Electrolyte disorders

Definition An electrolyte disorder is an imbalance of certain ionized salts (i.e., bicarbonate, calcium, chloride, magnesium, phosphate, potassium, and sodium) in the blood. Description Electrolytes are ionized molecules found throughout the blood, tissues, and cells of the body. These molecules, which are either positive (cations) or negative (anions), conduct an electric current and help to balance pH and acid-base levels in the body. Electrolytes also facilitate the passage of fluid between and within cells through a process known as osmosis and play a part in regulating the function of the neuromuscular, endocrine, and excretory systems. The serum electrolytes include:
• • • • • • •

Sodium (Na). A positively charged electrolyte that helps to balance fluid levels in the body and facilitates neuromuscular functioning. Potassium (K). A main component of cellular fluid, this positive electrolyte helps to regulate neuromuscular function and osmotic pressure. Calcium (Ca). A cation, or positive electrolyte, that affects neuromuscular performance and contributes to skeletal growth and blood coagulation. Magnesium (Mg). Influences muscle contractions and intracellular activity. A cation. Chloride (CI). An anion, or negative electrolyte, that regulates blood pressure. Phosphate (HPO4). Negative electrolyte that impacts metabolism and regulates acid-base balance and calcium levels. Bicarbonate (HCO3). A negatively charged electrolyte that assists in the regulation of blood pH levels. Bicarbonate insufficiencies and elevations cause acid-base disorders (i.e., acidosis, alkalosis).

Medications, chronic diseases, and trauma (for example, burns, or fractures etc.) may cause the concentration of certain electrolytes in the body to become too high (hyper-) or too low (hypo-). When this happens, an electrolyte imbalance, or disorder, results. Causes and symptoms Sodium HYPERNATREMIA Sodium helps the kidneys to regulate the amount of water the body retains or excretes. Consequently, individuals with elevated serum sodium levels also suffer from a loss of fluids, or dehydration. Hypernatremia can be caused by inadequate water intake, 1

water intoxication. including loop diuretics. and/or vomiting headache edema (swelling) muscle weakness and/or tremor paralysis disorientation slowed breathing seizures coma 2 . sertraline. haloperidol). or sodium retention (caused by excessive sodium intake or aldosteronism). Diuretics. diabetes insipidus. the illicit drug "ecstasy." and other pharmaceuticals can cause decreased sodium levels. certain drugs. kidney disease.excessive fluid loss (i. A 2004 study questioned the routine make-up of fluids prescribed for children and delivered intravenously (through a needle into a vein) in hospitals today. specific antipsychotics (lithium). The authors recommended only using IV fluids when necessary and then using isotonic saline. concentrated urine loss of elasticity in the skin irregular heartbeat (tachycardia) irritability fatigue lethargy heavy. Symptoms of hypernatremia include: • • • • • • • • • • • thirst orthostatic hypotension dry mouth and mucous membranes dark. excessive perspiration. or hyponatremia. Low sodium levels may also be triggered by inadequate dietary intake of sodium. and impairment of adrenal gland or kidney function.e. and prolonged vomiting or diarrhea). making it one of the most common electrolyte disorders. Symptoms of hyponatremia include: • • • • • • • • • nausea. abdominal cramping. corticosteroids.e. chlorpropamide. vasopressin. In addition. severe burns.. labored breathing muscle twitching and/or seizures HYPONATREMIA Up to 1% of all hospitalized patients and as many as 18% of nursing home patients develop hyponatremia. certain psychoactive drugs (i. and antihypertensive medications may cause elevated sodium levels. fluoxetine..

adrenal insufficiency. and adrenal gland impairments can all cause depletion of potassium levels in the bloodstream. kidney disease. multiple myeloma. cyclosporin. Cushing's syndrome. or Addison's disease. gastrointestinal bleeding. myocardial infarction (heart attack). and Paget's disease. lithium. Diuretic drugs. congestive heart failure. Symptoms may include: • • • • • weakness nausea and/or abdominal pain irregular heartbeat (arrhythmia) diarrhea muscle pain HYPOKALEMIA Severe dehydration. aldosteronism. and dietary phosphate deficiency. Symptoms of hypokalemia include: • • • • • • • weakness paralysis increased urination irregular heartbeat (arrhythmia) orthostatic hypotension muscle pain tetany Calcium HYPERCALCEMIA Blood calcium levels may be elevated in cases of thyroid disorder. multiple bone fractures. fasting.e. laxative abuse. ACE inhibitors. A substance known as glycyrrhetinic acid. Williams syndrome. Excessive use of calcium-containing supplements and certain over-the-counter medications (i. antacids) may also cause hypercalcemia. The condition may also be secondary to hypernatremia (low serum concentrations of sodium). In infants. which is found in licorice and chewing tobacco. as can heavy exercise. secondary hyperparathyroidism from maternal hypocalcemia. beta blockers. bulimia nervosa. certain penicillins. heparin. severe burns. Symptoms include: • fatigue 3 . metastatic cancer..Potassium HYPERKALEMIA Hyperkalemia may be caused by ketoacidosis (diabetic coma). and trimethoprim can increase serum potassium levels. kidney failure. long-term diuretic therapy. milk-alkali syndrome. lesser known causes may include blue diaper syndrome. can also deplete potassium serum levels.

