Magnesium Disorders Research Articles

Predictors of Nonelective Removal of Peripherally Inserted Central Catheters in Infants.

Nonelective removal of peripherally inserted central catheters (PICCs) due to complications continues to be a major concern in neonatal intensive care units (NICUs) around the world. Nonelective removal results in interruption of intravenous therapy, added costs, stress, and negative impacts on infant's health. Identification of predictors of complications that lead to nonelective removal of PICCs would allow for the initiation of preventive strategies to improve the quality of care. To identify predictors of nonelective removal of PICCs in neonates. A prospective cohort study with a sample of 524 PICC lines inserted in 436 neonates admitted to a tertiary-level NICU of a Brazilian hospital. Data were collected on all neonates between August 31, 2010, and August 30, 2012. Neonates were monitored daily from insertion of the catheter until its removal. Bivariate analysis and a logistic regression were conducted in order to identify predictors of nonelective removal. A diagnosis of a transitory metabolic disorder (hypoglycemia; disorders of calcium, magnesium, sodium, or potassium; or dehydration), previous PICC line insertion, insertion of dual-lumen polyurethane PICC, noncentral tip position, and multiple intravenous solutions in a single-lumen silicone PICC were predictors of nonelective removal of PICC lines. The avoidance of repeated PICC insertions, noncentral tip position, and placement of single-lumen silicone PICCs for administration of four or more intravenous solutions is suggested. Interventions should be explored that facilitate PICC insertion success and correct tip placement.

Prevalence and clinical impact of magnesium disorders in end-stage renal disease: a protocol for a systematic review.

BackgroundMagnesium plays a key role in maintaining internal homeostasis through actions in the musculoskeletal, nervous, endocrine and cellular messenger systems. Renal excretion is the major route of magnesium elimination from the body. A positive magnesium balance would be expected in renal failure. However, a compensatory decrease in tubular reabsorption is expected to operate to maintain adequate urinary magnesium excretion even when glomerular filtration rate is very low.Patients with end-stage renal disease and those on dialysis have impaired regulatory mechanisms, predisposing them to disturbances in magnesium levels. The effects of high or low magnesium can have deleterious health outcomes, which impact on the co-morbidities and outcomes of chronic renal disease. This systematic review aims to determine the prevalence and clinical outcomes of magnesium disorders in end-stage renal disease.Methods/DesignWe will undertake a comprehensive search of various databases, MEDLINE, PubMED, EMBASE, Cochrane Library, Cochrane Collaboration, CIHNAL (Ebsco), Web of Science and Google Scholar, for observational studies and clinical trials on magnesium disorders in end-stage renal disease using key terms to identify papers for inclusion. Paper selection and data extraction (where appropriate) will be performed in duplicate on socio-demographic characteristics of participants, diagnosis of end-stage renal disease, magnesium levels, prevalence and clinical outcomes. An assessment of quality will be performed using a modified Newcastle-Ottawa Scale (NOS), including identification of any bias, which may influence findings. Data will be pooled together according to whether the studies were on pre-dialysis, hemodialysis or peritoneal dialysis participants. References from individual papers will also be screened as appropriate. Paper organisation and data extraction and analysis will take place using Microsoft Excel® and Stata version 13®.DiscussionThis systematic review will represent a significant effort at pooling together information on prevalence and outcomes of magnesium disturbances amongst end-stage renal disease patients, which may guide further research and management of the disorders.Systematic review registrationPROSPERO: CRD42014014354Electronic supplementary materialThe online version of this article (doi:10.1186/s13643-015-0063-x) contains supplementary material, which is available to authorized users.

Protocolo de tratamiento de las alteraciones iónicas urgentes

The electrolyte disturbances has considerable prevalence in the general population and, even more important, in the hospital environment. Added to all of this it's an important cause of morbidity, increased hospital stay and sometimes even death. So it is essential a quick assessment of electrolyte status and establish early treatment. The electrolyte disorders in hospitalized patients often result from a wide variety of causes and limiting compensation mechanisms that are present in healthy individuals. This protocol will review the emergency treatment of the most frequent electrolyte disturbances, and those with greater clinical relevance, such as hyponatremia, present in up to 20% of critically ill patients, hypernatremia that associates an increased mortality, disorders of potassium, magnesium or calcium and phosphorus.

Magnesium physiology and clinical therapy in veterinary critical care.

