DOCSLIB.ORG

HYPERCALCEMIA in CHILDREN Smaranda Diaconescu, Nicoleta Gimiga, Claudia Olaru*, Marin Burlea “Grigore T

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
HYPERCALCEMIA in CHILDREN Smaranda Diaconescu, Nicoleta Gimiga, Claudia Olaru*, Marin Burlea “Grigore T RomanianJournalofOralRehabilitation Vol.6,No.3,JulyͲSeptember2014 HYPERCALCEMIA IN CHILDREN Smaranda Diaconescu, Nicoleta Gimiga, Claudia Olaru*, Marin Burlea “Grigore T. Popa" University of Medicine and Pharmacy - Ia܈i, Romania, Faculty of Medicine, Vth Pediatric Clinic, "Sf. Maria" Children's Hospital *Corresponding author: Claudia Olaru, MD, PhD Student “Grigore T. Popa" University of Medicine and Pharmacy - Ia܈i, Romania; e-mail: [email protected] ABSTRACT Hypercalcemia is less common in children than in adults, but is more likely to be clinically significant in younger patients as routine biochemical screening tests are rarely performed in children. The serum calcium levels are maintained through the interplay of parathyroid, renal, and skeletal factors. The most common causes of hypercalcemia are primary (hyperparathyroidism or cancer) but a variety of unusual etiologies must be considered in children. The initial approach to the medical treatment of severe or symptomatic hypercalcemia is to increase the urinary excretion of calcium. In most cases, hypercalcemia is due osteoclastic bone resorption, and the effective treatment is based on agents that inhibit or destroy osteoclasts . Parathyroid surgery is recommended for all children with primary hyperparathyroidism. Keywords: hypercalcemia, pediatrics, parathyroid Hypercalcemia is not a common pediatric regulatory hormones [2]. The three problem; the actual incidence in children is predominant sources of calcium and targets unknown, although it is less common than in for regulation are the bones, renal filtration adults. In adults, hypercalcemia is the primary and reabsorption, and intestinal absorption. malignancy-associated endocrine/electrolyte The major regulators of calcium levels are disorder; it is present in 5% of all parathyroid hormone (PTH) and vitamin D, malignancies, or in 15 per 100,000 total which target the bones, intestine, and kidney patients [1]. The normal values of blood to increase serum calcium. Calcitonin, a more calcium in children varies from 8.5 to 10.3 minor player in regulation, decreases serum mg%. Hypercalcemia is considered, calcium by its effects on bone and kidney. depending on age, at the following values: premature -> 9 mg%, term newborn -> 10, 4 Etiology mg%, child / adolescent -> 10.4 mg% . Most Hypercalcemia is caused by either primary of the body calcium (98% is in the skeleton hyperparathyroidism or cancer in over 90% of and only 2% is in circulation; half of this one cases. The rest of the etiologies are numerous. is free calcium (ionized) Ca++, (2)Primary hyperparathyroidism is a physiologically active. 1% is fastened to the pathologic and unregulated excess of PTH rest of the serum proteins. Calcium leading to elevated calcium. Malignancy is absorption and regulation involve a complex the most common cause of hypercalcemia interplay between multiple organ systems and that leads to inpatient care. Other less 91 RomanianJournalofOralRehabilitation Vol.6,No.3,JulyͲSeptember2014 frequent etiologies are bone diseases, determining the etiology may be more granulomatous conditions, and diet. In the important than the electrolyte imbalance case of malignancy or granulomatous disease, itself. Table 1. Calcium physiology Hormone Efect Bone Gut Kidney Ca reabsorbtion PTH K Ca L Po4 K Osteoclasts Indirect / Vit. D Po4 excretion K Ca K Po4 Vitamin D3 K Ca K Po4 Indirect action Indirect action absorbtion Inhibate Calcitonin L Ca L Po4 Indirect action Ca and Po4 excretion osteoclasts Hyperparathyroidism: rare instances a parathyroid carcinoma may Primary hyperparathyroidism ranges in account for the condition. severity from very mild and asymptomatic, to Less common etiologies: severe disease complicated by the Vitamin D is a fat-soluble vitamin that consequences of bone loss, including can become toxic when excessive amounts fractures