Intravenous Infusion Of Calcium Gluconate Research Articles

Optimising Ovulation Induction in PCOS

Biochemical, Metabolic and Endocrine changes in PCOS result in reproductive impairment in women with PCOS. Controlled ovarian stimulation (COS) may be associated with • Unpredictable response • Response may be slow • Hyper-response - OHSS • Risk of Cyst Formation • Poor oocyte quality • Miscarriage • Cycle cancellation So, the ovulation induction protocol should be efficacious and safe resulting in a singleton live birth, minimising complications, and risks like ovarian hyperstimulation syndrome (OHSS), multiple pregnancies and cancellation of cycles. For this special consideration should be given to prediction of response, pre-treatment, choosing the right ovulation induction (OI) protocol with right dose and analogue, using GnRH agonist trigger instead of hCG, preventing late follicular phase rise in progesterone, or following the segmentation protocol. We can maximize the success rates by stimulation individualization based on age, AMH, AFC and amended further for BMI. AMH is considered as more sensitive marker to define follicle excess than AFC as it appraises more follicle classes - preantral and early antral. One should probably use mild stimulation protocols where gonadotropins are given in combination with oral ovulogens or the low dose step up protocol. It is essential that we use GnRH antagonist protocol and administer GnRH agonist if there is risk of OHSS. If segmentation protocol is used one could also use the progesterone primed ovarian stimulation instead of GnRG antagonist. One could reduce the incidence of OHSS by laparoscopic ovarian drilling and use of Metformin and aspirin before assisted reproduction. If the patient is at risk of developing OHSS during stimulation then one could administer cabergoline, intravenous infusion of calcium gluconate or albumin and methylprednisolone. But freezing all embryos and transferring them in a subsequent cycle increase the efficacy and reduce complications of ART in PCOS women. Elective single embryo transfer(eSET) should be the norm to reduce the multiple pregnancy rate. Conclusion Thus, in all ART cycles individualised COS with freeze all and eSET could help in increasing the success of ART and reducing stress and anxiety and complications in these women.

Clinical profile and outcome of patients of common krait bite with features of neurotoxic envenomation, treated with intravenous calcium gluconate infusion in conjunction with AVS, a tertiary care center-based study

Background: Snake bite is one of the most neglected diseases in South East Asian region. Common Krait (CK) (Bungarus caeruleus) is the deadliest snake found in the dry zones of India. With the polyvalent anti-venom serum (AVS) remaining the cornerstone of treatment of neurotoxic snake envenomation, there is no universally accepted treatment for CK envenomation-associated neuroparalysis, except supportive measures. Aims and Objectives: Our study was conducted to describe the epidemiology, define clinical features, study outcome, and apparent efficacy of calcium gluconate in preventing or reversing neuromuscular paralysis with respiratory failure in CK bite patients. Materials and Methods: This study is a prospective observational study done on 52 CK bite patients. Patients were enrolled according to inclusion and exclusion criteria and were treated with AVS and calcium gluconate infusion according to National Standard Guideline, 2016. Patients developing severe respiratory muscle paralysis were offered mechanical ventilation. Results: Patients developed ptosis and dysphagia, pain abdomen, cyanosis, paralysis of jaw and tongue, perioral numbness, altered sensorium, dysphonia, ophthalmoplegia, and paradoxical breathing. 21.15% of patients developed respiratory failure and needed ventilator support with average critical care unit stay of 3 days and average stay on a ventilator of 2 days. 3 patients expired (case fatality rate 5.77%). The average hospital stay was 3.33 days. Conclusion: Our study shows that early intervention in patients of CK bite with neurotoxic envenomation, with calcium gluconate infusion, leads to less mortality and morbidity compared to other relevant studies. Further large-scale studies are required for better understanding and implementation.

Iatrogenic calcinosis cutis in a preterm infant.

