Infusion Of Calcium Gluconate Research Articles

Improved assessment of bone turnover by the PTH-(1-84)/large C-PTH fragments ratio in ESRD patients

The "intact" parathyroid hormone (PTH) assay recognizes PTH-(1-84) as well as amino terminally truncated PTH fragments, that is, large carboxyterminal PTH fragments (C-PTH fragments). The present study investigated whether the use of the plasma PTH-(1-84)/C-PTH fragment ratio enhances the noninvasive assessment of bone turnover in patients on dialysis. Bone biopsies and blood samples for determinations of routine indices of bone turnover and PTH peptides were obtained in 51 adult patients on dialysis not treated with drugs affecting bone such as vitamin D or corticosteroids. Blood levels of large C-PTH fragments were calculated by subtracting PTH-(1-84) from "intact" PTH. Patients were classified according to their levels of bone turnover based on histomorphometrically obtained results of activation frequency. Prediction of bone turnover by the various blood indices was done by using proper statistical methods. In addition, hypercalcemia was induced by calcium gluconate infusion in a subset of patients, and levels of PTH-(1-84), "intact" PTH, and PTH-(1-84)/C-PTH fragment ratio were determined. The PTH-(1-84)/C-PTH fragment ratio was the best predictor of bone turnover. A ratio> 1 predicted high or normal bone turnover (sensitivity 100%), whereas a ratio <1 indicated a high probability (sensitivity 87.5%) of low bone turnover. Calcium infusion resulted in decrease in PTH-(1-84)/C-PTH fragment ratio. The PTH-(1-84)/C-PTH fragment ratio predicts bone turnover with acceptable precision for biological measurements. Moreover, a change in serum calcium levels is one of the regulators of the relative amount of circulating PTH-(1-84) and its large C-PTH fragments.

Simplified citrate anticoagulation for continuous renal replacement therapy

Regional anticoagulation with trisodium citrate is an effective form of anticoagulation for continuous renal replacement therapy (CRRT) for patients with contraindications to heparin. However, because of the metabolic complications of trisodium citrate, it is a complicated technique requiring specialized dialysis solutions. We have designed a simplified protocol for citrate regional anticoagulation for CRRT. Two percent trisodium citrate was delivered at 250 mL/h via the prefilter port of a COBE PRISMA device, with the rate adjusted to maintain a postfilter ionized calcium (iCa++) <0.5 mmol/L. A central calcium gluconate infusion was used to maintain a systemic iCa++ at 1.1 mmol/L. A standard dialysate solution consisting of 0.9% saline, KCl 3 mmol/L, and MgSO4 1 mmol/L was delivered at 1000 mL/h. We retrospectively reviewed the outcomes and complications associated with this protoco1 in 29 patients treated from July 1999 to October 1999, evaluating the frequency of clotting of the dialyzer, bleeding complications, citrate toxicity, and patient mortality. The Kaplan-Meier curve for dialyzer survival demonstrated a 61% survival rate at 48 hours. There were no episodes of significant bleeding or citrate toxicity. Seventy-two percent of patients died for reasons unrelated to CRRT. A CRRT protocol using regional 2% trisodium citrate anticoagulation is not associated with significant bleeding complications or citrate toxicity, and represents a simplified approach compared with previous applications using 4% trisodium citrate.

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.

Continuous Renal Replacement Therapy in the Initial Management of Neonatal Hyperammonemia Due to Urea Cycle Defects