and osteitis fibrosa cystica (von are taken in over time. Self-dosing or is the Recklinghausen disease). Tertiary usual cause. Overdosing with 1,alpha- hyperparathyroidism occurs in chronic renal hydroxylated vitamin D metabolites failure. (alfacalcidol or calcitriol) can easily result in Malignancy: hypercalcemia and chronic administration Hypercalcemia may be associated with must be avoided or carefully monitored. malignancies in two ways: bony involvement Exaggerated supplementation with over-the- by the tumor may lead to massive osteoclastic counter products can also readily and activity (osteolytic lesions) when the calcium frequently lead to hypercalcemia. Vitamin D flux simply overwhelms homeostatic is also elevated in granulomatous disease mechanisms; a variety of tumors release such as sarcoidosis, berylliosis, tuberculosis. PTH-related peptide acting on PTH receptors The mechanism is enhanced conversion of [3]. From 25% to 30% of patients with cancer vitamin D by macrophages. Endocrine will develop hypercalcemia at some point diseases such as hyperthyroidism can lead to over the course of their disease. Common hypercalcemia and almost always malignancies that can lead to hypercalcemia hypercalciuria as a consequence of rapid bone include: multiple myeloma, leukemia, lung turnover; another pathologic conditions are and breast cancer. When malignancies cause adrenal insufficiency, pheochromocytoma, hypercalcemia, the tumor is typically very acromegaly. Iatrogenic causes includes advanced. Malignancies which produce milk-alkali syndrome caused by excess hypercalcemia may be associated with dietary milk or alkali (e.g., because of multiple endocrine neoplasia (MEN) type 1 dyspepsia) or excess calcium supplementation and MEN type 2a or isolated familial (e.g., in postmenopausal women) [4]. Other hyperparathyroidism. There is an association drugs are lithium and vitamin A derivates, of primary hyperparathyroidism with used for acne treatment and thiazides that neurofibromatosis and von Hippel-Landau. In affect renal mechanisms and rapid bone 92 RomanianJournalofOralRehabilitation Vol.6,No.3,JulyͲSeptember2014 turnover, thus both causing hypercalcemia transient hypercalcaemia. that reverses when the drugs are stopped. Immobilization in adolescents and young Clinical presentation people (Paget disease) causes massive bone First, the clinician should take a history demineralization and hypercalcemia. Older detailing any bone pain to suggest patients can also be subject to this problem, malignancy in metastatic locations of the long but the robust state of bone mineralization in bones. A history of weight loss would young people means there is a much larger identify malignancy more likely than mobile calcium pool to create and sustain the hyperparathyroidism. History may also hypercalcemia. Excess bone metabolism of identify symptoms of high calcium such as any etiology can lead to hypercalcemia. renal stones (typical of hyperparathyroidism, Congenital causes: familial hypocalciuric lethargy), easy fatigue, confusion, depression, hypercalcemia can be confused with irritability, constipation, and hypercalcemia due to hyperparathyroidism as polyuria/polydipsia. Classic GI symptoms abnormal calcium sensing in the parathyroid may also be present (nausea, vomiting, glands and kidneys leads to mild elevation of abdominal pain, peptic ulcer, pancreatitis). PTH and reduced calcium excretion. Chronic symptoms are more consistent with Williams syndrome - is a rare hyperparathyroidism, whereas more recent neurodevelopmental disorder characterized onset of symptoms suggests malignancy. by a distinctive, "elfin" facial appearance, Symptoms from calcium elevation are along with a low nasal bridge, an unusually typically not found unless the calcium is cheerful demeanor and ease with strangers; above 12 mg/deciliter. Severe symptoms and developmental delay coupled with strong coma are likely to appear when calcium gets language skills and cardiovascular problems, above 13 mg/deciliter [5, 6]. such as supravalvular aortic stenosis and Table 2. Clinical signs of Hypercalcemia Renal symptoms Nervous