safety of treatment with triamcinolone acetonide in calcinosis cutis following extravasation of calcium gluconate. Initially, 2 cc of 10% calcium gluconate was injected subcutaneously into two rabbits at seven sites on the shaved skin of the back. Another two rabbits were injected at the same sites with 0.5 cc of triamcinolone acetonide (10 mg/dl) after injection of 2 cc of 10% calcium gluconate. As a control, 2 cc of normal saline was injected into another rabbit in the same manner. These five rabbits were observed over the next 7 weeks and underwent pathologic examination at various intervals (on days 1, 3, 8, 15, 30, 37, 45). In the 10% calcium gluconate injected rabbits, nodules and large ulcerated lesions developed after 15 days. Multiple, linear, ulcerative and indurated masses were noted on day 37. The lesions healed progressively with a decrease in ulceration, and after 2 months, the masses disappeared gradually. Histologically, on day 15 calcium deposits were seen in the walls of the arteries, veins, dermis, and muscle fibers and epidermal necrosis was seen at the injection sites. From day 37 discharge of calcium deposits began to take place by means of transepidermal elimination. After 2 months, the calcium and mucin deposition was observed focally in the dermis. In the rabbits injected with 10% calcium gluconate and triamcinolone acetonide, mild erythema and induration were seen after day 15 at the injection sites; this gradually disappeared. After 30 days the injection sites were normal in appearance. Histologically, at day 15 calcium deposition was seen in the upper dermis, but after 1 month the injection sites were histologically normal. We suggest that intralesional injection of triamcinolone acetonide for the treatment of calcinosis cutis following extravasation of calcium gluconate is effective, probably due to its antiinflammatory effect and its role in facilitating the resorption of calcium in the tissue.

Administration, Topical↗
PubMed1994

Influence of intravenous calcium gluconate on saphenous vein graft flow in closed-chest patients.

The effects of calcium gluconate on hemodynamics and saphenous vein graft flow in a group of patients undergoing elective coronary artery bypass grafting who developed ionized hypocalcemia at the end of the surgical procedure were examined. The patients received a central venous bolus of 15 mg/kg of calcium gluconate. Heart rate (HR), arterial pressure (AP), central venous pressure (CVP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), and cardiac output were measured immediately before and 30, 60, 120, 180, and 240 seconds after injection of calcium gluconate. Systemic and pulmonary vascular resistance (SVR and PVR, respectively), cardiac index (CI), stroke volume index (SVI), and right and left ventricular stroke work index (RVSWI and LVSWI, respectively), were calculated. Venous bypass flow velocity (Vbypass-flow) was assessed using a Doppler probe that was attached to the left anterior descending artery (LAD) bypass intraoperatively. Calcium gluconate significantly increased MAP, SVR, and LVSWI from 67 +/- 3 mmHg (mean +/- SEM), 1,128 +/- 128 dyne.s.cm-5 and 25 +/- 3 g.m.beat/m to a maximum of 81 +/- 5 mmHg (P < 0.01), 1,401 +/- 196 dyne.s.cm-5 (P < 0.05), and 32 +/- 4 g.m/beat/m (P < 0.01), respectively. HR, CVP, PAP, PCWP, PVR, CI, SVI, and Vbypass-flow remained unaltered. It is concluded that calcium gluconate administered to moderately hypocalcemic patients increases arterial pressure mainly by peripheral vasoconstriction. Because the increase of arterial pressure, and, thereby, coronary perfusion pressure is not associated with an increase of LAD bypass flow, vasoconstriction in the coronary vascular bed distal to the venous graft cannot be ruled out, and deterioration of the myocardial oxygen supply/demand ratio is strongly suggested.

Aged↗
PubMed1981

A comparison of calcium gluconate and methocarbamol (Robaxin) in the treatment of Latrodectism (black widow spider envenomation).

Calcium gluconate and methocarbamol were compared by using an algorithmic treatment protocol on all cases of Latrodectus (black widow) envenomation seen over a period of 3 years. Six of 13 patients were effectively cured of their symptoms by calcium gluconate, while only one of 10 patients was relieved by methocarbamol. Calcium gluconate remains the drug of first choice for this syndrome. It was also noted that calcium gluconate was more effective in patients who presented 3 hours of more after they were bitten. Antivenom may be necessary in those who present with symptoms in less than 3 hours.

Adolescent↗
PubMed1996

Prevention of citrate reactions during therapeutic plasma exchange by constant infusion of calcium gluconate with the return fluid.