After completing this article, readers should be able to: 1. Describe the metabolic acidosis that may be seen in urea cycle defects. 2. Delineate the most important factor in determining neurologic outcome in urea cycle defects. 3. Explain the factors that affect the blood ammonia concentration in continuous renal replacement therapy (CRRT). 4. Delineate the most difficult issue in pursuing CRRT in neonates. 5. Describe the morbidities associated with CRRT. MP was born at 39 weeks' estimated gestational age by vaginal delivery to a 35-year-old gravida 3 para 2 woman who had an uncomplicated pregnancy. The 3- and 6-year-old female siblings of the patient were healthy. Apgar scores were 8 at 1 minute and 9 at 5 minutes. The newborn was discharged to home after a 2-day stay in the well baby nursery during which time she appeared to be alert and was breastfeeding appropriately. She presented to the emergency department less than 1 day later after her parents noted increasing lethargy and very poor feeding at home. She was admitted to the neonatal intensive care unit (NICU). Results of a complete blood count with differential count and C-reactive protein evaluation were unremarkable, but the patient progressed to worsening lethargy, respiratory failure, and abdominal distension requiring intubation within hours of admission. The anterior fontanelle was soft on admission physical examination. Further testing revealed a base deficit of 6.1 on arterial blood gas, serum ammonia level of 810 mcmol/L (1,134 mcg/dL), serum lactate level of 5.6 mmol/L (5.6 mEq/L), and serum pyruvate level of 0.06 mmol/L. Results of liver function tests were abnormal, and the infant had a prothrombin time of 35.9 seconds, a partial thromboplastin time of 54.3 seconds, and a fibrinogen concentration of 1.75 g/L (175 mg/dL). Genetic and nephrology consultations were requested immediately. Additional metabolic studies were obtained, including measurement of plasma amino …

Continuous intra-arterial infusion therapy in hydrofluoric acid burns.

To determine the effect of continuous intra-arterial calcium gluconate infusion therapy on patients suffering from hydrofluoric acid dermal burns of the digits, clinical treatment was performed prospectively on 10 patients from January 1997 to December 1998 at the burn care unit of Kaohsiung Medical University Hospital. An arterial catheter was inserted transcutaneously through the radial artery of the involved hand. After confirmation of the proper position of the catheter, calcium gluconate was infused continuously with an ambulatory infusion pump. Rapid pain relief was achieved immediately after infusion. The rate of infusion was then tapered down gradually, and treatment was completed with no major therapeutic complication. All injured digits of these 10 patients were successfully salvaged with good cosmetic appearance and complete functional preservation. Compared with other conventional therapies, continuous intra-arterial calcium gluconate infusion therapy proved to be a safe, rapid, simple, portable, and effective method for treating hydrofluoric acid dermal burns.

Hemodynamic effects of ionized calcium in horses anesthetized with halothane or isoflurane

Abstract Objectives To evaluate the effects of halothane and isoflurane on cardiovascular function and serum total and ionized calcium concentrations in horses, and to determine whether administration of calcium gluconate would attenuate these effects. Animals 6 clinically normal adult Thoroughbreds. Procedure Catheters were inserted for measurement of arterial blood pressures, pulmonary arterial blood pressures, right ventricular pressure (for determination of myocardial contractility), right atrial pressure, and cardiac output and for collection of arterial blood samples. Anesthesia was then induced with xylazine hydrochloride and ketamine hydrochloride and maintained with halothane or isoflurane. An IV infusion of calcium gluconate was begun 75 minutes after anesthetic induction; dosage of calcium gluconate was 0.1 mg/kg of body weight/min for the first 15 minutes, 0.2 mg/kg/min for the next 15 minutes, and 0.4 mg/kg/min for an additional 15 minutes. Data were collected before, during, and after administration of calcium gluconate. Results Halothane and isoflurane decreased myocardial contractility, cardiac index, and mean arterial pressure, but halothane caused greater depression than isoflurane. Calcium gluconate attenuated the anesthetic-induced depression in cardiac index, stroke index, and maximal rate of increase in right ventricular pressure when horses were anesthetized with isoflurane. When horses were anesthetized with halothane, a higher dosage of calcium gluconate was required to attenuate the depression in stroke index and maximal rate of increase in right ventricular pressure; cardiac index was not changed with calcium administration. Conclusions and Clinical Relevance IV administration of calcium gluconate may support myocardial function in horses anesthetized with isoflurane. (Am J Vet Res 1999;60:1430–1435)

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.