system Cardiac symptoms GI system Musculoskeletal system Renal stones CNS depressyon QT shortening Gastritis Arthralgia Polyuria Decreased reflexes Sinus tahycardia Pancreatitis Bone pain Nycturia Ventricular Constipation Spontaneous fractures Hematuria extrasystoles Anorexia Laboratory data plasma total calcium should be 8.5 to 10.5 The most common causes of mg/dl and the ionized calcium should be 4.6 hypercalcemia are primary to 5.1 mg/dl. The PTH is elevated in primary hyperparathyroidism and malignancy, hyperparathyroidism, despite elevated together accounting for 90% of cases. They calcium indicating a disconnect between the can be distinguished by ordering a serum regulating hormone and the ion regulated. In PTH level and a simultaneous repeat calcium malignancy, calcium is elevated either due to test. Total serum calcium is usually a humoral abnormality with a PTH-related satisfactory but if there is an elevated or peptide or due to bone destruction in markedly depressed plasma protein metastases. In cases of malignancy, the PTH concentration, the physiologically important might even be very low or barely detectable fraction is ionized calcium. Normal serum or since the elevated calcium should inhibit PTH 93 RomanianJournalofOralRehabilitation Vol.6,No.3,JulyͲSeptember2014 secretion. Hypercalcemia Medication IͲPTH PTHrP IͲPTH PTHrP High/N Low Low High Low/N Low/N Primary Vit.D PTHrP Urinary 1,25 Endocrinolog hyperparathyroid intoxication, calcium24h dihydroxyvita ical ism Malignancy, MilkͲalkali minD Figure 1.
Load more

Recommended publications
  • CARE PLAN Electrolyte and Fluid Imbalance
    CARE PLAN Electrolyte and Fluid Imbalance . Related to: Check all that apply Endocrine dysfunction Treatment/Drug side effects Urinary difficulties Nutritional deficiency Tissue trauma Renal dysfunction Post-op complications Trauma Other _____________ Status: Achieved/ Progressing/Not Date/Select Outcome Select Interventions Met (comment for negative variances) Serum electrolytes, Perform initial/routine BUN, blood gases will assessments, assess be within desired limits for neurological manifestations indicating electrolyte imbalance. Report findings to clinician (MD, PA, NP) promptly. Implement therapeutic actions (i.e., appropriate diet, administer replacement electrolytes—sodium bicarb, mag sulfate, etc., as ordered) Assess/monitor serum levels of electrolytes; report finding to MD promptly Monitor for associated complications Absence of cardiac Assess/monitor cardiac dysrhythmias rhythm Published by Cinahl Information Systems, a division of EBSCO Information Services. Copyright©2016, Cinahl Information Systems. All rights reserved. No part of this may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the publisher. Cinahl Information Systems accepts no liability for advice or information given herein or errors/omissions in the text. It is merely intended as a general informational overview of the subject for the healthcare professional. Cinahl Information Systems, 1509 Wilson Terrace,
    [Show full text]
  • Electrolyte Imbalance in Children with Severe Acute Malnutrition at a Tertiary Care Hospital in Pakistan: a Cross-Sectional Study
    Open Access Original Article DOI: 10.7759/cureus.10541 Electrolyte Imbalance in Children With Severe Acute Malnutrition at a Tertiary Care Hospital in Pakistan: A Cross-Sectional Study Mohammad Raza 1, 2 , Sohail Kumar 3 , Muzamil Ejaz 2 , Dua Azim 3 , Saad Azizullah 2 , Azhar Hussain 4, 5 1. Pediatrics, The Indus Hospital, Karachi, PAK 2. Pediatrics, Dow Medical College, Dr. Ruth K. M. Pfau Civil Hospital, Karachi, PAK 3. Internal Medicine, Dow Medical College, Dr. Ruth K. M. Pfau Civil Hospital, Karachi, PAK 4. Healthcare Administration, Franklin University, Columbus, USA 5. Medicine, Xavier University School of Medicine, Oranjestad, ABW Corresponding author: Mohammad Raza, [email protected] Abstract Background Malnutrition is a significant public health concern and a leading contributor to the global burden of children’s diseases, affecting 50 to 150 million children under the age of five years worldwide. Globally, undernutrition accounts for