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.

Denosumab-induced hypocalcemia post bariatric surgery—a severe and protracted course: a case report

BackgroundDenosumab is known to cause abnormalities in calcium homeostasis. Most of such cases have been described in patients with underlying chronic kidney disease or severe vitamin D deficiency. Previous bariatric surgery could also contribute to hypocalcemia and deterioration in bone health.Case presentationWe present a case of a 61-year-old Malay female with worsening bilateral limb weakness, paresthesia, and severe carpopedal spasm a week after receiving subcutaneous denosumab for osteoporosis. She had a history of gastric bypass surgery 20 years ago. Post gastric bypass surgery, she was advised and initiated on lifelong calcium, vitamin D, and iron supplementations that she unfortunately stopped taking 5 years after surgery. Her last serum blood tests, prior to initiation on denosumab, were conducted in a different center, and she was told that she had a low calcium level; hence, she was advised to restart her vitamin and mineral supplements. Laboratory workup revealed severe hypocalcemia (adjusted serum calcium of 1.33 mmol/L) and mild hypophosphatemia (0.65 mmol/L), with normal magnesium and renal function. Electrocardiogram showed a prolonged QTc interval. She required four bolus courses of intravenous calcium gluconate, and three courses of continuous infusions due to retractable severe hypocalcemia (total of 29 vials of 10 mL of 10% calcium gluconate intravenously). In view of her low vitamin D level of 33 nmol/L, she was initiated on a loading dose of cholecalciferol of 50,000 IU per week for 8 weeks. However, despite a loading dose of cholecalciferol, multiple bolus courses, and infusions of calcium gluconate, her serum calcium hovered around only 1.8 mmol/L. After 8 days of continuous intravenous infusions of calcium gluconate, high doses of calcitriol 1.5 μg twice daily, and 1 g calcium carbonate three times daily, her serum calcium stabilized at approximately 2.0 mmol/L. She remained on these high doses for over 2 months, before they were gradually titrated down to ensure sustainability of a safe calcium level.ConclusionThis case report highlights the importance of screening for risk factors for iatrogenic hypocalcemia and ensuring normal levels before initiating denosumab. The patient history of bariatric surgery could have worsened the hypocalcemia, resulting in a more severe presentation and protracted response to oral calcium and vitamin D supplementation.

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.

Single stage chest wall soft tissue reconstruction with ipsilateral pectoralis major turnover flap, rhomboid skin flap, and inferior nipple transposition

Extravasation injury is a well-known complication of central venous catheter placement, with potential for extensive soft tissue necrosis. Here, we describe the case of a patient who developed a large right chest well soft tissue defect, due to a chest wall abscess from calcium gluconate infusion via a right internal jugular central venous catheter. After multiple debridements, the chest wall defect was reconstructed with a single stage ipsilateral pectoralis major turnover flap, rhomboid skin flap, and inferior nipple transposition to match the contralateral nipple. There was no further infection, no nipple necrosis, and patient regained full range of motion of the ipsilateral shoulder.

ODP076 A Unique Case of Iatrogenic Hypermagnesemia Induced Symptomatic Hypocalcemia

