Infusion Of Gluconate Research Articles

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.

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

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.

Intravenous Versus Oral Iron Replacement in Patients with a Continuous-Flow Left Ventricular Assist Device.

Intravenous Versus Oral Iron Replacement in Patients with a Continuous-Flow Left Ventricular Assist Device.

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

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.

SAT-508 A Case Report Of Severe Hypercalcaemia Due To Iatrogenic (oral Supplements), Aki And Immobility

Introduction: Hypercalcaemia is a commonly encountered electrolyte imbalance.We report a case of severe hypercalcaemia which was resistant to conventional treatment approach. Case Report: A 52 year old lady presented to hospital with tiredness, constipation, confusion and reduced mobility for 3 weeks.She had complex past medical history including Papillary carcinoma of thyroid treated with total thyroidectomy and parathyroidectomy and Radioactive Iodine ablation 16 years ago and depression. She was taking Levothyroxine , oral calcium & 1-alfacalcidol. On physical examination, she was dehydrated and confused. Her biochemistry revealed Acute kidney Injury(AKI) with Urea: 15.6 (n:2.5-7.8mmol/l), Creatinine: 177 (n: 50-104 micromol/l), eGFR:32ml/min and corrected Calcium 5.71 (n:2.20-2.60mmol/l). PTH was suppressed at 0.1 (n:1.1-4.7pmol/l) and Vitamin D of 30 (n:50-250nmol/l). ECG showed shortened QTc. Initial management of her severe hypercalcaemia was by stopping her oral Calcium tablets and 1 alfacalcidol. She was treated with normal saline infusion.Pamidronate infusion was contraindicated because of AKI. She was therefore given Calcitonin infusion 400 International units resulting in improvement in her corr. Ca+ to 4.77 mmol/l within 24 hours. She continued to receive normal saline and her biochemistry improved. ECG changes were also resolved. Work up for non PTH dependent severe hypercalcaemia included a CT Thorax Abdomen Pelvis, which did not show any evidence of malignancy, bone lesions or nephrocalcinosis. Her Immunoglobulin electrophoresis was normal. Her severe hypercalcaemia was thought to be multifactorial - contributed by her oral calcium and 1 alphacalcidol supplements and exacerbated by immobility and acute kidney injury. After 5 days of hospital admission, her corr. Ca+ dropped to 2.11 mmol/l. Her calcium tablets and 1 alfacalcidol 1.5microgram OD were restarted.However, her bloods showed worsening hypocalcaemia with corr. Ca+ 1.50 mmol/l despite ongoing treatment with calcium gluconate infusion for 10 days. She was therefore started on Indapamide 2.5 mg once daily which was uptitrated to 5mg once daily. Her corr. Ca+ improved to 2.15mmol/l and she was discharged from hospital. Her bone profile has been followed up since discharge and calcium levels have been in normal range. Her Indapamide has now been discontinued. Conclusion: Although disorders of bone homeostasis are very commonly treated on medical wards, sometimes these electrolyte imbalances can be extremely severe and subsequent management could be quite challenging. Markedly high calcium levels due to primary hyperparathyroidism secondary to adenoma(parathyroid crisis) and malignancy have been reported in the past. However, our case report is the first to highlight such severe hypercalcaemia due to iatrogenic (oral supplements), AKI and immobility causes.

SUN-515 A Case report of Severe Persistent Hypocalcaemia due to Functional Hypoparathyroidism