approximately 33% of the deaths among under-fives. South Asia alone contributes to 50% and 38.8% of the world’s population of wasted and stunted children, respectively. In Pakistan, malnutrition is the leading cause of childhood mortality, accounting for nearly 35% of all deaths under five years of age. Severe acute malnutrition (SAM), the most severe form of malnutrition, is often associated with electrolyte imbalances. This study aimed to determine the frequency of electrolyte imbalance in children with SAM admitted at a tertiary care hospital. Methods This cross-sectional study includes 184 patients with SAM aged between 6 and 60 months, who were admitted at the inpatient Department of Pediatrics, Dr. Ruth K.
    [Show full text]
  • Electrolyte Imb-Hypercalcemia
    HYPERCALCEMIA (Last updated 01/10/2020; Last reviewed 03/11/2017; Reviewers: Rudy Tedja, DO, Bibek Karki, MBBS) PRESENTING COMPLAINT: Weakness, fatigue, constipation, depression FINDINGS A Check airway B ↓/N RR C ↑/N BP, ↓HR D Variable altered (V,P,U,D)* E Profound muscle weakness, bone pain LPC ↑Ca, ↑/↓/N PTH, ↑/↓/N P UPC Renal stone *V (verbal), P (pain), U (unconsciousness), D (delirious) UPC (point of care ultrasound) LPC (point of care labs) OTHER HISTORY Signs and symptoms Neurological: Lethargy, confusion, stupor, coma Cardiac: Shortened QT interval, supraventricular, ventricular arrhythmias, bradycardia Renal: Polyuria, nephrolithiasis, nephrogenic diabetes insipidus, renal insufficiency, renal tubular acidosis MSK: Bone pain GI: Nausea/vomiting, abdominal pain, pancreatitis Predisposing Conditions: Elderly are predisposed to neuropsychiatric symptoms and known history of malignancy DIFFERENTIAL DIAGNOSIS Other causes of drug induced or metabolic encephalopathy/coma, delirium, intracranial pathology OTHER INVESTIGATIONS Lab: Creatinine Severity: Mild: Calcium < 12 mg/dL; moderate: Calcium 12-14 mg/dL; severe: Calcium >14 mg/dL Monitoring: Calcium level every 8 hours THERAPEUTIC INTERVENTIONS Initial therapy 1 o Stop any offending agents, such as thiazides, lithium, exogenous calcium, vitamin A supplementation, vitamin D supplementation o Intravascular volume repletion with isotonic saline at initial rate of 200-300 ml/hr . Depending on renal function and history of CHF . Titrate rate of normal saline to goal urine
    [Show full text]
  • Hypernatremia at Admission Predicts Poor Survival
    Seo et al. BMC Palliative Care (2020) 19:94 https://doi.org/10.1186/s12904-020-00607-z RESEARCH ARTICLE Open Access Hypernatremia at admission predicts poor survival in patients with terminal cancer: a retrospective cohort study Min-Seok Seo1,2, In Cheol Hwang3*† , Jaehun Jung4*†, Hwanhee Lee3, Jae Hee Choi3 and Jae-Yong Shim2 Abstract Background: Although palliative care providers, patients, and their families rely heavily on accurate prognostication, the prognostic value of electrolyte imbalance has received little attention. Methods: As a retrospective review, we screened inpatients with terminal cancer admitted between January 2017 and May 2019 to a single hospice-palliative care unit. Clinical characteristics and laboratory results were obtained from medical records for multivariable Cox regression analysis of independent prognostic factors. Results: Of the 487 patients who qualified, 15 (3%) were hypernatremic upon admission. The median survival time was 26 days. Parameters associated with shortened survival included male sex, advanced age (> 70 years), lung cancer, poor performance status, elevated inflammatory markers, azotemia, impaired liver function, and hypernatremia. In a multivariable Cox proportional hazards model, male sex (hazard ratio [HR] = 1.53, 95% confidence interval [CI]: 1.15–2.04), poor performance status (HR = 1.45, 95% CI: 1.09–1.94), leukocytosis (HR = 1.98, 95% CI: 1.47–2.66), hypoalbuminemia (HR = 2.06, 95% CI: 1.49–2.73), and hypernatremia (HR = 1.55, 95% CI: 1.18– 2.03) emerged as significant predictors of poor prognosis. Conclusion: Hypernatremia may be a useful gauge of prognosis in patients with terminal cancer. Further large- scale prospective studies are needed to corroborate this finding.