Systemic and topical effects of intradermal hydrofluoric acid

A 35-year-old man attempted suicide by subcutaneous self-administration of hydrofluoric acid (5 cc of a domestic rust removal solution containing 7% hydrofluoric acid). A burn 9 × 7 cm in diameter immediately appeared at the injection site (left forearm and fold of the elbow). In the emergency department, the burn was copiously washed with isotonic solution and treated with cutaneous and subcutaneous injections of magnesium chloride, 10% solution of calcium gluconate, and 2% xilocain, then continuously maintained under topical treatment with calcium gluconate. Seven hours after injection, the patient was severely hypocalcemic (Ca ++ 0.64 mmol/L). Ten hours after injection, in addition to the persistent hypocalcemia (Ca ++ 0.81 mmol/L), hyponatremia (123 mmol/d), hypokalemia (3.4 mmol/L), and hypochloremia (95.6 mmol/L) had developed. The hypocalcemia was corrected with infusion of calcium gluconate (8.92 mEq of Ca ++ as total amount). The patient underwent surgical intervention 7 days after admission, followed by several interventions of plastic surgery.

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.]

An overview of therapeutic apheresis in pediatrics.

Therapeutic apheresis in pediatrics requires selected modifications due to the child's smaller size, blood volume, and developmental age. Red blood cell priming is used to prevent dilution of the child's hematocrit from the normal saline prime. Continuous flow cell separators maintain isovolemia. Discontinuous flow machines cause alterations in the blood volume which may be poorly tolerated by small and critically ill children. Whole blood volumes are calculated on 100 cc/kg for newborns and 70 cc/kg for toddlers and children. Although peripheral access may be used in older children, the majority of pediatric patients require central venous lines preferably the stiffer apheresis or dialysis double lumen catheters. Anticoagulants include heparin, anticoagulant citrate dextrose (ACD), or a combination of both. The heparin dose is titrated to achieve activated clotting times of 180-220 seconds. Children are more sensitive to the hypocalcaemic effects of ACD especially if citrated replacement products such as fresh frozen plasma are used. Prevention or treatment of low ionized calcium levels may include decreased citrate rates, calcium addition to 5% albumin replacement, calcium gluconate infusions, intravenous boluses of calcium chloride, or a change in anticoagulant. Apheresis risks can be reduced through adequate monitoring and preventive measures. The most commonly performed treatments are plasma exchanges and peripheral blood stem cell collections. Diversional activities appropriate for the child's developmental age are provided to allay anxiety, to divert attention, and to elicit cooperation. In conclusion, size and clinical condition are not exclusionary criteria for apheresis.

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.

Control of pulsatile and tonic parathyroid hormone secretion by ionized calcium.

To investigate the effect of changes in ionized calcium on instantaneous PTH secretion, we examined seven young healthy volunteers by 1-min blood sampling under conditions of normo-, hypo-, and hypercalcemia. After a baseline period of 75 min, ambient ionized calcium was either increased or decreased by 0.2 mmol/L for 105 min by clamped infusion of calcium gluconate or sodium citrate. The characteristics of PTH secretion were analyzed by a deconvolution technique, accounting for subject-specific plasma PTH disappearance half-life, as measured during the first 15 min of calcium infusion (range, 2.04-2.93 min). The process regularity of pulsatile PTH secretion was evaluated by an approximate entropy statistic. Under baseline conditions, 32% of total PTH secretion was released in a pulsatile fashion, with a burst frequency of 6.9 +/- 0.8 h-1 and a PTH mass per burst of 2.6 +/- 0.9 pmol/L. The remaining 68% of total secretion was attributed to tonic hormone release. During the initial 30 min of induced hypocalcemia, pulsatile secretion increased by 1140%, whereas tonic secretion did not change. The preferential increase in pulsatile PTH secretion was mediated by a combined rise in burst frequency and mass released per burst. During subsequent steady state hypocalcemia, the tonic secretion rate increased (255% of baseline), whereas burst frequency and burst mass decreased (to 103% and 189% of the baseline values), restoring the baseline ratio of tonic to pulsatile PTH secretion. The regularity of PTH release increased during steady state hypocalcemia. During hypercalcemia, tonic secretion, burst mass, and burst frequency decreased by 75%, 82%, and 32%, respectively, and remained constant throughout the clamp period. We conclude that acute hypocalcemia elicits an immediate pulsatile and a delayed tonic secretory response of the parathyroid gland with increased regularity of PTH release. Acute hypercalcemia suppresses both the pulsatile and the tonic component of PTH secretion.