Abstract Introduction Magnesium plays a role in production, release, and end-organ responsiveness of parathyroid hormone (PTH) and calcium homeostasis. Hypomagnesemia has been well documented to cause hypocalcemia by impaired secretion of PTH or PTH resistance. Iatrogenic hypermagnesemia in pregnant patients receiving intravenous magnesium for suppression of premature labor and pre-eclampsia is an uncommon cause of hypocalcemia. We are reporting a case of symptomatic hypocalcemia caused by iatrogenic hypermagnesemia in post-partum mother, who had high PTH in contrast to previous case reports. CaseA 28-year-old G4P1122 female, postpartum day 16 was admitted for headache, slurred speech, and vomiting. She was found to have elevated blood pressures and was started on IV magnesium for postpartum preeclampsia. On her first day, she received a 4g bolus of magnesium sulfate followed by 2g as maintenance for seizure prophylaxis. The following morning, the patient awoke complaining of numbness/tingling in both arms and twitching in her face and eyelids. Later that day, she had developed bilateral spontaneous carpopedal spasm as well. Labs drawn at that time revealed ionized calcium 0.78mmol/L (1.18-1.32 mmol/L), corrected calcium 7.42mg/dL (8.5-10.1), vitamin D 25-OH 45ng/mL (30-100), PTH 149.1pg/mL (18.5-88), phosphorus 2.9mg/dL (2.3-4.6), GFR116mL/min (>60) and magnesium 3.5mg/dL (1.4-2.2). Patient was started on IV calcium gluconate infusion along with calcium carbonate 1g QID and vitamin D3 5000 units daily. By the evening of the second day, patient's carpopedal spasm and paresthesia completely resolved. Repeat labs demonstrated improved ionized calcium of 1.17mmol/L (1.18-1.32), corrected calcium of 9.78mg/dL (8.5-10.1), and magnesium of 1.5mg/dL (1.4-2.2). Patient was discharged on calcium carbonate 1g TID and Vitamin D3 5000 units daily. Patient self-discontinued calcium and vitamin D supplementation a week after discharge. Repeat labs one week later showed normal corrected calcium, magnesium, and PTH levels. Conclusion Our patient developed transient, symptomatic hypocalcemia with elevated PTH secondary to iatrogenic hypermagnesemia, which improved with intravenous calcium. Hypomagnesemia is a known cause of hypocalcemia, but hypermagnesemia is a significantly less recognized etiology. Hypermagnesemia can cause low PTH due to activation of calcium sensing receptors resulting in inhibition of PTH secretion. Hypermagnesemia can also blunt the peripheral effect of PTH and promote hypercalciuria. Previous studies showed PTH can peak by the end of magnesium infusion but still result in hypocalcemia, although this is an uncommon clinical presentation. Our case highlights this aspect of elevated PTH after the completion of IV Magnesium infusion but still unable to correct hypocalcemia due to PTH resistance from hypermagnesemia. This calls attention to another underrecognized sequalae of hypermagnesemia: blunting of peripheral tissues response to PTH. Clinicians should be aware of development of hypocalcemia with both hypo- and hypermagnesemia as well as the underlying pathophysiology. Presentation: No date and time listed

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.

Calcium gluconate infusion is not as effective as dopamine agonists in preventing ovarian hyperstimulation syndrome.

The aim of the study was to compare the effectiveness of calcium gluconate and cabergoline therapy in the prevention of ovarian hyperstimulation syndrome (OHSS). Eight hundred and forty-five women who underwent GnRH antagonist protocol and at high risk for developing OHSS were divided into two groups, those given cabergoline (n=435) or calcium gluconate (n=410). In cabergoline group, 0.5 mg of cabergoline was administered once daily p.o. starting on the day of ovulation trigger and continued until the following 8 days. In calcium gluconate group, intravenous calcium gluconate was administered daily for four days starting on the day of oocyte pickup (OPU). 10 ml of 10% calcium gluconate solution was dissolved in 200 ml of physiological saline and administered by intravenous route within 40 minutes. Infusion was started within the first 30 minutes following the OPU and continued on the 1st, 2nd and 3rd days after OPU. Mild OHSS was developed in 367 (89%) patients receiving calcium gluconate infusion, while 251 patients (57%) in the cabergoline group developed mild OHSS. The frequency of mild OHSS in the calcium group was significantly higher than the cabergoline group (p<.001). Moderate OHSS was observed in 32 people (7.8%) in the calcium gluconate group, while it was observed in 184 people in the cabergoline group (42.3%). Calcium gluconate infusion significantly reduced the development of moderate OHSS compared to cabergoline therapy (p<.001). Severe OHSS developed in 11 patients (2.7%) in the calcium gluconate group, while severe OHSS did not develop in those given cabergoline (0%, p<.001). Clinical pregnancy, live birth and abortion rates were similar in the two groups. When logistic regression analysis was performed, a significant correlation was found between age, BMI, AMH, the number of antral follicle count, OHSS history, paracentesis, progesterone on the day of hCG, 2 PN zygotes, and HbA1c levels and the development of OHSS. No correlation was found between the use of metformin or cetrotide and the development of OHSS. Calcium gluconate treatment is not effective in the prevention of OHSS.