    [Show full text]
  • Childhood Sustained Hypercalcemia: a Diagnostic Challenge
    ORI GI NAL AR TIC LE DO I: 10.4274/jcrpe.4247 J Clin Res Pediatr Endocrinol 2017;9(4):315-322 Childhood Sustained Hypercalcemia: A Diagnostic Challenge Nisa Eda Çullas İlarslan1, Zeynep Şıklar2, Merih Berberoğlu2 1Ankara University Faculty of Medicine, Department of Pediatrics, Ankara, Turkey 2Ankara University Faculty of Medicine, Department of Pediatric Endocrinology, Ankara, Turkey What is already known on this topic? Hypercalcemia is a rare finding in children which may be due to a wide variety of factors and possibly left undiagnosed in mild elevations, while carrying the potential to lead to serious complications if proper intervention is not achieved. What this study adds? Suspicion of hypercalcemia and measurement of serum calcium level in children with clinical findings not attributable to any other clinical condition is essential. In case of hypercalcemia, young infants are more vulnerable to development of nephrolithiasis and should be evaluated as soon as possible. Abstract Objective: This study aimed to call attention to hypercalcemia, a rare finding in children which carries the potential of leading to serious complications without proper intervention. Methods: Diagnosis, treatment, and clinical course of children with sustained hypercalcemia admitted between the years 2006-2016 were reviewed. Group 1 [parathyroid hormone (PTH)-dependent] consisted of patients with high/unsuppressed PTH levels and group 2 (PTH-independent) included cases with normal/suppressed PTH levels. Results: Twenty patients (11 male, 9 female) with a median age of 6.25 (0.03-17.88) years were evaluated. Symptoms were mostly related with the gastrointestinal system, while six patients (30%) were asymptomatic. Physical examination findings were diverse, non-specific, and normal in four patients (20%).