Extravasation phlebitis over the right forearm of a preterm newborn persisted beyond 3 weeks of limb care. The initial swelling evolved into a firm, non-tender, non-erythematous induration. The newborn was born as a singleton preterm birth at 32 weeks of gestation with a birth weight of 2.1 Kg (81 percentile) due to antepartum hemorrhage in a primigravida mother. The chart review suggested intravenous calcium gluconate infusion at 80 mg/kg per day for 2 days because of low ionized calcium (0.70 mmol/L) and seizures on day 2 of life.

PSAT189 Severe Hypocalcemia and Hypophosphatemia Associated with Denosumab use in a Chronic Myeloid Leukemia Patient on Imatinib

Abstract Background Hypocalcemia and hypophosphatemia are known side effects of Denosumab, especially in presence of risk factors including underlying chronic kidney disease, osteoblastic metastasis, high bone turnover states, vitamin D deficiency and preexisting hypocalcemia. We report a unique case of prolonged severe hypocalcemia and hypophosphatemia in a patient with CML on Imatinib, treated with Denosumab for osteoporosis. Clinical case A 73-year-old lady with history of CML, on Imatinib for 4 years and osteoporosis with a chronic L1 compression fracture treated with her second dose of Denosumab 3-months back, presented with complaints of numbness and tingling involving the entire body. Labs revealed severe hypocalcemia (calcium 5.6 mg/dL, ionized calcium 2.93 mg/dL), severe hypophosphatemia, (phosphorus of 0.5mg/dL) and a low normal magnesium level of 1.5mg/dL, with normal ALP, liver and kidney function parameters. Of note she had normal calcium, phosphorus and vitamin D levels before receiving denosumab. Further work-up revealed an elevated PTH level of 241 pg/mL, normal 25 hydroxy vitamin D level of 26.0 ng/ml, slightly low 1,25 (OH) vitamin D of 16pg/ml and an elevated FGF 23 of 299RU/mL (normal <180RU/mL). Her calcium and phosphorus levels remained suboptimal despite treatment with up to 24 grams of calcium carbonate supplementation daily, K-phos 1 packet QID and calcitriol 0.25 mcg TID. 24-hour urine calcium and phosphorus levels were low at 4mg/day and 0.2mg/day respectively. Fractional excretion of phosphate was 13.63%, suggesting renal phosphorus wasting, likely from an elevated FGF23. Bone scan showed no metastatic lesion. After discussion with oncology, Imatinib was held inpatient and she was started on intravenous calcium gluconate infusion, and continued on Calcitriol, vitamin D3 and K-phos supplementation. After receiving almost 18gm of calcium gluconate intravenously over 2 days, her hypocalcemia and hypophosphatemia resolved with improvement in symptoms. Conclusion Hypocalcemia is a recognized adverse effect of Denosumab that is seen in patients with underlying risk factors. Emerging data now suggests the deregulatory effect of long term Imatinib therapy on bone formation by inhibition of osteoclastic activity along with transient increase in osteoblastic activity leading to retention and sequestration of calcium and phosphate in bone, resulting in hypocalcemia and hypophosphatemia. Ours is the first reported case of severe hypocalcemia and hypophosphatemia observed in a CML patient on Imatinib after receiving Denosumab, with resistance to high dose oral calcium and phosphate supplementation, requiring intravenous supplementation and transient discontinuation Imatinib. The elevated FGF 23 likely played a key role in severe hypophosphatemia. This unique case addresses the prospect of occurrence of severe hypocalcemia and hypophosphatemia in patients on Imatinib receiving Denosumab, while questioning the possibility of potentiation of the osteoclast inhibitory effect of this medication when used in patients on long term Imatinib therapy. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Optimization of infusional calcium gluconate for prevention of hypocalcemic reactions during therapeutic plasma exchange.