• • • • • • • • constipation depression confusion muscle pain nausea and vomiting dehydration increased urination irregular heartbeat (arrhythmia) HYPOCALCEMIA Thyroid disorders. hyperparathyroidism. burns. and diuretic use. severe burns. sepsis. is a common cause of hypomagnesemia. Hypermagnesemia is characterized by: • • • • • lethargy hypotension decreased heart and respiratory rate muscle weakness diminished tendon reflexes HYPOMAGNESEMIA Inadequate dietary intake of magnesium. digestive system disorders. often caused by chronic alcoholism or malnutrition. Addison's disease. aldosteronism. Other causes include malabsorption syndromes. vitamin D deficiency. and medications such as heparin and glucogan can deplete blood calcium levels. pancreatitis. or an overdose of magnesium salts. irritability) dry skin brittle nails facial twitching Magnesium HYPERMAGNESEMIA Excessive magnesium levels may occur with end-stage renal disease. Lowered levels cause: • • • • • • muscle cramps and spasms tetany and/or convulsions mood changes (depression. kidney failure. Symptoms of low serum magnesium levels include: • • • leg and foot cramps weight loss vomiting 4 .

Severe depletion of serum chloride levels causes metabolic alkalosis. twitching. Symptoms include: • • • • weakness headache nausea cardiac arrest HYPOCHLOREMIA Hypochloremia usually occurs as a result of sodium and potassium depletion (i. resulting in hyperchloremic metabolic acidosis. Drugs such as boric acid and ammonium chloride and the intravenous (IV) infusion of sodium chloride can also boost chloride levels.e. hyponatremia. hypokalemia). and tremors seizures muscle weakness arrthymia Chloride HYPERCHLOREMIA Severe dehydration. This alkalization of the bloodstream is characterized by: • • • • mental confusion slowed breathing paralysis muscle tension or spasm 5 . traumatic brain injury. and aldosteronism can also cause hyperchloremia.• • • • muscle spasms. kidney failure.. hemodialysis.

hyperparathyroidism. hypoparathyroidism. kidney disease. and Trousseau's sign. hemodialysis. acromegaly. kidney failure. and prolonged diuretic therapy can also diminish blood phosphate levels. the provider will test reflexes. malnutrition. perform a complete physical examination. systemic infection. hemodialysis. the physician will also check for Chvostek's sign. and intestinal obstruction can all cause phosphate retention and build-up in the blood. Individuals with mild hyperphosphatemia are typically asymptomatic. and prescribe appropriate laboratory tests. but signs of severe hyperphosphatemia include: • • • • tingling in hands and fingers muscle spasms and cramps convulsions cardiac arrest HYPOPHOSPHATEMIA Serum phosphate levels of 2 mg/dL or below may be caused by hypomagnesemia and hypokalemia.Phosphate HYPERPHOSPHATEMIA Skeletal fractures or disease. a reflex test that triggers an involuntary facial twitch. hypothyroidism. Cushing's syndrome. or phlebotomist. vitamin D deficiency. Because electrolyte disorders commonly affect the neuromuscular system. Serum electrolyte imbalances can be detected through blood tests. a muscle spasm that occurs in response to pressure on the upper arm. diabetic ketoacidosis. Symptoms of severe hypophosphatemia include: • • • muscle weakness weight loss bone deformities (osteomalacia) Diagnosis Diagnosis is performed by a physician or other qualified healthcare provider who will take a medical history. and analyzed at a lab. 6 . diabetic ketoacidosis. The disorder occurs concurrently with hypocalcemia. discuss symptoms. Severe burns. There are typically few physical signs of mild phosphate depletion. Blood is drawn from a vein on the back of the hand or inside of the elbow by a medical technician. If a calcium imbalance is suspected. alcoholism.