    [Show full text]
  • Serum Calcium and Magnesium Abnormalities in Patients with Status
    Pakistan Journal of Neurological Sciences (PJNS) Volume 10 | Issue 3 Article 6 12-2015 Serum calcium and magnesium abnormalities in patients with status epilepticus: a single centre tertiary care experience Uzma Jamil Pakistan Institute of Medical Sciences,Islamabad Mazhar Badshah Pakistan Institute of Medical Sciences,Islamabad Ali Zohair Nomani Pakistan Institute of Medical Sciences,Islamabad Muhammad Irshad Pakistan Institute of Medical Sciences,Islamabad Jamal Janjua Pakistan Institute of Medical Sciences,Islamabad Follow this and additional works at: http://ecommons.aku.edu/pjns Part of the Neurology Commons Recommended Citation Jamil, Uzma; Badshah, Mazhar; Nomani, Ali Zohair; Irshad, Muhammad; and Janjua, Jamal (2015) "Serum calcium and magnesium abnormalities in patients with status epilepticus: a single centre tertiary care experience," Pakistan Journal of Neurological Sciences (PJNS): Vol. 10: Iss. 3, Article 6. Available at: http://ecommons.aku.edu/pjns/vol10/iss3/6 INTRODUCTION and burden of PSD is likely to happen because of the decline in mortality after stroke and ageing of Stroke is the major cause of physical disability in adults, populations.1 The 24 year study also indicated that the second most common cause of dementia, and the prevalence of Post stroke Dementia associated with third leading cause of death (after coronary-artery lacunar stroke was 7 times higher than other types of diseases and cancers).2 Vascular cognitive impairment stroke, including Intracerebral hemorrhage6. According is decline caused by ischemic, hemorrhagic, or oligemic to Nys et al., a high proportion of stroke survivors injury to the brain as a consequence of cerebrovascular developed the cognitive impairment within 3 months of disease.It is one of the main causes of dependency in stroke.
    [Show full text]
  • The Co-Existence of Vulvar Lichen Sclerosus, Ulcerated Calcinosis Cutis, and Dermatomyositis: Coincidence Or Immunological Mechanism?
    Lichen Sclerosus, Calcinosis Cutis and Dermatomyositis Ann Dermatol Vol. 23, Suppl. 3, 2011 http://dx.doi.org/10.5021/ad.2011.23.S3.S375 CASE REPORT The Co-Existence of Vulvar Lichen Sclerosus, Ulcerated Calcinosis Cutis, and Dermatomyositis: Coincidence or Immunological Mechanism? Didem Didar Balcı, M.D., Ebru Çelik, M.D., Gökhan Sarıkaya, M.D., Jülide Zehra Yenin, M.D., Esin Atik, M.D.1 Departments of Dermatology, 1Pathology, Faculty of Medicine, Mustafa Kemal University, Antakya-Hatay, Turkey Calcinosis cutis is a condition characterized by the de- proximal extensor myopathy. Calcinosis cutis is frequently position of calcium salts in the skin and subcutaneous accompanied by juvenile dermatomyositis (JDM). Ulcera- tissues, and patients suffering from it encounter various tion may be observed in the lesions of calcinosis cutis1,2. connective tissue disorders, such as dermatomyositis (DM), Cases of the co-existence of ulcerated calcinosis cutis and scleroderma, and systemic lupus erythematosus. Although adult DM have been rarely reported3,4. The current case is calcinosis cutis is frequently accompanied by juvenile presented due to the relatively rare incidence of ulcerated dermatomyositis, rare cases have been reported in adult calcinosis cutis in patients with adult DM, as well as the patients with DM. On the other hand, lichen sclerosus (LS) is co-existence of vulvar lichen sclerosus (LS), which has not a chronic inflammatory disease of the skin and mucosal been reported previously to the best of our knowledge. surfaces. In the present report, we present a rare case of a 71-year-old patient with DM accompanied by ulcerated CASE REPORT calcinosis cutis and vulvar LS.