We sought to optimize direct intravenous infusion of calcium gluconate (CaGlu) for maintaining plasma ionized calcium concentration ([Ca2+ ]) and preventing hypocalcemic reactions during 34 consecutive 1-volume therapeutic plasma exchanges (TPEs) in eight patients. CaGlu, 2 g in 50 mL of 0.9% NaCl, was prepared by our hospital pharmacy and infused at either 1.0 or 1.6 g/h during alternate TPE. Plasma [Ca2+ ] was monitored at intervals of 20 to 30 minutes. At 1 g/h of CaGlu, plasma [Ca2+ ] fell by 8.35% after 40 to 50 minutes and then plateaued. At 1.6 g/h of CaGlu, plasma [Ca2+ ] fell by 6% after 20 to 30 minutes and then plateaued. The difference at 40 to 50 minutes was significant (P = .015). Hypocalcemic reactions were noted in three patients during 5 of 17 TPE at 1.0 g/h (all after 40 to 60 minutes) but 0 of 17 TPE at 1.6 g/h (P = .044). CaGlu at 1.6 g/h stabilized plasma [Ca2+ ] and appears to prevent hypocalcemic reactions during TPE.

Slight hypercalcemia is not associated with positive responses in the Comet Assay in male rat liver

Maintenance of physiological levels of intracellular and extracellular calcium is essential for life. Increased intracellular calcium levels are involved in cell death (apoptosis and necrosis) and are associated with positive responses in the Comet assay in vitro. In addition, high calcium and vitamin D intakes were reported to induce apoptosis in adipose tissue in obese mice and to increase DNA-migration in the Comet assay. To investigate increased serum concentration of calcium as a potential confounding factor in the regulatory Comet assay in vivo, we induced mild hypercalcemia in male Wistar rats by 3-day continuous intravenous infusion of calcium gluconate and performed the Comet assay in the liver in line with regulatory guidelines.The results of the study showed that mild increases in serum calcium concentration (up to 1.4 times above the concurrent control) and increased urinary calcium concentration (up to 27.8 times above the concurrent control) results in clinical signs like mild tremor, faster respiration rate and decreased activity in a few animals. However, under the conditions of the study, no increase in the %Tail DNA in the Comet assay and no indication of liver damage as determined by histopathological means were observed. Thus, mild increases in plasma calcium did not lead to positive results in a genotoxicity assessment by the Comet assay in the rat liver. This result is important as it confirms the reliability of this assay for regulatory evaluation of safety.

Fatal Electrolyte Abnormalities Following Enema Administration

A 90-year-old man was admitted to the Emergency Department with severe congestive heart failure and kidney failure. His medical history included successful surgery for prostatic carcinoma, aortocoronary bypass surgery, and cardiac pacemaker implantation. The patient was regularly taking digoxin, enalapril, aspirin, transdermal nitrate, and furosemide. At admission, the patient was hyperkalemic (Table 1), and therapy with sodium polystyrene sulfonate and ethacrynic acid was started immediately. The diuretic therapy was continued after his admission to the Nephrology and Dialysis Department on the second day of hospitalization. An ultrasound examination in which the kidneys appeared small and hyperechoic confirmed chronic renal impairment. On the evening of the sixth day of hospitalization, 2 enemas (120 mL each) were administrated 30 min apart to relieve prolonged constipation. The patient vomited the following night, and a nasogastric tube was inserted. The next morning, the patient showed signs of dehydration and was hypotensive (blood pressure, 90/40 mmHg). The patient's abdominal distension prompted an abdominal radiograph, which showed signs of intestinal obstruction. Laboratory findings revealed severe hypocalcemia [3.7 mg/dL (0.93 mmol/L); reference interval, 8.5–10.5 mg/dL (2.13–2.63 mmol/L)] and alterations in the plasma concentrations of other major plasma ions (Table 1). An intravenous infusion of calcium gluconate was started immediately, and an abdominal computed tomography evaluation was requested. The severe electrolyte abnormalities were confirmed after analysis of a second blood sample drawn after 1.5 h, which revealed severe hyperphosphatemia [30.0 mg/dL (9.69 mmol/L); reference interval, 2.5–4.5 mg/dL (0.81–1.45 mmol/L)] without signs of overt acidosis. In the meantime, the abdominal computed tomography scan revealed paralytic ileus. Emergent hemodialysis was planned, but despite intensive treatment, the patient's electrocardiogram showed an increased QT interval. He finally went into cardiac arrest and died before hemodialysis could begin. View this table: Table 1. Laboratory findings for the patient during hospitalization. The enemas were given on the evening of day 6.a ### QUESTIONS TO CONSIDER 1. Which laboratory tests are useful in the evaluation of a patient with severe hypocalcemia? 2. What …