We have examined the effectiveness of intravenous calcium gluconate infusion in the prevention of citrate reactions during therapeutic plasma exchange. Over 3 years, 636 procedures were performed on 90 patients, mostly for treatment of neurological disorders. Return fluid consisted of 4-5% human serum albumin in 0.9% NaCl. Anticoagulant ACD-A was used at a starting ratio of 1:16. Whole blood flow rates were 70-80 ml/min. Treatments were divided into three groups for management of citrate reactions: Group A (360 treatments) were managed using simple measures only, including slowing the whole blood flow rate, altering the ACD:whole blood flow ratio, and oral calcium carbonate wafers; Group B (102 treatments) received small intravenous boluses of 10% calcium gluconate, us to 25 ml during the procedure; Group C (174 treatments) received constant infusion of calcium gluconate (10 ml/liter of return fluid) during the procedure. Citrate reactions occurred in 35.6% of Group A and 29.4% of Group B treatments (P = 0.3), but in only 8.6% of Group C treatments (P < 0.0001). Men with and without reactions were the same age (mean 63.3 vs. 61 years, P = 0.0823), but women with reactions were younger than women without reactions (mean 49.9 vs. 57.9 years, P < 0.0001). Supplementation of the return fluid with calcium gluconate is an effective, convenient, and well-tolerated method for prevention of citrate toxicity during therapeutic plasma exchange procedures using albumin-based return fluid.

Adolescent↗
PubMed1994

Development of a mutant strain of Aspergillus niger and optimization of some physical factors for improved calcium gluconate production.

In the course of mutation studies of Aspergillus niger strain AB with ethylene imine (1:4000), a mutant A. niger AB 501, produced greater amount of calcium gluconate in the culture broth (88.0 g/lit) as against the parent strain (36.0 g/lit) by the surface culture method of fermentation. This mutant was then exposed to UV-rays and a mutant, A.niger AB 1801, was found to produce high calcium gluconate in the culture broth (120 g/lit). The optimum cultural conditions for the production of calcium gluconate by A.niger AB 1801 were pH, 6.5; period of incubation, 9 days; volume of medium in 1 litre flask, 150 ml; temperature, 30 degrees C, volume of inoculum, 7.5 ml of cell suspension containing 2.6 x 10(7) spores and age of inoculum, 6 days old spores of A. niger AB 1801. The maximum yield of calcium gluconate to the above conditions was 168 g/lit. The cultural conditions that support maximum cultural growth did not, however, give optimal yield of calcium gluconate because after having yielded the maximum of calcium gluconate the growth of organism continued to increase further.

Aspergillus niger↗
PubMedDate not supplied

A biochemical and histologic rationale for the treatment of hydrofluoric acid burns with calcium gluconate.

Hydrofluoric acid has unique properties that make it attractive for a variety of industrial and household uses. Exposure to dilute and concentrated solutions of hydrofluoric acid can lead to severe pain and tissue necrosis. Local treatment with topical calcium gluconate and subdermal injections of 0.5 ml 10% solution of calcium gluconate per cm2 of affected tissue has been advocated but frequently fails to relieve the patient of pain. Intraarterial infusion of calcium gluconate has been advocated for these patients, but several reports have been made of massive soft-tissue loss associated with such therapy. The purpose of this study was to show what, if any, were the microscopic effects on the distal arterial tree of intraarterial infusion of calcium gluconate. By studying 1 micron-thick cuts of distal rat aortas after proximal infusion of concentrated (10%) and dilute (2%) calcium gluconate, we were able to show that the incidence of microperforations in the intima and media of the rat aorta increased with the concentration of calcium gluconate. We conclude that intraarterial infusions should be reserved for only the most severe cases of hydrofluoric acid burns unresponsive to local therapy.

Animals↗
PubMed1993

Effect of nicardipine on the reversal of magnesium toxicity by calcium gluconate in nonpregnant rabbits.

OBJECTIVE: To determine whether nicardipine, a dihydropyridine, inhibits the ability of calcium gluconate to reverse magnesium-induced toxicity. METHODS: The reversal of magnesium-induced neuromuscular blockade of skeletal muscle in the presence of nicardipine was assessed using a nerve stimulator. Nicardipine (12 mg) or an equivalent volume of saline was administered intramuscularly to 19 nonpregnant rabbits in a randomized, blinded manner. Magnesium sulfate, 800 mg, was then infused intravenously in all animals, an amount sufficient to cause toxicity as measured by depression of skeletal muscle twitch and by average serum levels of 10.4 mEq/L. Calcium gluconate (300 mg) was then infused in all animals, and reversal of neuromuscular blockade was measured using the nerve stimulator to compare the saline- and nicardipine-treated groups. RESULTS: Administration of calcium gluconate was equally effective in reversing magnesium-induced toxicity in both the control and test groups. CONCLUSION: Nicardipine does not block the ability of calcium gluconate to reverse magnesium-induced neuromuscular blockade.

Animals↗
PubMed1975

Roentgen patterns of extravasation of calcium gluconate in the tissues of the neonate.