    [Show full text]
  • Prevalence of Patient Load with Electrolyte Abnormalities Presenting to Emergency Department at a Tertiary Care Hospital
    International Journal of Health Sciences and Research Vol.10; Issue: 6; June 2020 Website: www.ijhsr.org Original Research Article ISSN: 2249-9571 Prevalence of Patient Load with Electrolyte Abnormalities Presenting To Emergency Department at a Tertiary Care Hospital Abdul Wahid Bhat1, Basil Wahid Bhat2 1Additional Professor Emergency Medicine, 2Medical Student, Sher-I-Kashmir Institute of Medical Sciences, Soura Srinagar, Kashmir Corresponding Author: Abdul Wahid Bhat ABSTRACT Disturbances in electrolytes are frequently observed in the emergency departments. There were 12500 patients admission (episodes) with various electrolyte abnormalities studied to check the prevalence of electrolyte imbalance in the patients admitted in the emergency department of a tertiary care hospital. Hyper and hypo abnormalities in Potassium, sodium and calcium were the common abnormalities and were present in 40.7%, 36.16% and 6.7% respectively. Patients with malignancy pre dominantly had electrolyte imbalances particularly hyponatremia, hypokalemia and hypercalcemia. Because of the high incidence rate of chronic co morbid conditions with electrolyte imbalance have multiple admission to ED, The ED physicians must be acknowledged and understand the dynamics of fluid and electrolyte balance and their early correction in patients admitted for short term care in the emergency department. The routine measurement of these electrolytes in all patients admitted in emergency department may be warranted for early detection and correction of any derangement in various electrolytes. Key words: Episodes, Electrolyte imbalance, hyponatremia, hyponatremia, hyperkalemia, hypokalemia, hypocalcaemia, hypercalcemia INTRODUCTION sulphate and phosphate being the major Disturbances in electrolytes are anions. Electrolyte imbalances are frequently observed in the emergency commonly observed in many medical and department (ED) and have important surgical conditions.
    [Show full text]
  • Electrolyte Imbalance
    Electrolyte Imbalance An electrolyte is a substance in the bloodstream that regulates important body functions. Some electrolytes are potassium, magnesium, sodium, phosphorous and calcium. Electrolytes are necessary so that muscles, organs (like the heart) and organ systems (like the nervous system) work properly. Electrolyte levels can be measured when blood is drawn for testing. If the levels are too high or too low, this is called an electrolyte imbalance. Causes of Electrolyte Imbalance There are many causes of an electrolyte imbalance, including: Loss of body fluids from vomiting, diarrhea, sweating or high fever. Chemotherapy. Medications, such as furosemide (Lasix®), that help patients with water retention. Antibiotics, such as AmBisome® and Cancidas®. Immunosuppressants, such as cyclosporine. Poor diet or not getting enough vitamins from food. Symptoms Common symptoms of electrolyte imbalance include irregular heartbeat, confusion, fatigue, lightheadedness, blood pressure changes, muscle weakness or twitching, numbness and seizures. In general, a person with an electrolyte imbalance does not feel very well or want to be involved in much activity. Electrolyte Imbalances in Patients Common electrolyte imbalances in patients include low potassium and low magnesium. The easiest way to replace the body’s supply is to eat foods that are rich in potassium and magnesium. Some examples of potassium-rich foods are: Dried fruits such as raisins, prunes, apricots and dates. Fruits such as bananas, strawberries, watermelon, oranges and cantaloupe. Dried vegetables such as beans and peas. Fresh meats like turkey, fish and beef. Baked potato (with skin). Some examples of magnesium-rich foods are: Peanuts and peanut butter. Broccoli, spinach, okra, squash, corn and brown rice.
    [Show full text]
  • “Hyponatremia in Stroke: Cerebral Salt Wasting Versus Syndrome of Inappropriate Anti-Diuresis”
    IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-ISSN: 2279-0853, p-ISSN: 2279-0861.Volume 15, Issue 7 Ver. II (July. 2016), PP 00-00 www.iosrjournals.org “Hyponatremia in Stroke: Cerebral Salt Wasting Versus Syndrome of Inappropriate Anti-Diuresis” Dr. Kumar Natarajan, Md,Ficp1, Dr. Mithra Prasad2 1(Professor And HOD, Department Of Medicine , Coimbatore Medical College/ Tamil Nadu Dr.MGR University, India) 2 (Post Graduate, Department Of Medicine , Coimbatore Medical College/ Tamil Nadu Dr.MGR University, India) Abstract: Hyponatremia is the most common electrolyte imbalance in neurologic patients. The causes of hyponatremia are varied, but in neurologically ill patients, is most commonly attributed to Syndrome of Inappropriate Anti-diuresis and Cerebral Salt Wasting. Both these entities are cerebral in origin but have distinct pathophysiology, prognosis and treatment options. The importance of distinguishing both lies in the fact that the therapy indicated for one if used for the other, can be deleterious. SIADH is a subclinically volume expanded state due to inappropriate anti-diuresis.. In stroke SIADH occurs due to AVP secretion inappropriate to the osmotic threshold. It thus requires fluid restriction as the treatment. CSW, on the other hand, is essentially a volume depleted state, which occurs due to the combined effects of decreased sympathetic outflow and increased natriuretic peptides and needs rigorous volume repletion. Hyponatremia, especially Cerebral Salt Wasting, occurring in the setting of stroke has been shown to worsen the prognosis of stroke, increase morbidity, short and long term mortality, and cause a poorer discharge disposition.. The purpose of this study is to observe the occurrence of SIADH vs CSW in the setting of stroke and to study the short term mortality, morbidity and discharge disposition among the two entities.