Parathyroid gland function in secondary hyperparathyroidism.

The parathyroid glands play a critical role in the maintenance of calcium homeostasis. It has been suggested that the set-point for calcium-regulated parathyroid hormone (PTH) release is higher in uremic patients than normal subjects. However, these assessments of parathyroid gland function have been performed using methods that differed from the original four-parameter model. Dynamic testing of the parathyroid glands has been performed with standardized infusions of calcium gluconate and sodium citrate in dialysis patients with secondary hyperparathyroidism and in normal volunteers. In addition, similar studies have been carried out before and after 4 months of intermittent calcitriol therapy. The derived values for the set-point were 1.21 + 0.04 mmol/l and 1.24 + 0.06 mmol/l, respectively in control and dialyzed patients (NS). Furthermore, the values for set-point were 1.21 + 0.01 and 1.22 + 0.01 mmol/l (NS), before and after calcitriol therapy. In addition, when subjects were grouped according to the severity of secondary hyperparathyroidism, the set-point calcium-regulated PTH release did not differ between the groups. Calcitriol therapy alters the secretory capacity of the parathyroid glands during hypocalcemia. The degree of parathyroid enlargement and the type of cell proliferation may be more important determinants of the severity of secondary hyperparathyroidism.

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.

The effect of graded calcium infusions on rhythmic blood pressure oscillations in normal man

This study was designed to determine whether calcium contributes to the regulation of rhythmic oscillations in blood pressure. Six normal subjects received sequential 1-h infusions of calcium gluconate (1.5, 3.0 and 4.5 mg calcium/kg/h) during continuous blood pressure (Finapres) monitoring. The plasma ionized calcium ([Ca2+]) concentration increased from 4.6 +/- 0.07 mg/dl to 5.97 +/- 0.20 mg/dl (p < 0.01) with infusion. The mid-frequency (0.07-0.14 Hz, Mayer wave) power spectrum of diastolic blood pressure was depressed slightly following the first dose but increased significantly following the final dose (p < 0.05). The high-frequency (0.15-0.40 Hz) power spectrum of systolic blood pressure decreased following the first dose (p < 0.05) and subsequently remained low. The low-frequency (0.02-0.6 Hz) power spectrum was not affected. These results demonstrate that graded hypercalcaemia affects blood pressure oscillations in man. Our data suggest that the amplitude of the Mayer wave, a clinical marker of sympathetic vascular tone, is modulated in part by calcium.

Pyrogen reactions to human serum albumin during plasma exchange

Reactions to human serum albumin (HSA) in therapeutic plasma exchange (TPE) are rare. Nevertheless, older literature describes possible adverse effects, including specific immune responses to albumin or other proteins, and reactions due to contaminating organisms or pyrogen. During an eight day period three patients in our unit had unusual reactions after infusion of 1.5-2 L of HSA. Patient 1 had trembling that persisted for 20 min. Patient 2 had shaking for 40 min despite calcium gluconate infusion, and fever to 100.8 degrees F. Patient 3 had severe rigors that subsided after 90 min when meperidine was finally given, and fever to 103.5 degrees F. Record reviews revealed that all three patients had received HSA from the same lot, and that only one other TPE patient had received HSA from that lot. Neither our pharmacy nor the manufacturer was aware of other reactions associated with that lot. Material from a bottle only partially infused to patient 3 was negative in culture and was negative for pyrogen when retested by the manufacturer. Nevertheless, because patients 1 and 2 had each had multiple previous uneventful TPEs and because all three patients tolerated subsequent TPEs without incident when another brand of HSA was used, we conclude that these patients had pyrogen reactions to the implicated HSA lot. This experience illustrates the value of cluster recognition in arousing suspicion of unusual reactions to HSA and the value of recorded lot numbers in pursuing such suspicions. Apheresis personnel should be aware of the potential for pyrogen reactions with HSA and should record lot numbers of all fluids infused during TPE.