Introduction: Severe Hypocalcaemia is generally seen in clinical practice in patients following thyroid or parathyroid surgery .We report a case of severe hypocalcaemia with unusual presentation and etiology with challenging management. Case report: A 49 year old gentleman presented to hospital with unexpected, unintentional severe weight loss (20kg over 2 months), vomiting, diarrhoea, muscle cramps and pins & needles in both hands. His past medical history included beta thalassemia trait. He had a recent bereavement in his family and therefore had attributed his symptoms to the grieving process. He had no significant or relevant family history of note.Physical examination revealed positive Chvostek and Trousseau’s signs. His initial biochemistry showed corrected calcium of 0.86 (Normal range:2.20-2.60 mmol/l), Magnesium 0.58 (Normal range:0.7-1.0mmol/l), K+:3.3(Normal range:3.5-5.3mmol/l),Parathyroid hormone(PTH) suppressed at 0.7(Normal range:1.1-4.7pmol/l) and 25 OH Vitamin D 25(Normal range:50-250nmol/l).ECG showed long QTc.He wasn’t taking any proton pump inhibitor. He was started on intravenous magnesium infusion (6g of MgSO4 in 500 ml Normal saline), Calcium Gluconate infusion (100ml of 10% Ca. Gluconate in 1000mls of Normal saline at 50-100 ml/hr), Calcium carbonate tablets and Cholecalciferol 20,000 units daily(for 10 days). His corrected calcium gradually improved and he noticed immediate resolution of his symptoms. His CT chest,Abdomen,Pelvis did not show any evidence of malignancy and Gastroscopy showed mild erosive gastritis.He was reviewed by Gastroenterology but no other cause for significant weight loss and gastrointestinal symptoms was found. He was thought to be having Severe Hypocalcaemia due to Functional Hypoparathyroidism caused by Magnesium and Vitamin D deficiency. He was discharged on oral calcium and cholecalciferol tablets. He represented to hospital a month later with corr. Ca+ of 1.57mmol/l. Vitamin D had improved to 90nmol/l, however, PTH was still suppressed at 0.8pmol/l.His calcium carbonate tablets were increased to daily dose of 3g per day and he was also started on 1-alfacalcidol 250 nanograms BD. Subsequent review in ambulatory clinic revealed that he was still hypocalcaemic at 1.75mmol/l. His 1-alfacalcidol was increased to 500 nanograms BD. He continues to be on this treatment, has gained weight and is asymptomatic. Conclusion: Although calcium abnormalities are commonly treated on medical wards, it is very rare to see such severe hypocalcaemia in the absence of any significant pathology. Understanding the physiology of calcium homeostasis is vital to guide appropriate management, especially in situations of clinical emergency which can be very challenging, as we have highlighted in our case.

Extracorporeal life support for severe cardiogenic shock induced by diltiazem intoxication

Introduction. Management of cardiogenic shock caused by severe drug intoxication is always challenging. In case of multidrug intoxication, a result, despite aggressive medical therapy, is often unpredictable. Utilization of extracorporeal life support devices in these cases has been suggested and reported results are promising. Case report. We presented a case of profound cardiogenic and distributive shock caused by suicidal intoxication with diltiazem and anionic surfactant ingestion in a 36-year-old woman. The patient ingested more than 90 tablets of diltiazem of 90 mg (ingested dose of 8.1 g), and 4 pieces of household toilet refresh agent containing anionic surfactant. During the admission, systemic blood pressure was 65/40 mmHg, heart rate 45 beats per minute, with signs of metabolic acidosis. The patient underwent several repeated gastric lavages. Emergent fluid resuscitation, calcium gluconate, insulin and vasopressive agents (dopamine and noradrenaline) infusions were administered with negligible effect. Due to progressive and refractory cardiogenic shock with signs of multiorgan failure, a decision was made to put the patient on venoarterial extracorporeal membrane oxygenator. Immediately after starting the extracorporeal membrane oxygenation, diuresis was established. During the next 36 h, an adequate end-organ perfusion was achieved with complete reversal of multiorgan failure. After the successful restoration of all major organ functions, the patient was successfully decannulated and discharged from the hospital after 10 days in a good condition. Conclusion. In severe cases of refractory cardiogenic and distributive shock due to diltiazem and other poison intoxication, venoarterial extracorporeal membrane oxygenation could allow additional circulatory support providing the bonus time for endogenous clearance of toxins. Venoarterial extracorporeal membrane oxygenation could be used in conjunction with the optimal medical therapy aiming to the restoration of end-organ perfusion and allowing for intrinsic drug and toxin metabolism and natural elimination.