Improving management of severe hypoparathyroidism: a case series.

Hypoparathyroidism is considered a rare endocrine disease. Despite being a deficiency of parathyroid hormone, the standard therapy is based on oral calcium and active vitamin D supplementation. This approach provides satisfactory management in most cases but may be inadequate for patients in the most complex spectrum of the disease. Other therapies are being explored, and among them, the use of recombinant human parathyroid hormone (PTH) has proved to decrease the requirements of calcium and active vitamin D to reach adequate therapeutic goals. We aimed to provide information on the effectiveness of the current recombinant parathyroid hormone analogs in the clinical management of difficult to control cases of hypoparathyroidism. We report our experience using teriparatide and PTH (1-84) through five complex cases of hypoparathyroidism of diverse etiologies. We describe each case and report the effectiveness of treatment in clinical practice. Four patients with postsurgical hypoparathyroidism and one patient with autoimmune hypoparathyroidism, all of them with suboptimal control under the standard treatment with calcium and calcitriol supplements or calcium gluconate infusion, are presented. They were all started on teriparatide or PTH (1-84), and all of them showed a diminishment of symptoms and were able to maintain normocalcemia without parenteral calcium despite a reduction of oral treatment. This article highlights the effectiveness and safety of hormonal replacement treatment in difficult to manage hypoparathyroidism and provides evidence which justifies its off-label prescription in the case of teriparatide. We consider that this treatment should be considered in cases in which standard treatment fails to reach adequate therapeutic goals.

The Unusual Suspect: Hypocalcemia in Preeclampsia After Magnesium Infusion

Background: Magnesium plays a vital role in calcium homeostasis. Magnesium sulfate is used in obstetric populations for the management of preeclampsia and eclampsia. Hypocalcemia secondary to iatrogenic hypermagnesemia is an uncommon complication. We report a case of symptomatic hypocalcemia due to hypermagnesemia. Clinical Case: A 26-year-old female with type 1 diabetes at 33 weeks gestation was admitted for preeclampsia. She had severe hypertension and proteinuria, and the decision to induce labor was made. She was started on a magnesium sulfate drip and remained on the drip for 33 hours. Magnesium levels peaked at 7.5 mg/dL (1.7–2.5 mg/dL). The magnesium drip was suspended after delivery. She complained of mild tingling and numbness in her hands, feet, and perioral area. Shortly after delivery, she had a pre-syncopal event. The laboratory evaluation revealed a calcium of 5.9 mg/dL (8.4–10.4) with an albumin of 2.2 g/dL (3.7–5.5), magnesium of 4.2 mg/dL, phosphorus 2.2 mg/dL (2.3–4.6) and GFR above 60 mL/min/1.73m2 . Spot urine calcium to creatinine ratio was 0.17 mg/dL. The 25-hydroxy vitamin D level was low at 12 ng/mL (20–100). The parathyroid hormone (PTH) level was inappropriately normal at 21.7 pg/mL (12–88). She had no history of hypocalcemia, and calcium level obtained six months before the presentation was normal. She received one calcium gluconate infusion, was then started on a continuous calcium gluconate infusion for symptomatic hypocalcemia. She also received oral supplementation of calcium and vitamin D. The calcium levels normalized within 24 hours as the hypermagnesemia resolved from the discontinuation of the magnesium drip. The subsequent PTH level was 38.8 pg/mL. She was discharged on vitamin D supplements. She had no recurrence of hypocalcemia. Conclusion: Our case highlights the effect of magnesium infusion on the parathyroid gland leading to profound symptomatic hypocalcemia. Magnesium plays an essential role in the secretion of PTH. Transient hypoparathyroidism can occur due to hypomagnesemia and hypermagnesemia (tocolytic therapy). In hypomagnesemia, the parathyroid gland secretes insufficient PTH, and the renal and skeletal response to PTH is reduced. In hypermagnesemia, the magnesium activates the extracellular calcium-sensing receptor, subsequently causing inhibition of the parathyroid gland. Amelioration of hypermagnesemia leads to the normalization of parathyroid function. Health care providers should be aware of this phenomenon, especially in the obstetric population receiving magnesium infusion. The monitoring of calcium levels may be necessary for this patient population. The laboratory testing should include magnesium in the evaluation of hypocalcemia.