Effects of Single Dose Calcium Gluconate Infusion in Hypocalcemic Preterm Infants

We conducted a prospective, double-blind study of 43 preterm infants to examine the effect of a single calcium gluconate infusion as therapy for neonatal hypocalcemia on serum calcium concentrations and hypocalcemic signs in preterm infants with low total serum calcium concentrations. Total and ionized serum calcium was measured and signs of irritability, jitteriness, and twitching were scored (scale 0-9) by blinded observers before and after receiving one dose of either calcium gluconate (100 mg/kg) or placebo (normal saline). Total and ionized serum calcium increased 3 to 6 hours following the calcium, but not the placebo, infusion. Of the infants with hypocalcemic signs, the average score of hypocalcemic signs decreased in the 11 calcium-treated infants; the 12 infants with hypocalcemic signs showed no change of hypocalcemic signs following treatment with placebo. We conclude from this study that a single dose of calcium gluconate (100 mg/kg) in hypocalcemic preterm infants raise total and ionized serum calcium and decrease clinical signs of hypocalcemia.

In vivo assessment of left atrial contractile performance in normal and pathological conditions using a time-varying elastance model.

Contractile function of the ex vivo, isolated left atrium (LA) has been described by a time-varying elastance, but this atrial chamber property has not been shown in vivo. Instantaneous LA pressure-volume (P-V) relations were studied in 12 anesthetized, autonomically blocked, atrially paced dogs. LA volume was calculated from orthogonal sonomicrometer pairs using a cast-validated formula. Data were collected during increases in LA pressure produced by a phenylephrine bolus (200 to 400 micrograms IV). Isochronal P-V points from 5 beats, representing a wide range of atrial pressures, were fitted by linear regression analysis (range of R2, .92 to .99). There were significant time-dependent increases in the slopes [E(t)] and small but statistically insignificant decreases in the volume axis intercepts [VO(t)] of the instantaneous LA P-V relations during atrial contraction; maximal elastance (Emax) occurred 29 +/- 16 milliseconds before atrial end systole (minimal LA volume). Emax was not significantly different than the slopes of either the nonisochronal end-systolic P-V relation (Ees) or the nonisochronal maximal P-to-V relation (EmaxPV): 5.5 +/- 2.8, 4.3 +/- 1.5, and 5.4 +/- 4.2 mm Hg/mL, respectively. In 7 dogs, data were collected both before and after a rapid infusion of calcium gluconate (1 to 2 g IV). Emax increased significantly with a calcium-induced increase in inotropic state (4.5 +/- 1.6 to 5.7 +/- 1.8 mm Hg/mL, P < .01), but the volume axis intercept was unchanged (3.6 +/- 0.7 versus 3.4 +/- 1.9, P = NS). In 4 additional dogs with heart failure (mean LA pressure, 26 +/- 6 mm Hg) produced by 3 weeks of rapid right ventricular pacing, LA stroke volume was significantly greater than and elastance determinations were similar to those of normal dogs. However, the effects of calcium infusion on LA function were attenuated in these animals. We conclude that (1) in the intact heart, LA contraction may be approximated by time-varying elastance with time-dependent changes in E(t) and that (2) LA systolic P-V relations using either the nonisochronal maximum P-to-V ratio or end systole may be useful as an estimate of Emax, are highly linear and sensitive to calcium-induced changes in inotropic state, and may be useful in identifying LA chamber adaptation to chronic hemodynamic loads.

L'acide fluorhydrique : un toxique méconnu

Hydrofluoric acid has widespread uses in industry and at home. Its mechanism of toxicity is the basis of a specific treatment. Cutaneous burns are the most common form of toxicity and the consequences can be catastrophic. Its insidious presentation can delay any therapeutic action, except if the physician is aware about it. A case report underlines the beneficial action of the intra-arterial infusion of calcium gluconate.