A Case of Life-threatening Amlodipine and Atenolol Overdose

ABSTRACTTreating a patient of amlodipine-atenolol poisoning is nightmare for a physician. In high dose both the drugs individually cause severe bradycardia and hypotension. In combination they cause severe cardiovascular depression. Here we report a case of 66-year-old obese, hypertensive, depressed male, who presented to emergency 9 hours after consumption of 25 tablets of amlodipine-atenolol (5 mg+50 mg). On evaluation, he had refractory bradycardia, hypotension and acute kidney injury (AKI). Eventually he developed cardiac arrest. He was revived after 5 minutes of cardio-pulmonary resuscitation (CPR). He was successfully managed with gastric lavage, fluids, inotropes, atropine, isoprenaline and subsequently with calcium gluconate infusion, high-dose insulin euglycemia therapy (HIET) and lipid emulsion therapy. Glucagon infusion was also planned but it was not available. Patient hemodynamics improved and on 8th day he got the discharge. Our case exemplifies the importance of timely and aggressive management of lethal overdose of amlodipine-atenolol poisoning.How to cite this article: Tale S, Kumar M, Ghosh S, Bhalla A. A Case of Life-threatening Amlodipine and Atenolol Overdose. Indian J Crit Care Med 2019;23(6):281–283.

Predicting effects on oxaliplatin clearance: in vitro, kinetic and clinical studies of calcium- and magnesium-mediated oxaliplatin degradation

This study evaluated the impact of calcium and magnesium on the in vitro degradation and in vivo clearance of oxaliplatin. Intact oxaliplatin and Pt(DACH)Cl2 were measured in incubation solutions by HPLC-UV. A clinical study determined changes in plasma concentrations of calcium and magnesium in cancer patients and their impact on oxaliplatin clearance. Kinetic analyses modelled oxaliplatin degradation reactions in vitro and contributions to oxaliplatin clearance in vivo. Calcium and magnesium accelerated oxaliplatin degradation to Pt(DACH)Cl2 in chloride-containing solutions in vitro. Kinetic models based on calcium and magnesium binding to a monochloro-monooxalato ring-opened anionic oxaliplatin intermediate fitted the in vitro degradation time-course data. In cancer patients, calcium and magnesium plasma concentrations varied and were increased by giving calcium gluconate and magnesium sulfate infusions, but did not alter or correlate with oxaliplatin clearance. The intrinsic in vitro clearance of oxaliplatin attributed to chloride-, calcium- and magnesium-mediated degradation predicted contributions of <2.5% to the total in vivo clearance of oxaliplatin. In conclusion, calcium and magnesium accelerate the in vitro degradation of oxaliplatin by binding to a monochloro-monooxalato ring-opened anionic intermediate. Kinetic analysis of in vitro oxaliplatin stability data can be used for in vitro prediction of potential effects on oxaliplatin clearance in vivo.

Severe ovarian hyperstimulation syndrome: Can we eliminate it through a multipronged approach?

BackgroundPrevention of severe Ovarian Hyperstimulation Syndrome (OHSS), a potentially fatal complication of controlled ovarian hyperstimulation has been the aim of all fertility experts. Various pharmacologic and non-pharmacologic interventions have been instituted but the results have been conflicting. These preventive strategies were administered in isolation or as a combination of few aiming to eliminate this iatrogenic sequel. This study aimed to eliminate severe OHSS by multipronged approach incorporating almost all preventive modalities available in patients at high risk for this dreadful complication. MethodsIt was a prospective observational study wherein 112 high risk patients planned for IVF were studied. The multipronged approach was in the form administering calcium gluconate infusion, cabergoline, albumin infusion, GnRH antagonist in luteal phase in addition to elective cryopreservation of embryos. The primary outcome measure was incidence of severe OHSS in the study group and the rate of hospitalisation. The secondary outcome measure was the number of days required for complete recovery and resolution of signs and symptoms. ResultsOut of the 112 high risk patients only one patient (1/112; 0.9%) developed severe OHSS with an overall incidence of 0.095% of severe OHSS in all the cycles. There was no biochemical or haematological derangement in any of the high risk patients. ConclusionAlthough this is the first study evaluating the multipronged approach in preventing the dreaded complication of severe OHSS, it does add to the knowledge that targeting the various pathophysiological pathways at different time frames will bring about prevention of OHSS but further randomised studies may reveal superiority of one intervention over the other.