Calcium gluconate is irritating to soft tissues and can produce tissue necrosis and slough; Radiographs of the part following extravasation initially show only soft tissue swelling. A variable pattern of soft tissue calcification then develops in one to three weeks, and gradually is completely resorbed over several months' time. The cause of the soft tissue calcifications may be quite puzzling, if the incident of calcium gluconate extravasation has been overlooked.

Arteriosclerosis↗
PubMed1997

Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity.

STUDY OBJECTIVE: To describe regional intravenous infusion of calcium gluconate as a therapy for hydrofluoric acid (HF) burns of the forearm, hand, or digits. METHODS: This study describes seven patients with HF burns. Calcium gluconate, 10 mL of 10% solution with 30 to 40 mL normal saline solution, was injected intravenously into the affected limb using a Bier block technique. Ischemia was maintained for 20 to 25 minutes. Therapy was considered successful if significant reduction of pain and tenderness was noted after tourniquet release. RESULTS: Seven patients were treated. HF concentration varied from 5% to 49%. Exposure sites included the forearm (two cases), thenar eminence and digits (two cases), or digits only (three cases). Complete pain resolution occurred on tourniquet release in four patients (two with burns to the forearm, two with burns to digits only). One patient had partial relief (thenar but not digital exposure site), and two had no relief of symptoms. Intraarterial calcium gluconate perfusion was subsequently administered to the three patients with persistent subungual and pulp, or thenar pain. Recovery was complete in all cases. No adverse effects were noted. CONCLUSION: Regional intravenous infusion of calcium gluconate should be considered a therapeutic option in HF burns of the forearm, hand, or digits when topical therapy fails.

Adult↗
PubMed1999

Therapeutic effect of topical calcium gluconate for hydrofluoric acid burn--time limit for the start of the treatment.

BACKGROUND: There are few studies regarding the time-dependent effectiveness of topical calcium gluconate treatment for the experimental hydrofluoric acid (HF) burn. METHODS: For producing a HF-burn, a drop of 46% or 23% HF solution was put on the back of rats for 3 minutes followed by washing with tap water. Calcium gluconate jelly or ointment was then applied to the burn area at various time intervals. The ointment was applied once a day thereafter. RESULTS: The topical calcium gluconate treatment was much more effective if the application was started within 3 hours. On the other hand, if the application was started after 6 hours or more, there was no difference between the groups and the non-treatment groups. CONCLUSIONS: It is suggested that practitioners should be ready to prepare quickly the calcium gluconate ointment to treat a HF burn, since the calcium gluconate ointment is not commercially available in Japan.

Administration, Topical↗
PubMedDate not supplied

Extravasation of calcium gluconate concomitant with osteomyelitis in a neonate.

Extravasation of calcium gluconate is not an uncommon complication in neonatal units, which may result in skin and soft tissue inflammation, injury and even infection. We report an 11-day-old preterm infant who developed osteomyelitis at an infiltrated intravenous site through which calcium gluconate was infused. The patient was initially treated conservatively as a simple calcium-infiltrate. Clinical condition deteriorated until proper antibiotic treatment was given. We exclude other possible causes and assume that calcium-infiltrate had an important role in the pathogenesis. We conclude that osteomyelitis should be considered in a patient with calcium extravasation whose soft tissue inflammation does not improve as expected. Furthermore, using a diluted calcium solution and checking the insertion site frequently in order to identify extravasation earlier would prevent the complication.

Calcium Gluconate↗
PubMed1977

Effect of calcium gluconate infusion on renin in the dog.

We have previously reported that infusion of CaCl2 into the renal artery of the dog inhibits renin release. To evaluate the possible importance of the anion delivered with calcium, similar experiments were performed in 10 dogs with equivalent amounts of calcium gluconate (0.3 mg. of Ca++ per kilogram of body weight per minute). The experiment consisted of three successive 15 minute control periods, followed by three 15 minute calcium gluconate infusion periods and two 15 minute recovery periods. During calcium gluconate infusion, mean serum Ca++, and ECa++, ENa+, and EFNa+ from the infuses kidney increased (p less than 0.005). Systolic blood pressure (142 mm. Hg +/- 8S.E.), renal blood flow (137 ml. per minute +/- 11 S.E.), creatinine clearance, and aldosterone excretion (12.0 ng. per 15 minute +/- 1.5 S.E.) did not change (p less than 0.3). Renal venous PRA (28.4 ng. per millileter per hour +/- 7.5 S.E.) decreased (p less than 0.014). The per cent decrease of PRA correlated (r = -0.70) with the per cent increase EFNa+ (p less than 0.001). Calcium gluconate had a lesser (p less than 0.01) inhibitory effect on renin than CaCl2, despite greater excretion of Ca++ and Na++ during calcium gluconate infusion. Taken together, the results indicate that Ca++ inhibits renin release, although the extent of the inhibition is modified by the anion accompanying Ca++. The effect of Ca++ on renin may be mediated by NaCl transport across the macula densa.

Animals↗