• Journal of Chest Surgery
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• v.25 no.2
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• pp.188-193
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• 1992

Life-threatening cardiac arrhythmia is a frequent complication of open heart surgery. There are many causes of postoperative cardiac arrhythmias. Electrolyte imbalance such as hypokalemia and acidemia are major causes of ventricular arrhythmias. Infrequently, however, antiarrhythmic agents and /or hypomagnesemia induce[s] a ventricular arrhythmia such as "torsade de pointes" by increasing the repolarization time of myocardium, Recently, we have experienced two cases of "Torsade de pointes" associated with hyp-omagnesemia after replacement of mitral valve and one of whom after use of procainamide. Intravenous infusion of magnesium immediately and successfully abolished the torsade de pointes in both cases.intes in both cases.

• Korean Journal of Veterinary Research
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• v.49 no.4
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• pp.355-359
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• 2009

A miniature schnauzer (8 years old, male castrated), diagnosed as diabetes mellitus 6 months ahead, were referred to the Veterinary Medical Teaching Hospital of our University with hindlimb stiffness, facial rubbing and tetany. Serum chemistry showed severe hypocalcemia, hypomagnesemia, and measured iPTH (intact pharathyroid hormone) concentration was low (< 3.0 pmol/L). Consistent rate injection of calcium gluconate (282 mg/kg over 30 min) resulted in prompt relief of the tetany. Then typical treatment for hypoparathyroidism (calcium gluconate and dihydrotachysterol per os) with magnesium administration could control the neuromuscular signs. Diabetes mellitus is being controlled by insulin therapy and prescription diet. Hypomagnesemia in diabetic dog may be induced hypoparathyrodism.

• Asian-Australasian Journal of Animal Sciences
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• v.2 no.3
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• pp.275-276
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• 1989

• Journal of Korean Neurosurgical Society
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• v.66 no.3
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• pp.332-339
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• 2023

Objective : The present study aimed to investigate the clinical characteristics of electrolyte imbalance in patients with moderate to severe traumatic brain injury (TBI) who underwent craniotomy and its influence on prognosis. Methods : A total of 156 patients with moderate to severe TBI were prospectively collected from June 2019 to June 2021. All patients underwent craniotomy and intracranial pressure (ICP) monitoring. We aimed to explore the clinical characteristics of electrolyte disturbance and to analyze the influence of electrolyte disturbance on prognosis. Results : A total of 156 patients with moderate and severe TBI were included. There were 57 cases of hypernatremia, accounting for 36.538%, with the average level of 155.788±7.686 mmol/L, which occurred 2.2±0.3 days after injury. There were 25 cases of hyponatremia, accounting for 16.026%, with the average level of 131.204±3.708 mmol/L, which occurred 10.2±3.3 days after injury. There were three cases of hyperkalemia, accounting for 1.923%, with the average level of 7.140±1.297 mmol/L, which occurred 5.3±0.2 days after injury. There were 75 cases of hypokalemia, accounting for 48.077%, with the average level of 3.071±0.302 mmol/L, which occurred 1.8±0.6 days after injury. There were 105 cases of hypocalcemia, accounting for 67.308%, with the average level of 1.846±0.104 mmol/L, which occurred 1.6±0.2 days after injury. There were 17 cases of hypermagnesemia, accounting for 10.897%, with the average level of 1.213±0.426 mmol/L, which occurred 1.8±0.5 days after injury. There were 99 cases of hypomagnesemia, accounting for 63.462%, with the average level of 0.652±0.061 mmol/L, which occurred 1.3±0.4 days after injury. Univariate regression analysis revealed that age, Glasgow coma scale (GCS) score at admission, pupil changes, ICP, hypernatremia, hypocalcemia, hypernatremia combined with hypocalcemia, epilepsy, cerebral infarction, severe hypoproteinemia were statistically abnormal (p<0.05), while gender, hyponatremia, potassium, magnesium, intracranial infection, pneumonia, allogeneic blood transfusion, hypertension, diabetes, abnormal liver function, and abnormal renal function were not statistically significant (p>0.05). After adjusting gender, age, GCS, pupil changes, ICP, epilepsy, cerebral infarction, severe hypoproteinemia, multivariate logistic regression analysis revealed that hypernatremia or hypocalcemia was not statistically significant, while hypernatremia combined with hypocalcemia was statistically significant (p<0.05). Conclusion : The incidence of hypocalcemia was the highest, followed by hypomagnesemia, hypokalemia, hypernatremia, hyponatremia and hypermagnesemia. Hypocalcemia, hypomagnesemia, and hypokalemia generally occurred in the early post-TBI period, hypernatremia occurred in the peak period of ICP, and hyponatremia mostly occurred in the late period after decreased ICP. Hypernatremia combined with hypocalcemia was associated with prognosis.

• Korean Journal of Veterinary Service
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• v.13 no.2
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• pp.154-161
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• 1990

This survey was carried out to investigate the fatality of the newborn beef calves in three ranches in Cheju area. The results were summarized as follows : 1. The fatality rate was 5.8%(67 calves) from the total 1, 160 calves examined. 2. There were pneumonia(46%), enteritis(16%), suckling disorder(13%), theileriasis (4%). and hypomagnesemia(4%) in dead calves. 3. Most of dead calves(78%) with 52cases died within 30days postparturition. 4. Bacteria-induced fatal diseases in newborn calves within 30 days postparturition might be closely associated with maternal immunity by the lack of immnunoglobalin of strum.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.14 no.1
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• pp.86-90
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• 2011

Wilson's disease is an autosomal recessive disorder of copper metabolism consequence of which leads to accumulation of copper in the liver, brain, cornea and other tissues. The manifestations are more likely to be hepatic in the early childhood and neurological in the adolescents. In addition, the abnormalities that develop during disease progression may result in other manifestations such as hematologic, endocrine, or renal findings. We report a thirteen year-old girl who manifested tetany shortly after the initial diagnosis of Wilson's disease. Despite aggressive calcium, magnesium and vitamin D replacement, the hypocalcemia and hypomagnesemia did not respond to the therapy promptly. It took more than three weeks for blood levels of the minerals to be normal. We concluded that tetany occurred in our patient because of hypoparathyroidism as a rare complication of Wilson disease, vitamin D deficiency resulting from various conditions, and inconclusive hypomagnesemia.