Improvement of Fabry disease pain with calcium gluconate infusions given at time of agalsidase beta therapy

Fabry disease (FD) is a lysosomal storage disorder (LSD) that involves the cochleovestibular system. Tinnitus and progressive sensorineural hearing loss are frequent complains. A stabilization of hearing function has been reported with enzyme replacement therapy (ERT). This study aims to characterize the inner ear involvement, identify factors associated to hearing loss and evaluate the effect of ERT on the hearing function of FD patients.We reviewed the clinical records of patients with confirmed diagnosis of FD followed in a Reference Centre on LSD in the North of Portugal.We included a total of 122 patients with a mean age of 47.1 ± 17.6 years and 48.3% males. Hearing loss was reported by 26.2% of the patients and 23.0% mentioned tinnitus. Pure tone audiometry revealed sensorineural hearing loss in 36.9% of the cases. FD patients presented worse age-adjusted hearing thresholds in all analysed frequencies compared to the normal population (p = .001). Patients with hearing loss presented a significantly higher value of microalbuminuria (p = .001) and a higher frequency of acroparesthesias (p = .032). Patients presented a comparable hearing level one year after starting ERT (p = .384).In FD, hearing loss is common and age-matched hearing thresholds by frequency are worse than in the general population. Hearing loss was associated to the presence of acroparesthesias and higher values of microalbuminuria. Hearing loss stabilized in patients under ERT. A careful cochleo-vestibular evaluation should be part of the clinical assessment of FD.

Hypocalcaemia, Hypoglycaemia, Macrosomia and Congenital Cryptorchidism in a Male Offspring of a Mother with Overweight and Gestational Diabetes Mellitus

AbstractThis paper reports a case of a male infant born to a 32-year-old multiparous mother with overweight (BMI 28.5kg/m2) and gestational diabetes mellitus (GDM). The mother had fasting hyperglycaemia (range 5.7- 6.0mmol/L) noted at 24 weeks of pregnancy and was managed with diet alone. There is no family history of diabetes mellitus and the mother did not have pre-eclampsia. Physical examination of the infant revealed macrosomia (birthweight, 4600g) and bilateral congenital cryptorchidism. The baby suffered severe hypoglycaemia (blood glucose 1.7mmol/L) and hypocalcaemia (total serum calcium 1.03mmol/L), manifesting with seizures. He was successfully managed with 10% dextrose water and calcium gluconate infusion, using standard protocol. His karyotype is 46 XY. The patient was discharged from admission at the age of 10 days and was referred to the paediatric endocrinologist at the tertiary hospital. By 8 weeks of age, the right testis was noticed to have descended into the right scrotum. At the age of 3 months, the left testis was still not palpable either in the inguinal canal or the scrotal sac. The patient was lost to follow up. Conclusion: Diet-treated maternal overweight in association with GDM could potentially increase the risk for hypocalcaemia, hypoglycaemia, macrosomia and congenital cryptorchidism in the offspring, highlighting the need for physicians to assess for the presence of these morbidities in such infants.

Near-fatal cardiac arrhythmia during intravenous calcium administration for symptomatic neonatal hypocalcemia: A case report

A seven-day-old male neonate presented with symptomatic hypocalcemia in the form of generalized seizure activity for three minutes. He arrived at the pediatric emergency department in a postictal state. His clinical examination was unremarkable, but his initial laboratory evaluation revealed marked hypocalcemia and hypomagnesemia. The patient received intravenous boluses of calcium gluconate for correction. The patient had bradycardia during the first calcium gluconate infusion, and on the second infusion, he developed frequent premature ventricular contractions, which progressed into polymorphic ventricular tachycardia. Arrhythmia reverted to sinus rhythm after discontinuation of the calcium gluconate infusion without the need for chemical/electrical cardioversion. Subsequently, two extra doses of intravenous calcium gluconate for persistent hypocalcemia were administered safely. The patient was discharged home successfully in a good general condition after stabilization. The emergence of bradycardia during calcium gluconate infusion should be considered a red flag since it can trigger serious cardiac arrhythmia, especially in the presence of electrolyte abnormalities such as hypocalcemia and hypomagnesemia. We report this case to stress the need for continuous cardiac monitoring of children on calcium gluconate infusion even if proper dose, dilution, and rate of infusion are used, as serious cardiac arrhythmia can be unpredictable and may develop at any time.