A Case of Vocal Cord Paralysis and Severe Hypocalcemia

Background: Tetany is the hallmark of hypocalcemia. Vocal cord paralysis is a rare presenting symptom of hypocalcemia, especially without signs of overt tetany or seizures. Clinical case: 18 year old man with history of iron deficiency anemia and dyslipidemia presented with aphasia, right sided upper and lower extremity weakness and facial tingling for 3 days. Physical exam was notable for aphasia, pallor, positive Chvostek and Trousseau sign. Admission labs showed BUN 127 mg/dL (n 8–26 mg/dL), creatinine 12.74 mg/dL (n 0.8–2.00 mg/dL), calcium 5.2 mg/dL (n 8.5–10.5 mg/dL), magnesium (1.8–2.4 mg/dL), phosphorus 10.3 (2.4–4.8 mg/dL), alkaline phosphatase 126 (8–120 U/L), albumin 3.3 g/dL (n 3.0–5.0 g/dL), 25 OH VitD3 9.1 ng/mL (n 30–80 ng/mL), PTH 594 pg/mL (n 15–65 pg.mL), COVID 19 PCR negative. Aphasia resolved with 1 gram calcium gluconate infusion. Patient underwent emergent hemodialysis. He was placed on calcium carbonate 1500 mg oral three times daily, calcitriol 1 mcg oral twice daily, ergocalciferol 50,000 IU weekly, sevelamer carbonate 1600 mg tablet three times daily. Kidney biopsy showed membranoproliferative pattern glomerulonephritis with C3 deposits. He was discharged on hemodialysis and referred to a transplant center. Conclusion: Vocal cord paralysis is rare in adults and mostly seen in patients with pseudohypoparathyroidism caused by hypomagnesaemia.2,3 Identifying vocal cord paralysis as an atypical presentation of hypocalcemia secondary to acute kidney failure requires prompt recognition and treatment.