    [Show full text]
  • Electrolyte Imbalance
    Electrolyte Imbalance For Providers Myth: Volume depletion and electrolyte imbalance are interchangeable terms. Fact: While we often use these terms interchangeably, they are actually different conditions and require different treatment. Volume depletion is the loss of salt and water. Residents with volume depletion may show changes to the BUN and creatinine or present with new orthostatic hypotension. Treatment of volume depletion requires replacement of both sodium and water, usually with normal saline. Electrolyte imbalance is loss of water only. In true dehydration, the sodium is always elevated. Treatment of residents with electrolyte imbalance requires replacement of water deficit with oral water (mild electrolyte imbalance) or with intravenous fluids. Giving a patient with true electrolyte imbalance (hypernatremia) normal saline is likely to worsen their condition. Myth: Electrolyte imbalance can be diagnosed by physical exam. Fact: While there are some signs on physical exam that may lead you to think about electrolyte imbalance such as dry tongue or dry axilla, these are nonspecific. The diagnosis of electrolyte imbalance is a laboratory diagnosis. You need to get at least a BMP. Dehydration is diagnosed by hypernatremia (deficit of free water). Volume depletion is diagnosed by changes to the BUN and creatinine. Myth: If a patient has a G-tube, then I don’t need to place an IV to hydrate them. Fact: For residents with mild to moderate electrolyte imbalance, you may be able to hydrate them through their g-tube. However, for severe electrolyte imbalance or volume depletion, you likely still need to place an IV as the ability of the gut to absorb fluids will limit your ability to replenish fluids quickly enough for these residents.
    [Show full text]
  • University of Illinois, December 2003
    Case #1 Case Presented by Virginia C. Fiedler, MD, Michelle Bain, MD and Alexander L. Berlin, MD History of Present Illness: This 9-year-old African American girl presented with hair shedding and patchy hair loss since infancy. Additionally, her hair has been brittle. Her scalp is comfortable, without pruritus. The patient’s mother has also noticed deviations of multiple finger joints since the age of 3 along with more recent similar changes in toe joints. These changes are not associated with pain or joint swelling. The patient denies decreased body sweating, but she does note increased sweating in the areas of scalp hair loss. Past Medical History: Febrile seizures as a child Multiple finger and toe joint deviations starting at 3 years of age History of ankle deformities treated with braces for 2 years Medications: None Allergies: No known drug allergies Family History: No history of autoimmune or other skin disorders; no joint abnormalities Social History: Patient is a 4th grade student and is doing well in school Review of Systems: Denies visual problems or arthralgias Diet is adequate for protein Physical Examination: The patient had patchy alopecia that was most pronounced in the ophiasis distribution and also involved the vertex. The affected areas had miniaturized hair follicles. Hair pull test was positive for 5-6 hairs in catagen and telogen phases. Ears were not low-set. There was an increased distance between the nose and the upper lip, and the philtrum was difficult to appreciate. The patient had retained deciduous teeth, as well as hypodontia and partial anodontia.
    [Show full text]