Refractory hypocalcemia precipitated by dual infection with typhoid fever and hepatitis A in a patient with congenital hypoparathyroidism

AbstractWe present this rare occurrence of a 17 yr old boy, a known case of congenital hypoparathyroidism, who presented with fever and jaundice for 8 days and 2 episodes of generalised tonic-clonic seizures. Premorbidly patient was on regular oral calcium supplementations with normal serum calcium levels. Investigations revealed severe hypocalcaemia (3.2 mg/dL), low 25 hydroxyvitamin D levels and hypomagnesaemia. The marked elevation of serum bilirubin was accompanied by derangement of liver enzymes. Microbiological investigations were confirmatory for both hepatitis A and typhoid fever. In spite of the aggressive management with intravenous calcium gluconate infusion, refractory hypocalcaemia persisted with recovery only after gradual decline in the bilirubin levels. We inferred that the cholestatic process produced by both acute viral hepatitis A and typhoid fever precipitated this state of refractory hypocalcaemia in the previously well preserved patient.

Sporotrichoid-like calcinosis cutis and calcifications in vessel walls and eccrine sweat glands following intravenous infusion of calcium gluconate

Sporotrichoid-like calcinosis cutis and calcifications in vessel walls and eccrine sweat glands following intravenous infusion of calcium gluconate

Do we need sick-day guidelines for hypoparathyroidism?

Do we need sick-day guidelines for hypoparathyroidism?

Stimulation of Adrenal Chromaffin Cell Proliferation by Hypercalcemia Induced by Intravenous Infusion of Calcium Gluconate in Rats

Increased incidence of adrenal pheochromocytoma is frequently encountered in rat carcinogenicity studies. In some of the studies, the finding is judged to be due to a rat-specific mechanism of carcinogenesis caused by a disturbance of calcium homeostasis. However, direct evidence that the proliferation of chromaffin cells in the adrenal medulla is induced solely by hypercalcemia is not available. In this study, calcium gluconate was intravenously infused for 7 days to rat chromaffin cells by a tail cuff method, and cumulative labeling with bromodeoxyuridine (BrdU) was carried out to evaluate the proliferative activity. The serum calcium concentration was dose-dependently increased, and a high calcium concentration was stably sustained from day 2 to 7. In the adrenal medulla, BrdU-positive chromaffin cells increased in the calcium gluconate-treated animals, and the BrdU-labeling index increased in a dose-dependent manner. In addition, an increased BrdU-labeling index of chromaffin cells was shown to correlate with the serum calcium concentration. Our results demonstrate that hypercalcemia directly enhances the proliferative activity of chromaffin cells and that the proliferative activity is correlated with the serum calcium concentration.

Efficacy of an Intravenous Calcium Gluconate Infusion in Controlling Serum Calcium after Parathyroidectomy for Secondary Hyperparathyroidism

Intravenous calcium gluconate has been used to prevent postoperative hypocalcaemia (POH) following parathyroidectomy for secondary hyperparathyroidism in chronic kidney disease (CKD). Retrospective data were obtained for 36 patients with CKD stage 4 and 5 after parathyroid surgery, correlating albumin-corrected serum calcium with the infusion rate of calcium gluconate. Calcium flux was characterised along with excursions out of the target calcium range of 2 to 3 mmol/L. With this data, an improved titration regimen was constructed. Mean peak efflux rate (PER) from the extracellular calcium pool was 2.97 mmol/h occurring 26.6 hours postoperatively. Peak calcium efflux tended to occur later in cases of severe POH. Eighty-one per cent of patients had excursions outside of the target calcium range of 2 to 3 mmol/L. Mean time of onset for hypocalcaemia was 2 days postoperatively. Hypocalcaemia was transient in 25% and persistent in 11% of patients. A simple titration regimen was constructed in which a 10% calcium gluconate infusion was started at 4.5 mL/h when serum calcium was <2 mmol/L, then increased to 6.5 mL/h and finally to 9.0 mL/h if calcium continued falling. Preoperative oral calcium and calcitriol doses were maintained. Blood testing was done 6-hourly, but when a higher infusion rate was needed, 4-hourly blood testing was preferred. Monitoring was discontinued if no hypocalcaemia developed in the fi rst 4 days after surgery. If hypocalcaemia persisted 6 days after surgery, then the infusion was stopped with further monitoring for 24 hours.