Denosumab Induced Severe Prolonged Hypocalcemia in Metastatic Prostate Cancer

Background: Denosumab is a RANK-l inhibitor that, in addition to the treatment of osteoporosis, is used in patients with advanced cancer and metastatic bone disease to prevent skeletal-related events. Although denosumab is generally safe and effective, it can cause hypocalcemia which in some patients can be severe and life threatening. We present a case of severe prolonged hypocalcemia after a single dose of denosumab in a patient with metastatic prostate cancer. Case: A 78-year-old male with a past medical history of stage 4 prostate cancer on antiandrogen treatment with GnRH antagonist presented with severe hypocalcemia. Physical exam revealed a blood pressure 125/80 mm Hg, pulse 115 per min and weight 135 lb with negative Chvostek’s and Trousseau’s signs. The electrocardiogram showed supraventricular tachycardia with prolonged QTc interval of 503 ms (<430 ms). Labs showed serum calcium 4.9mg/dL (8.5–10.5), albumin 2.5g/dL (3.6–5.1), corrected calcium 5.7 mg/dL, ionized serum calcium 0.64mmol/L (1.05–1.3), creatinine 1.10mg/dL (0.7–1.2), eGFR >60, phosphorus 2.0mg/dL (2.5–4.5), magnesium 1.9 mg/dL (1.6–2.6), 25-OH vitamin D 29.7 ng/mL (30–100), 1,25 dihydroxy vitamin D 174 pg/mL (18–64), iPTH 244.0 pg/mL (11–68) and PSA 1860 ng/mL. Three weeks prior to presentation, the patient received 120 mg of subcutaneous denosumab. Pre-treatment serum calcium was 9.2 mg/dL (8.5–10.5), and Tc-99m bone scan showed multiple osteoblastic osseous metastatic lesions involving both axial and appendicular skeleton. The patient was diagnosed with denosumab-induced severe hypocalcemia and started on intravenous (IV) calcium gluconate infusion, oral phosphate 250 mg twice daily, and ergocalciferol 50,000 IU twice weekly. He required IV calcium gluconate up to 10 g per day in addition to oral calcium carbonate 2 g t.i.d. for 2 weeks to resolve hypocalcemia and normalize QTc interval. Patient was discharged to nursing home on calcium carbonate 2 g q.i.d. with IV calcium gluconate as needed to keep corrected calcium >8.0 mg/dL. After discharge he required up to 4 g of IV calcium and 8 g of oral calcium per day. Unfortunately, he presented again with severe hypocalcemia 5 weeks after discharge. In addition to current regimen of oral and IV calcium boluses, low dose calcitriol was started. We were only able to maintain his serum calcium>8.0 mg/dL by administering high daily dose of oral calcium carbonate 8 g /day and calcitriol 2 mcg daily. Due to poor prognosis, he was transitioned to hospice care and died 2 weeks later. Discussion: There are not many case reports on severe prolonged hypocalcemia secondary to denosumab in cancer patients but normal kidney function. Our patient remained on high dose of calcium even 101 days after denosumab administration. Reference: 1. Milat F et al. Prolonged hypocalcemia following denosumab therapy in metastatic hormone refractory prostate cancer. Bone. 2013 Aug 1;55(2):305–8.

Hypermagnesemia in a 20-month-old healthy girl caused by the use of a laxative: a case report

BackgroundHypermagnesemia can be a fatal condition and should be diagnosed early on. Most reports of hypermagnesemia have been of adults with impaired renal function. We describe the case of a pediatric patient without renal dysfunction who developed severe hypermagnesemia.Case presentationA healthy 20-month-old Asian girl presented to our emergency department with episodes of vomiting and a reduced level of consciousness. The neurological examination showed a symmetric decrease in muscle tone, and the deep tendon reflexes were decreased. On admission, her magnesium (Mg) level was 11.0 mg/dL after receiving magnesium oxide for 4 days because of constipation. She was immediately administered calcium gluconate infusion (3.9 mEq), and then was continuously infused with it (0.23 mEq/h) as a Mg antagonist to cardiac side effects. She was kept hydrated with 0.9% sodium chloride to maintain good urine output to excrete the Mg. The level of the serum Mg decreased to 2.4 mg/dL, enabling her to regain consciousness. During 5 years of follow-up, she was neurologically well, without the recurrence of hypermagnesemia.ConclusionsEven in the absence of significant renal dysfunction, the prescription of a laxative containing Mg for constipation can result in severe hypermagnesemia. In addition, the symptoms of hypermagnesemia are nonspecific, and early diagnosis is difficult unless it is actively suspected.

SAT-404 Neonatal Hypocalcemic Seizures in Offspring of a Mother with Familial Hypocalciuric Hypercalcemia Type 1 (FHH1)