SOCIETY FOR ENDOCRINOLOGY EMERGENCY ENDOCRINE GUIDANCE: Emergency management of acute hypocalcaemia in adult patients

In this addendum to the above paper, the Society for Endocrinology Clinical Committee and the original authors provide additional advice on the dose equivalence of calcium gluconate and calcium chloride. The ‘Severe hypocalcaemia’ section, which appeared in the September 2016 issue of Endocrine Connections (volume 5, page G8, https://doi.org/10.1530/EC-16-0056 reads as follows: Severe hypocalcaemia Severe hypocalcaemia: serum calcium <1.9 mmol/L and/or symptomatic at any level below reference range. This is a medical emergency Administer i.v. calcium gluconate Initially, give 10–20 mL 10% calcium gluconate in 50–100 mL of 5% dextrose i.v. over 10 min with ECG monitoring. This can be repeated until the patient is asymptomatic. It should be followed up with a calcium gluconate infusion as follows: Dilute 100 mL of 10% calcium gluconate (10 vials) in 1 L of Normal saline or 5% dextrose and infuse at 50–100 mL/h. (Calcium chloride can be used as an alternative to calcium gluconate, but it is more irritant to veins and should only be given via a central line) Titrate the rate of infusion to achieve normocalcaemia and continue until treatment of the underlying cause has taken effect The Society for Endocrinology Clinical Committee and the original authors now provide this additional advice on the dose equivalence of calcium gluconate and calcium chloride, as follows: Each 10 mL vial of 10% calcium gluconate contains 2.2 mmol of calcium. Calcium chloride for i.v. administration is available in a number of preparations including, commonly, 10 mL of 7.35% calcium chloride (which contains 5 mmol of calcium) and 5 mL of 14.7% calcium chloride (which also contains 5 mmol of calcium). Great care should be taken since other preparations are also available. If using calcium chloride in place of calcium gluconate, 4.4 mL of 7.35% calcium chloride or 2.2 mL of 14.7% calcium chloride for i.v. administration should therefore be used as equivalent to 10 mL of 10% calcium gluconate. If other calcium chloride preparations are used, the required volume should be calculated, aiming to achieve 2.2–4.4 mmol i.v. loading bolus followed by a 1.1–2.2 mmol/h maintenance infusion.

Maintenance of Serum Ionized Calcium during Exercise Attenuates the Exercise-Related Increase in Bone Resorption

Exercise is recommended to build or maintain bone mass, but there is evidence that vigorous or prolonged exercise is associated with bone loss under certain conditions. It is our contention that disruptions in calcium homeostasis during exercise lead to increases in parathyroid hormone (PTH) and bone resorption. PURPOSE: To determine if preventing the decline in serum ionized calcium (iCa) during exercise attenuates the increases in PTH and a marker of bone resorption (carboxy-terminal collagen crosslinks (CTX)). METHODS: Healthy, cycling-trained men (n=11, aged 18-45y) underwent two identical one-hour cycling bouts at ~75% VO2peak under conditions of calcium gluconate versus half-normal saline infusion. Blood was sampled every 5 minutes to adjust the calcium infusion rate, with a goal to maintain serum iCa at ~0.2 mg/dL above baseline. The same infusion protocol was replicated under the saline condition. Blood samples to assess PTH, CTX, bone formation (procollagen type 1 amino procollagen (P1NP)), and total calcium (tCa) were taken every 15 minutes during exercise and hourly for 4 hours post-exercise. RESULTS: Serum iCa was successfully maintained above baseline during Ca infusion and was significantly different from the saline condition during exercise (all time points p<0.01). Compared to saline, the Ca infusion markedly reduced the increase in serum PTH during exercise (p=0.004) and the suppression of PTH persisted throughout the 4-hour recovery period (all p<0.01). Similarly, the increase in CTX during exercise was suppressed with Ca infusion (p=0.003) and remained below the saline condition through recovery (all p<0.001). tCa was also a significantly higher during exercise (p<0.001) with Ca infusion, but values were similar during recovery (all p>0.10). There were no differences between conditions for P1NP at any time points (all p>0.10). CONCLUSIONS: The increase in bone resorption was attenuated when the exercise-related decline in serum iCa was prevented, suggesting a calcium-dependent relationship. There was no effect of Ca infusion on P1NP, but the duration of post-exercise sampling may have been too short to capture any changes. The results are limited to young, trained, men during cycling exercise. Future research should investigate sex- and age-differences and other exercise modalities.