Hypercalcaemia and calcitonin inhibit prolactin secretion.

The authors investigated the effect of acute hypercalcaemia induced by a 2-hour intravenous infusion of calcium gluconate (8.9 mg Ca2+/kg b. w.) on the lactotrophic secretory reserve assessed by the test with insulin hypoglycaemia (delta PRL) and the effect of an intravenous bolus of 50 IU synthetic salmon calcitonin on the lactotrophic secretory reserve assessed by means of the TRH test (delta PRL). Acute hypercalcaemia inhibits PRL levels stimulated by insulin hypoglycaemia (p less than 0.01) as well as delta PRL (p less than 0.01). Calcitonin reduces PRL levels at rest and TRH stimulated levels (p less than 0.05 and p less than 0.01, respectively) as well as delta PRL (p less than 0.01). The prolactin inhibiting effect of calcitonin resembles markedly the effect of hypercalcaemia. The exact mechanism of these changes and the physiological impact of calcitonin on the regulation of PRL secretion is not known.

The management of tumor lysis syndrome

The manifestation of tumor lysis syndrome (TLS) occurs when the destruction of tumor cells releases breakdown products that overwhelm the excretory mechanisms of the body. A cardinal sign is hyperuricemia, leading to uric acid nephropathy. Other signs are hyperkalemia, hyperphosphatemia and secondary hypocalcemia. Conventional management of TLS consists of aggressive intravenous hydration, diuretic therapy, urinary alkalization, and inhibition of urate production by high-dose allopurinol. Urate oxidase has been used in the management of patients at risk for TLS and recently the recombinant urate oxidase rasburicase was developed. Several data indicate that rasburicase is effective and well tolerated in the prevention and treatment of chemotherapy-induced hyperuricemia. Treatment options of hyperkalemia include sodium polystyrene sulfonate, hypertonic glucose and insulin, loop diuretics, and bicarbonate. Treatment of hyperphosphatemia reduces dietary phosphate intake and includes phosphate binders such as aluminum hydroxide and aluminum carbonate. When recurrent hypocalcemia is present, a continuous intravenous infusion of calcium gluconate can be initiated. Hemodialysis should be considered for every patient with excessively elevated uric acid, phosphate and/or potassium and in those patients with acute renal failure to control urinary volume and manage uremia.

Effects of P5, a novel oxazolo(3,2-a)pyridine derivative with a long-acting antihypertensive activity, on different agonist-mediated pressor responses in pithed rats.