Background: Familial hypocalciuric hypercalcemia type 1 (FHH1) is caused by loss-of-function mutations of the calcium-sensing receptor (CaSR), and considered to be a benign condition associated with mild-to-moderate hypercalcemia (1). However, the children of parents with FHH1 can develop a variety of disorders of calcium homeostasis in infancy. Objective: To further characterise the range of calcitropic phenotypes in the children of a mother with FHH1. Methods: We assessed a three generation FHH kindred by clinical, biochemical and mutational analysis following informed consent. Results: The kindred comprised a hypercalcemic male, his daughter who had hypercalcemia and hypocalciuria, and her four children, of whom two had asymptomatic hypercalcemia, one was normocalcemic, and one suffered from transient hypocalcemic seizures during infancy. The hypocalcemic infant had a serum calcium of 1.57 mmol/L (normal, 2.0-2.8) and PTH of 2.2 pmol/L (normal, 1.0-9.3) as a consequence of maternal hypercalcemia, and required treatment with I-V calcium gluconate infusions. Mutational analysis identified a novel heterozygous p.Ser448Pro CaSR variant in the hypercalcemic family members, but not in the children with hypocalcemia or normocalcemia. Three-dimensional modelling using a reported crystal structure of the dimeric CaSR showed the mutated Ser448 residue to be located in the CaSR extracellular domain, and predicted the p.Ser448Pro variant to disrupt a hydrogen bond interaction across the extracellular CaSR dimer interface. The variant Pro448 CaSR, when expressed in HEK293 cells, was shown to significantly impair CaSR-mediated intracellular calcium mobilisation and mitogen-activated protein kinase (MAPK) responses following stimulation with extracellular calcium, thereby demonstrating it to represent a loss-of-function mutation. Conclusion: These studies have identified a novel loss-of-function CaSR mutation which caused asymptomatic hypercalcemia in a mother and her children who had inherited the mutation. However, one child who did not inherit the mutation developed transient neonatal hypocalcemic seizures as a consequence of maternal hypercalcemia. These findings highlight the importance of assessing serum calcium and undertaking CaSR mutational analysis in the newborn offspring of a mother with FHH1. Reference: (1) Hannan FM, Kallay E, Chang W, Brandi ML, Thakker RV. The calcium-sensing receptor in physiology and in calcitropic and noncalcitropic diseases. Nat Rev Endocrinol. 2018; 15(1): 33-51.

Medical Management of Primary Hyperparathyroidism in Pregnancy: A Case Report and Brief Literature Review

There is no established standard of care for the medical management of primary hyperparathyroidism in pregnancy for those patients who are not surgical candidates. We present a case of primary hyperparathyroidism in the third trimester that was managed with cinacalcet and a literature review on the various modalities for the medical management of primary hyperparathyroidism in pregnancy. The primary aim of this case report is to document a case of hyperparathyroidism in pregnancy that was managed medically and to perform a brief systematic review of the literature available on the medical management of primary hyperparathyroidism in pregnancy. The secondary aim is to contribute to the literature available on the use of cinacalcet in pregnancy. A 37-year-old woman with untreated primary hyperparathyroidism presented at 32 weeks of gestation with hypercalcemia that was not amenable to surgical intervention. We treated her with increasing doses of cinacalcet with improvement in her serum calcium until developing pre-eclampsia which prompted emergent cesarean delivery of the infant. The neonate developed respiratory distress after delivery but did not develop hypocalcemia after birth. The neonate became transiently hypercalcemic in the setting of calcium gluconate infusions given to prevent hypocalcemia. The patient underwent surgical removal of a parathyroid adenoma and required calcium supplementation for 1 month afterwards. Hypercalcemic crisis during pregnancy is associated with significant maternal and fetal morbidity. There is limited information regarding the medical management of primary hyperparathyroidism due to the lack of high-powered studies and prospective studies owing to the relative rarity of the condition. No serious adverse maternal events were reported for either bisphosphonate or cinacalcet use. Adverse neonatal events include transient hypocalcemia of the infant with cinacalcet use and possibly low birth weight, infantile hypocalcemia, and shortened gestational periods with bisphosphonate use. J Endocrinol Metab. 2020;10(2):49-53 doi: https://doi.org/10.14740/jem624

Severe Amlodipine Toxicity: A Case Rescued with Extracorporeal Membrane Oxygenation.