To review magnesium physiology including absorption, excretion, and function within the body, causes of magnesium abnormalities, and the current applications of magnesium monitoring and therapy in people and animals. Magnesium plays a pivotal role in energy production and specific functions in every cell in the body. Disorders of magnesium can be correlated with severity of disease, length of hospital stay, and recovery of the septic patient. Hypermagnesemia is seen infrequently in people and animals with significant consequences reported. Hypomagnesemia is more common in critically ill people and animals, and can be associated with platelet, immune system, neurological, and cardiovascular dysfunction as well as alterations in insulin responsiveness and electrolyte imbalance. Measurement of serum ionized magnesium in critically or chronically ill veterinary patients is practical and provides information necessary for stabilization and treatment. Tissue magnesium concentrations may be assessed using nuclear magnetic resonance spectroscopy as well as through the application of fluorescent dye techniques. Magnesium infusions may play a therapeutic role in reperfusion injury, myocardial ischemia, cerebral infarcts, systemic inflammatory response syndromes, tetanus, digitalis toxicity, bronchospasms, hypercoagulable states, and as an adjunct to specific anesthetic or analgesic protocols. Further veterinary studies are needed to establish the frequency and importance of magnesium disorders in animals and the potential benefit of magnesium infusions as a therapeutic adjunct to specific diseases. The prognosis for most patients with magnesium disorders is variable and largely dependent on the underlying cause of the disorder.

Magnesium and the Acute Physician

Magnesium deficiency, and to a lesser extent magnesium excess, is commonly encountered in patients admitted to the Acute Medical Unit. It is important that acute physicians are able to identify those at risk of these states and initiate appropriate investigation and treatment. This article aims to provide the reader with a sound understanding of magnesium physiology and its effect at a cellular level. The causes, symptoms and treatment of magnesium disorders are discussed along with a review of evidence regarding the therapeutic use of magnesium.

Volatile Anesthetics Reduce Biochemical Markers of Brain Injury and Brain Magnesium Disorders in Patients Undergoing Coronary Artery Bypass Graft Surgery

Neuropsychological disorders are some of the most common complications of coronary artery bypass graft (CABG) surgery. The early diagnosis of postoperative brain damage is difficult and mainly based on the observation of specific brain injury markers. The aim of this study was to analyze the effects of volatile anesthesia (VA) on plasma total and ionized arteriovenous magnesium concentrations in the brain circulation (a-vtMg and a-viMg), plasma matrix metalloproteinase-9 (MMP-9), and glial fibrillary acidic protein (GFAP) in adult patients undergoing CABG surgery. An observational study. The Department of Cardiac Surgery in a Medical University Hospital. Studied parameters were measured during surgery and in the early postoperative period. Patients were assigned to 3 groups: group O, patients who did not receive VA; group ISO, patients who received isoflurane; and group SEV, patients who received sevoflurane. Ninety-two patients were examined. CABG surgery increased MMP-9 and GFAP. The highest MMP-9, GFAP, and the most dramatic disorders in a-vtMg and a-viMg were noted in group O. Cardiac surgery increased plasma MMP-9 and GFAP concentrations. Changes in MMP-9, GFAP, and arteriovenous tMg and iMg were significantly higher in group O. Volatile anesthetics, such as ISO or SEV, reduced plasma MMP-9, GFAP concentrations, and disturbances in a-vtMg and a-viMg.

Electrolyte and metabolic disturbances in the critically ill

Electrolyte and metabolic disturbances are common in the critically ill patient. Hyponatraemia in the most frequent abnormality and is often caused by SIADH. Sodium should be corrected at a rate of < 10 mmol/day. Hypernatraemia is caused by a loss of free water, including diabetes insipidus after head injury. Treatment is replacement of water and DDAVP in DI. Disorders of potassium cause cardiac arrhythmias, including cardiac arrest. In severe hypokalaemia IV, KCl may be given at a max rate of 40 mmol/hour. Treatment of hyperkalaemia includes calcium chloride, then redistributing and ultimately removing potassium. Disorders of magnesium cause cardiac arrhythmias, muscle weakness and fits. Calcium is required by excitatory processes such as neuromuscular conduction and contraction. Hypercalcaemia is treated by rehydration with normal saline then excretion with bisphosphonates. Phosphate is an intracellular cation essential for cellular processes. Hyperphosphataemia may need treatment with haemofiltration as it is usually caused by renal failure. Metabolic disturbances include disorders of (1) hypothalamic-pituitary-adrenal axis, the most important being acute adrenal insufficiency. Treatment is replacement steroids; (2) thyroid emergencies, including thyroid storm, which if not recognized and treated has a high mortality, and myxoedema coma treated with replacement thyroid hormones; (3) diabetic emergencies, including DKA and HONK. DKA arises due to an absolute insulin deficiency causing hyperglycaemia and ketogenesis. This leads to dehydration, hypovolaemia and a metabolic acidosis due to impaired tissue perfusion. HONK is associated with profound hyperglycaemia, dehydration without ketosis. It develops more insidiously in an older age group and has a higher mortality.