Amlodipine overdose with hypotension and noncardiogenic pulmonary edema

Amlodipine overdose can be a life threatening situation when it is manifested as noncardiogenic pulmonary edema. Treatment remains challenging when it is complicated with refractory hypotension and pulmonary edema. Here we describe a 23 year old female with history of ingestion of 45 tabs (5mg) of amlodipine as a suicidal intent and presented within 36 hours to the hospital. High flow oxygen, IV fluids, calcium gluconate infusion and antibiotics were used for the management. After 7 days of hospital stay, patient was discharged with full recovery. Nepalese Heart Journal 2016; 13(1): 27-29

Aortic Hemostasis and Resuscitation: Preliminary Experiments Using Selective Aortic Arch Perfusion With Oxygenated Blood and Intra-aortic Calcium Coadministration in a Model of Hemorrhage-induced Traumatic Cardiac Arrest.

Selective aortic arch perfusion (SAAP) uses a thoracic aortic balloon occlusion catheter for heart and brain perfusion in cardiac arrest to achieve return of spontaneous circulation (ROSC). SAAP with oxygenated stored blood was studied in a model of hemorrhage-induced cardiac arrest. The study hypothesis was that intra-aortic calcium coadministration would be required to maintain normal aortic arch blood ionized calcium during SAAP and to achieve ROSC. Twelve anesthetized, domestic swine underwent severe hemorrhage and liver injury resulting in cardiac arrest. Whole blood and packed red blood cells (RBCs) stored in citrate anticoagulant served as perfusates for SAAP. Experiments were performed with four combinations of SAAP with oxygenated stored blood and intra-aortic calcium gluconate infusion: 1) whole blood without calcium, 2) whole blood with calcium, 3) lactated Ringers-diluted packed RBCs with calcium, and 4) normal saline-diluted packed RBCs with calcium. Aortic arch blood ionized calcium was monitored. Occurrence of ventricular dysrhythmias, success rate for ROSC, and the need for simultaneous intra-aortic calcium infusion were assessed. Selective aortic arch perfusion using whole blood without intra-aortic calcium (n = 2) resulted in severe aortic blood ionized hypocalcemia, refractory ventricular fibrillation, and no ROSC. SAAP using whole blood with intra-aortic calcium (n = 4) resulted in ROSC in all four animals. Two of four developed ventricular fibrillation that was successfully defibrillated. SAAP using packed RBCs with intra-aortic calcium resulted in ROSC in all six animals, but the intra-aortic calcium dose needed to maintain normal aortic arch blood ionized calcium levels was one-third of that needed for SAAP with whole blood. Dilution of packed RBCs with lactated Ringers (n = 2) resulted in formation of small clots in the perfusion circuit which were not seen with packed RBCs diluted with normal saline (n = 4). Selective aortic arch perfusion with stored whole blood or packed RBCs requires simultaneous intra-aortic calcium infusion to overcome citrate anticoagulant calcium binding, avoid refractory ventricular fibrillation, and allow for ROSC.

Donor gluconate rescues livers from uncontrolled donation after cardiac death

Ischemia from organ preservation or donation causes cells and tissues to swell owing to loss of energy-dependent mechanisms of control of cell volume. These volume changes cause substantial preservation injury, because preventing these changes by adding cell impermeants to preservation solutions decreases preservation injury. The objective of this study was to assess if this effect could be realized early in uncontrolled donation after cardiac death (DCD) livers by systemically loading donors with gluconate immediately after death to prevent accelerated swelling injury during the warm ischemia period before liver retrieval. Uncontrolled DCD rat livers were cold-stored in University of Wisconsin solution for 24 hours and reperfused on an isolated perfused liver (IPL) device for 2 hours or transplanted into a rat as an allograft for 7 days. Donors were pretreated with a solution of the impermeant gluconate or a saline control immediately after cardiac death. Livers were retrieved after 30 minutes. In vivo, gluconate infusion in donors immediately before or after cardiac death prevented DCD-induced increases in total tissue water, decreased vascular resistance, increased oxygen consumption and synthesis of adenosine triphosphate, increased bile production, decreased lactate dehydrogenase release, and decreased histology injury scores after reperfusion on the IPL relative to saline-treated DCD controls. In the transplant model, donor gluconate pretreatment significantly decreased both alanine aminotransferase the first day after transplantation and total bilirubin the seventh day after transplantation. Cell and tissue swelling plays a key role in preservation injury of uncontrolled DCD livers, which can be mitigated by early administration of gluconate solutions to the donor immediately after death.