ABSTRACTAmlodipine is a widely prescribed drugs for the management of hypertension. Its toxicity is associated with severe myocardial depression and refractory hypotension. We present a case of a 28-year-old female known case of seizure disorder and depression who got admitted to our hospital with a history of consumption of 80 tablets of 5 mg amlodipine (total 400 mg). Patient presented to our hospital after 23 hours following consumption of the drug. Patient was managed in the intensive care unit (ICU) with mechanical ventilation support and intravenous infusion of noradrenalin, adrenalin, insulin-dextrose, and calcium gluconate. Due to refractory hypotension, venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated on the same day. Patient was successfully managed and discharged home on the 8th day. This report highlights a rare case of a massive amlodipine overdose (400 mg) and ECMO as a rescue therapy.How to cite this articleSutar A, Venkategowda PM, Murthy A, Chikkaswamy SB. Severe Amlodipine Toxicity: A Case Rescued with Extracorporeal Membrane Oxygenation. Indian J Crit Care Med 2020;24(5):365–366.

HIGH DOSE AMLODIPINE POISONING TREATED WITH HIGH INSULIN EUGLYCEMIC THERAPY

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Calcium channel blockers (CCB) are one of the most commonly prescribed anti-hypertensive medications. CCB poisoning is life-threatening due to myocardial suppression and severe refractory hypotension. To date, there are no specific recommendations on when to initiate high insulin euglycemic therapy (HIET). Management has been aimed at achieving adequate vasopressor support with epinephrine, norepinephrine, and dopamine. fluid resuscitation, and calcium are also provided. Recently, case series have reported successful outcomes in treating CCB poisoning with HIET. CASE PRESENTATION: A 72 year old female presented to the ED with lethargy and dizziness after attempting to commit suicide by ingesting 100 tablets of Amlodipine 5 mg twelve hours prior to presentation, per report of the patient and family. Patient had a past medical history of macular degeneration, depression, cataract and hypertension. Upon presentation the patient’s physical exam was significant for a blood pressure of 87/53 mmHg, a temperature of 98.4 °F, a heart rate of 98 and a respiratory rate of 18. The cardiovascular exam showed a regular rhythm and normal heart sounds. The remainder of the exam was unremarkable. Electrocardiogram showed normal sinus rhythm of 97 with no evidence of any conduction delays. Abnormal labs included a serum sodium of 134, ALT of 110 and AST of 88. Renal function and blood counts were normal. The patient’s blood pressure began to decrease dramatically, prompting the initiation of HIET, calcium gluconate infusion and vasopressor support within the first 4 hours after presentation. The patient required continuous infusion of insulin with D10, calcium gluconate infusion, and close monitoring of both calcium and glucose for three days after admission. On day 6, she became normotensive and no longer required vasopressor support. DISCUSSION: Dihydropyridine CCB’s block L-type calcium channels, which cause smooth muscle relaxation with no-to-minimal effect on the myocardium in usual doses. At higher and more toxic doses, it can block sodium channels in the myocardium causing myocardial suppression. CCB poisoning in high doses can be fatal. However, there are no clear guidelines outlining the time to initiate HIET in CCB poisoning. In this case HIET had a positive outcome, but it was started almost 16-18 hours after ingestion of the calcium channel blocker. This presents the question of whether or not timing of HIET initiation could decrease ICU stay and mortality.In addition, it is unclear wether HIET should be used concurrently with vasopressor support as a first-line therapy. CONCLUSIONS: Patients who present with CCB poisoning due to higher dose ingestions require more aggressive therapy in order to demonstrate clinical improvement. Data in past years have supported the use of HIET in these patients, but appropriate time of HIET initiation has not been established. Reference #1: St-Onge M, Dubé PA, Gosselin S. et.al. Treatment for calcium channel blocker poisoning: a systematic review. Clinical Toxicology. 2014.1;52(9):926-44. Reference #2: Kumar K, Biyyam M, Bajantri B, et.al. Critical Management of Severe Hypotension Caused by Amlodipine Toxicity Managed With Hyperinsulinemia/Euglycemia Therapy Supplemented With Calcium Gluconate, Intravenous Glucagon and Other Vasopressor Support: Review of Literature. Cardiology research. 2018;9(1):46. Reference #3: St-Onge M, Anseeuw K, Cantrell FL, et.al. Experts consensus recommendations for the management of calcium channel blocker poisoning in adults. Critical care medicine. 2017;45(3):e306. DISCLOSURES: No relevant relationships by ahmad alkhatatneh, source=Web Response No relevant relationships by Razan Elsayed, source=Web Response