Tight junction biology and kidney dysfunction

The epithelial tight junction (TJ) has three major functions. As a "gate," it serves as a regulatory barrier separating and maintaining biological fluid compartments of different composition. As a "fence," it generates and maintains the apicobasal polarity of cells that form the confluent epithelium. Finally, the TJ proteins form a trafficking and signaling platform that regulates cell growth, proliferation, differentiation, and dedifferentiation. Six examples are selected that illustrate the emerging link between TJ dysfunction and kidney disease. First, the glomerular slit diaphragm (GSD) is evolved, in part, from the TJ and, on maturation, exhibits all three functions of the TJ. GSD dysfunction leads to proteinuria and, in some instances, podocyte dedifferentiation and proliferation. Second, accumulating evidence supports epithelial-mesenchymal transformation (EMT) as a major player in renal fibrosis, the final common pathway that leads to end-stage renal failure. EMT is characterized by a loss of cell-cell contact and apicobasal polarity, which are hallmarks of TJ dysfunction. Third, in autosomal dominant polycystic kidney disease, mutations of the polycystins may disrupt their known interactions with the apical junction complex, of which the TJ is a major component. This can lead to disturbances in epithelial polarity regulation with consequent abnormal tubulogenesis and cyst formation. Fourth, evidence for epithelial barrier and polarity dysregulation in the pathogenesis of ischemic acute renal failure will be summarized. Fifth, the association between mutations of paracellin-1, the first TJ channel identified, and clinical disorders of magnesium and calcium wasting and bovine renal fibrosis will be used to highlight an integral TJ protein that can serve multiple TJ functions. Finally, the role of WNK4 protein kinase in shunting chloride across the TJ of the distal nephron will be addressed.

European Resuscitation Council Guidelines for Resuscitation 2005: Section 7. Cardiac arrest in special circumstances

Electrolyte abnormalities can cause cardiac arrhythmias or cardiopulmonary arrest. Life-threatening arrhythmias are associated commonly with potassium disorders, particularly hyperkalaemia, and less commonly with disorders of serum calcium and magnesium. In some cases therapy for life-threatening electrolyte disorders should start before the laboratory results become available.

Hyponatremia and Heart Failure—Pathophysiology and Implications

Fluid and electrolyte disturbances are a common feature of heart failure. Among the electrolyte disturbances that occur in heart failure, disorders of potassium and magnesium have traditionally received the most attention. Abnormalities involving either of these actions serve as risk factors for sudden cardiac death/arrhythmias. More recently, a growing appreciation has emerged for the importance of hyponatremia in the heart failure patient. Hyponatremia is multifactorial in origin, and its presence correlates with disease severity and outcome. There are few effective therapies for hyponatremia, and those that are available are not viewed as offering specific survival benefits per se. The recent availability of vasopressin receptor antagonists, however, offers a different approach to the management of this complex electrolyte disturbance, but one that is still evolving as to the scope of its clinical benefits.

Do intracellular, extracellular or urinary magnesium concentrations predict renal retention of magnesium in critically ill patients?

Magnesium disorders are common in hospitalized patients. In patients with low or normal magnesium, the intravenous magnesium loading test has been demonstrated to be a sensitive test to assess magnesium deficiency in critically ill patients. However, it is more time consuming and more difficult than the measurement of intracellular or extracellular magnesium concentrations. This study evaluated whether erythrocyte, plasma and urinary magnesium concentrations predict renal magnesium retention measured by th magnesium loading test. One-hundred-and-three intensive care patients (36 females, 67 males) in a tertiary care centre and 41 healthy subjects (13 females, 28 males) took part in this prospective study. Intracellular, total plasma, ionize extracellular and urinary magnesium concentrations were measured and also magnesium retention by intravenous magnesium loading test. Total plasma magnesium concentration was poorly correlated with magnesium retention (r = 0.36 r2 = 0.13) and was the only parameter that significantly predicted magnesium retention in intensive care patients (P < 0.01). However, only 10% of the magnesium retention data were linked to the total plasma magnesium concentration. Total plasma magnesium concentration predicts magnesium retention in critically ill intensive care patients but not intracellular and urinary magnesium concentrations. Only a small proportion of the magnesium retention was due to the total plasma magnesium concentration.