• Childhood Kidney Diseases
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• v.16 no.2
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• pp.121-125
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• 2012

Gitelman syndrome is an autosomal recessive renal tubular disorder characterized by hypokalemic metabolic alkalosis, and it is distinguished from Batter syndrome by hypomagnesemia and hypocalciuria. This disorder is caused by mutation in SLC12A3 gene which encodes thiazide-sensitive $Na^+-Cl^-$cotransporter (NCCT) which is expressed in the apical membrane of cells, lining distal convoluted tubule. A 8-year old boy who presented with Rolandic epilepsy, and horseshoe kidney accidentally showed clinical features of metabolic alkalosis, hypokalemia, hypocalciuria without hypomagnesemia. So we identified a heterozygote mutation and an abnormal splicing in the SLC12A3 gene, encoding NCCT. The mutation was detected in the exon 15 and 22 of SLC12A3 gene.

• Clinical and Experimental Pediatrics
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• v.57 no.1
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• pp.1-18
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• 2014

Channelopathies are a heterogeneous group of disorders resulting from the dysfunction of ion channels located in the membranes of all cells and many cellular organelles. These include diseases of the nervous system (e.g., generalized epilepsy with febrile seizures plus, familial hemiplegic migraine, episodic ataxia, and hyperkalemic and hypokalemic periodic paralysis), the cardiovascular system (e.g., long QT syndrome, short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia), the respiratory system (e.g., cystic fibrosis), the endocrine system (e.g., neonatal diabetes mellitus, familial hyperinsulinemic hypoglycemia, thyrotoxic hypokalemic periodic paralysis, and familial hyperaldosteronism), the urinary system (e.g., Bartter syndrome, nephrogenic diabetes insipidus, autosomal-dominant polycystic kidney disease, and hypomagnesemia with secondary hypocalcemia), and the immune system (e.g., myasthenia gravis, neuromyelitis optica, Isaac syndrome, and anti-NMDA [N-methyl-D-aspartate] receptor encephalitis). The field of channelopathies is expanding rapidly, as is the utility of molecular-genetic and electrophysiological studies. This review provides a brief overview and update of channelopathies, with a focus on recent advances in the pathophysiological mechanisms that may help clinicians better understand, diagnose, and develop treatments for these diseases.

• Journal of Chest Surgery
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• v.33 no.1
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• pp.51-59
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• 2000

Background: Magnesium is one of the important intracellular cations. Hypomagnesemia is common after an open heart surgeryand may affect the development of posoperative arrhythmias. The aims of this study were to identify 1) the severity of the hypomagnesemia 2) the adequate dose of the magnesium replacement and 3) the effect of magnesium replacement on the postoperative arrhythmias. Material and Method: The serum magnesium level was measured in 20 patients in whom magnesium was replaced postopertively(6gm at the operative day 4gm at the 1st postoperative day and 2gm at the 2nd postoperative day) and compared with that of the 13 patients in whom magnesium was not replaced postopertively The serum magnesium level was normalized after magnesium replacement. We analyzed the development of arrhythmias in the patients groups who did not receive magnesium and were operated on between Oct. 1994 and Oct. 1995(Group I; n=206) and who received the magnesium postoperatively and were operated on between Nov. 1995 and Aug. 1996(Group II; n=133) Result: There were no differences in the preoperative risk factors and the rate of postoperative supraventricular or ventricular tachyarrhythmia occur-rences irrespectivel of the magnesium replacement. Magnesium replacement could prevent the aggrevation of the occurrence of postoperative arrhythmias in high risk groups of ventricular tachyarrhytnmia in old age but magnesium could not prevent postoperative arrhythmia in other high risk groups. Conclusion: The magnesium replacement after open heart surgery could prevent the development of ventricular tachyarrhythmias especially in old age groups but could not prevent atrial tachyarrhthmias.

• Childhood Kidney Diseases
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• v.8 no.1
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• pp.68-73
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• 2004

Both Gitelman syndrome and Bartter syndrome are autosomal recessively inherited renal tubular disorders characterized by hypokalemic metabolic alkalosis, salt wasting and normal to low blood pressure. Gitelman syndrome is caused by mutations in the thiazide-sensitive Na-Cl cotransporter (NCCT) and distinguished from Bartter syndrome, which is associated with mutations of several genes, by the presence of hypomagnesemia and hypocalciuria. In most of the patients with Gitelman syndrome, the disease manifests with transient episodes of muscular weakness and tetany in the adult period, but, often, is asymptomatic. We report here an 11 years-old female with Gitelman syndrome who presented with aggravation of epileptic seizure. The diagnostic work-up showed typical clinical features of metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. We also identified a heterozygote mutation($^{642}$CGC(Arg)>TGC(Cys)) and an abnormal splicing in the SLC12A3 gene encoding NCCT.