Feeding and postruminal infusion of calcium gluconate to lactating dairy cows

Gluconic acid was proposed as a prebiotic for nonruminants; however, a ruminant application is undescribed. The first experiment was a 5 × 5 Latin square with five test doses of calcium gluconate (...

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.

SUN-516 Fahr's Syndrome: A Rare Sequela of Hypoparathyroidism

Fahr’s syndrome (FS) is rare, progressive neurodegenerative disorder characterized by bilateral symmetric calcifications in the basal ganglia and cerebral cortex. Etiology of FS includes endocrine disorder, mitochondrial disease, dermatological or infectious disease. The prevalence of FS due to hypoparathyroidism (HP) is unknown. The presentation varies from movement disorders, pyramidal signs, neuropsychiatric manifestations to cognitive impairment. Case: We present a 46-year-old female with history of Grave’s disease s/p subtotal thyroidectomy, postsurgical HP and hypothyroidism for over two decades. She had history of chronic nonadherence with medications and clinic visits. Serum calcium levels were consistently below 7 mg/dl. She was found unresponsive and required intubation. Vital signs were within normal range. Physical examination except for neurological exam was unremarkable. Laboratory data: serum calcium- 6.2 mg/dl (8.4-10.2 mg/dl), ionized calcium- 0.77 mmol/L (1.13-1.32 mmol/L), phosphate - 6.4 mg/dl (2.7-4.5 mg/dl), 25 vitamin D- 21 ng/ml ( 30-100 ng/ml ), PTH- 7 pg/ml (15-65 pg/ml ), magnesium- 1.5 mg/dl (1.6-2.6 mg/dl ), creatinine - 5.16 mg/dl ( 0.4-1.1 mg/dl), WBC- 19.6 x 103/ uL (4-10 x 103/uL), TSH- 35 IU/ml (0.27-4.2 IU/ml), Free T4 – 0.96 ng/dl (0.9-1.7 ng/dl), lactate – 1.4 mmol/L (0.5 – 2.2 mmol/L). Urine toxicology was negative. EKG revealed prolonged QTc of 524 msec. Head CT showed no acute pathology however, revealed extensive bilateral calcifications of the dentate nuclei, basal ganglia, thalami and white matter, leading to consideration of FS. Calcium rose above 8 mg/dl with treatment (calcium gluconate infusion; oral calcium acetate and calcitriol via nasogastric tube). However, her mentation improved only after serum calcium remained above 8 mg/dl for the next five days. She regained consciousness and was oriented but mentation did not return to baseline. Conclusion: Although FS with extensive intracranial calcifications is a rare sequela of HP, HP is the most common cause of FS. The pathogenesis of these brain calcifications is not clear. Our patient had long standing HP and chronic non-adherence to medications. Her age at the time of diagnosis of FS rules out mitochondrial disorders. Her clinical presentation, extensive intracranial calcification with characteristic distribution and the absence of infection, dermatological lesions, traumatic or toxic causes or family history favor the diagnosis of FS. The progression of FS is thought to be associated with the calcium/phosphorus ratio, severity and duration of hypocalcemia. This emphasizes the importance of early stabilization of serum calcium level in HP to prevent development of complications. In most patients, clinical improvement and reversal of neuropsychiatric symptoms is notable after the correction of hypocalcemia. Hence, early recognition of HP as an etiology of FS is critical.