Disorders of calcium, phosphorus, and magnesium

Disorders of calcium, phosphorus, and magnesium

Magnesium and Affective Disorders

There are several findings on the action of magnesium ions supporting their possible therapeutic potential in affective disorders. Examinations of the sleep-electroencephalogram (EEG) and of endocrine systems point to the involvement of the limbic-hypothalamus-pituitary-adrenocortical axis as magnesium affects all elements of this system. Magnesium has the property to suppress hippocampal kindling, to reduce the release of adrenocorticotrophic hormone (ACTH) and to affect adrenocortical sensitivity to ACTH. The role of magnesium in the central nervous system could be mediated via the N-methyl-d-aspartate-antagonistic, γ-aminobutyric acidA-agonistic or a angiotensin II-antagonistic property of this ion. A direct impact of magnesium on the function of the transport protein p-glycoprotein at the level of the blood-brain barrier has also been demonstrated, possibly influencing the access of corticosteroids to the brain. Furthermore, magnesium dampens the calciumion-proteinkinase C related neurotransmission and stimulates the Na-K-ATPase. All these systems have been reported to be involved in the pathophysiology of depression. Despite the antagonism of lithium to magnesium in some cell-based experimental systems, similarities exist on the functional level, i.e. with respect to kindling, sleep-EEG and endocrine effects. Controlled clinical trials examining the effect of Mg in affective disorder are warranted.

Disorders of Serum Potassium, Sodium, Magnesium and Chloride

SummaryFluid and electrolyte imbalances are frequently encountered in a variety of medical and surgical disorders therefore requiring the clinician's astute evaluation of his/her patient's fluid and electrolyte status. Disorders involving the gastrointestinal tract, kidneys, and endocrine organs will frequently cause abnormalities in sodium, potassium, magnesium, and chloride balance. An accurate initial assessment of serum electrolyte concentrations and monitoring during the treatment is essential in order to maintain electrolyte homeostasis. Failure to do so can lead to severe clinical consequences for the patient and change a diagnostic triumph into a therapeutic failure. This presentation provides an overview of the etiologies, clinical signs, and therapeutic approaches to electrolyte disorders in the critically ill animal. (Vet. Emerg. &amp; Crit. Care, 9:209–217, 1999)

Fluid and electrolyte disorders

OBJECTIVE: To review the major concepts involving electrolyte disorders in pediatrics, with special emphasis on the diagnosis and treatment.METHOD: Systematic literature review, searching through classic pediatric textbooks, periodic electronic databases, such as Medline, Lilacs and other sources. RESULTS: Electrolyte disorders are among the most common events in pediatric medical practice, specially in emergency care, where, depending upon the magnitude, they may represent significant risk to patient life or to the development of permanent sequelae. Dehydration, independent of etiology, has its importance defined by the severity of water deficit (mild, moderate or severe) and by the proportion of sodium waste in relation to water deficit (isotonic, hypotonic and hypertonic), and should be correctly recognized to guide adequate treatment. Sodium disorders have major risks of central nervous system compromise and potassium disorders are specially linked to cardiac arrhythmia, always deserving special attention and care. On the other hand, calcium, phosphorus and magnesium disorders are more related to neuromuscular function alterations and, although less threatening, they need adequate recognition and management.CONCLUSION: Knowledge of the several mechanisms involved in water and electrolyte metabolism is crucial to the correct comprehension, diagnosis and management of fluid and electrolyte disorders in pediatrics.

Magnesium disorders and cardiovascular diseases.

AbstractThe evidence linking magnesium disorders with the pathogenesis and treatment of various cardiovascular diseases will be reviewed.

Disorders of calcium, phosphorus, and magnesium

Assistant Professor of Medicine University of Missouri-Kansas City School of Medicine Kansas City, Missouri

Gene mapping of mineral metabolic disorders.

Recent advances in the techniques of molecular biology and cytogenetics have enabled the localization of several mutant genes which result in disorders of phosphate, calcium, magnesium and water homeostasis. Thus, the genes causing X-linked hypophosphataemic rickets, Lowe's syndrome, Di George syndrome, X-linked recessive hypoparathyroidism, multiple endocrine neoplasia Type I, primary hypomagnesaemia and X-linked nephrogenic diabetes insipidus have been mapped. The molecular and genetic studies which localized these disease genes are described and the implications of this gene mapping in genetic counselling and in further elucidation of the mineral metabolic defects are discussed.