1. An oxazolo(3,2-a)pyridine derivative P5, described chemically as (+/-)-ethyl-7-(3-nitrophenyl)-5,8a-dimethyl-6-methoxycarbonyl-2,3,8,8a-tetrahydro-7H-oxazolo[3,2-a]pyridin-8-carboxylate, is a novel compound that has been synthesized as a possible antihypertensive prodrug of the 1,4-dihydropyridine type. Its antihypertensive activity was described in a previous study by the authors (Morán, Martin, Velasco, Martin, San Roman, Caballero, Puebla, Medarde & San Feliciano, 1997). 2. The aim of this work was to establish in vivo, the possible mechanisms participating in this antihypertensive action. Accordingly, we examined the effect of P5 on the pressor responses induced in pithed rats by noradrenaline (an alpha1-, alpha2- and beta-adrenoceptor agonist), xylazine (an alpha2-adrenoceptor agonist), methoxamine (an alpha1-adrenoceptor agonist), angiotensin I, angiotensin II, L-NAME (a nitric oxide synthase inhibitor) and BayK 8644 (a calcium channel agonist) and compared them with those of nifedipine, used as the reference drug. 3 Intravenous (i.v.) administration of P5 (2.5-10 mg kg(-1)) inhibited the pressor responses to noradrenaline (1 microg kg(-1)), xylazine (80 microg kg(-1)), angiotensin I (0.5 microg kg(-1)), angiotensin II (0.5 microg kg(-1)), BayK 8644 (30 microg kg(-1)) and L-NAME (10 mg kg(-1)). Nifedipine (10 microg kg(-1), i.v.) reduced the pressor responses to all these agonists and also to methoxamine (2 microg kg(-1)). 4. However, P5 was more effective than nifedipine in inhibiting these responses and its inhibitory effect lasted longer. Intravenous infusion of calcium gluconate (1 ml kg(-1) min(-1)) reversed the reduction in the pressor responses as a result of nifedipine. The effects of P5 were only reversed at 2-3 h after administration. 5 These results suggest that P5 has a strong capacity to inhibit the pressor responses to several agonists after its i.v. administration and that such effects are related to its potent antihypertensive activity.

Spider Bite Envenomation in Al Baha Region, Saudi Arabia

The purpose of this study was to highlight the clinical features of spider bite envenomation, a subject which has not, to our knowledge, been previously published in Saudi Arabia. Ten patients (8 males and 2 females) aged between 13 and 75 years (mean 36.8) were hospitalized at King Fahad Hospital, Al Baha, with the diagnosis of spider bites during the 9-year period from June 1988 to May 1997. One of the patients was bitten on the right hand by a brown spider, causing severe cellulitis and tissue necrosis, and requiring surgical debridement and pedicle skin flap graft. The nine other patients (90%) had bites from black spiders identified as black widow spiders. Two of the nine (22.2%) suffered only local reactions in the form of pain, erythema and swelling at the site of bite. The remaining seven (77.8%), had varying symptoms of systemic envenomation, including pulmonary edema, myocardial dysfunction with elevated creatinine kinase, electrocardiographic and echocardiographic abnormalities, progressive paresthesia, generalized body ache, etc. Therapy included analgesics, muscle relaxants, intravenous infusion of calcium gluconate and oxygen where indicated. Specific antivenin therapy was available for only four of the nine patients (44%) with black widow spider bite. Antivenin therapy still produced dramatic relief of the symptoms in the patient with pulmonary edema, even after a delay of 30 hours. Spider bite envenomation should be considered in the differential diagnosis of acute surgical abdomen and myocardial infarction.

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. [Graudins A, Burns MJ, Aaron CK, Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity. Ann Emerg Med November 1997;30:604-607.]

Aging alters calcium regulation of serum concentration of parathyroid hormone in healthy men.

We examined the effect of aging on the relationship between the concentrations of blood ionized calcium and of serum parathyroid hormone (PTH) in 22 healthy men [9 elderly (age 74 +/- 2 yr) and 13 young (age 39 +/- 1 yr)] in whom the glomerular filtration rate was > 70 ml/min. Throughout a 24-h period, serum concentrations of PTH in the elderly men were twice those in the young men, whereas blood ionized calcium did not differ between the two groups. With intravenous infusion of calcium gluconate, the minimum PTH concentration was two- to threefold higher in the elderly men. With infusion of NaEDTA. the maximum PTH concentration was 20% higher in the elderly men. The calcium set point for PTH release was higher in the elderly than in the young men (4.71 +/- 0.04 vs. 4.54 +/- 0.03 mg/dl, respectively, P < 0.005). In these healthy men, the age-related increase in serum PTH could not be attributed to a sustained decrease in concentration of either blood ionized calcium or 1,25-hydroxyvitamin D. These findings suggest that, with aging, the relationship between calcium and PTH is altered such that at any given level of calcium, the concentration of PTH is higher.

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.

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 2 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, up 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. © 1996 Wiley-Liss, Inc.