It may also be recommended for renal patients suffering from severe hypermagnesemia. When they are mild. when treated quickly and appropriately. However. can reverse electrolyte depletion. If medications such as diuretics triggered the imbalance.4 mg/dL (total Ca. However.1 mEq/L (plasma) Chloride. 1. Hemodialysis treatment may be required to reduce serum potassium levels in hyperkalemic patients with impaired kidney function. For example. 8. and death. Prevention Physicians should use caution when prescribing drugs known to affect electrolyte levels and acid-base balance. Fluid and electrolyte replacement therapy. serum) Magnesium. Severe hypernatremia has a mortality rate of 40-60%. Individuals with kidney disease. electrolyte imbalances in and of themselves are usually effectively reversed. Other blood tests that determine pH levels and acid-base balance may also be performed. nutritional changes may be prescribed. serum).5-4. transient hyperphosphatemia is usually fairly benign.5 mEq/L (serum) Calcium.Normal levels of electrolytes are: • • • • • • Sodium. If the disorder is caused by poor diet or improper fluid intake. age. adults) Standard ranges for test results may vary due to differing laboratory standards and physiological variances (gender. long-term elevations of blood phosphate levels can lead to potentially fatal soft tissue and vascular calcifications and bone disease. 135-145 mEq/L (serum) Potassium. and other factors). and other 7 .5 mg/dL (plasma. 2. coma. Prognosis A patient's long-term prognosis depends upon the root cause of the electrolyte disorder.7-5.8-10. 100-108 mEq/L (serum) Phosphate.4-2. either intravenously or by mouth. and severe serum phosphate deficiencies (hypophosphatemia) can cause encephalopathy. some electrolyte imbalances have few to no symptoms and may pass unnoticed.2 mg/dL (unbound Ca. Treatment Treatment of electrolyte disorders depends on the underlying cause of the problem and the type of electrolyte involved. 3. thyroid problems. discontinuing or adjusting the drug therapy may effectively treat the condition.5-5. Death is commonly due to cerebrovascular damage and hemorrhage resulting from dehydration and shrinkage of the brain cells. 4.

When they start to feed a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. Usually occurs in the treatment of peptic ulcer. Tetany A disorder of the nervous system characterized by muscle cramps.conditions that may place them at risk for developing an electrolyte disorder should be educated on the signs and symptoms. Aldosteronism A condition defined by high serum levels of aldosterone. Malnourished patients' intracellular phosphate stores can be depleted despite normal serum phosphate concentrations. and numbness of the extremities Refeeding Syndrome Is underdiagnosed and undertreated.35-7. Also known as postural hypotension. such as a cellular wall. and the lower concentration solute is drawn across the membrane into the higher concentration solute (osmosis). Key Terms Acid-base balance A balance of acidity and alkalinity of fluids in the body that keeps the pH level of blood around 7.1 Starting to eat again after a period of prolonged starvation seemed to precipitate cardiac failure.45. Instead fat and protein stores are catabolised to produce energy. spasms of the arms and legs. Bulimia nervosa An eating disorder characterized by binging and purging (self-induced vomiting) behaviors. a hormone secreted by the adrenal gland that is responsible for increasing sodium reabsorption in the kidneys. This results in an intracellular loss of electrolytes. but treatable Refeeding syndrome was first described in Far East prisoners of war after the second world war. Milk-alkali syndrome Elevated blood calcium levels and alkalosis caused by excessive intake of milk and alkalis. Orthostatic hypotension A drop in blood pressure that causes faintness or dizziness and occurs when one rises to a standing position. Addison's disease A disease characterized by a deficiency in adrenocortical hormones due to destruction of the adrenal gland. Osmotic pressure Pressure that occurs when two solutions of differing concentrations are separated by a semipermeable membrane. in particular phosphate. The pathophysiology of refeeding syndrome has now been established.2 In starvation the secretion of insulin is decreased in response to a reduced intake of carbohydrates. This stimulates 8 .

93% (28/30) achieved a serum phosphate concentration of 0. Serum phosphate. and when phosphate is measured the importance of grossly abnormal results may not be recognised. coma.7 Typically regimens recommend multiple infusions based on weight. other groups. cancer. with clinical end 9 . arrhythmias. The treatment seemed safe. In addition the exact degree of hypophosphataemia requiring treatment remains to be determined. Warrington. In the United Kingdom patients with anorexia nervosa. such as hypokalaemia and hypomagnesaemia. this should be started at a reduced calorific rate (25-50% of estimated requirements) to reduce the risk of refeeding syndrome developing. Fresenius Kabi. calcium. but these complex regimens may be impractical on general wards. it is the largest published series of the treatment of severe hypophosphataemia due to refeeding syndrome. would not require adjustment for weight. Serum phosphate concentrations of less than 0. the early clinical features of refeeding syndrome are non-specific and may go unrecognised.cellular uptake of phosphate. alcoholism. which include rhabdomyolysis.50 mmol/l (normal range 0. When these patients require artificial feeding (enteral or parenteral). Measurement of serum phosphate may not be done in patients at risk. Treatment of refeeding syndrome can be helped by the input of hospitals' nutrition teams. This treatment was effective. and some patients after operations are known to be at risk of refeeding syndrome. and the optimal regime therefore remains to be determined. When hypophosphataemia occurs it should be corrected in addition to other electrolyte abnormalities. If after 24 hours the serum phosphate concentration remains low or falls subsequently then further phosphate should be administered. which can lead to profound hypophosphataemia.40 mmol/l) can produce the clinical features of refeeding syndrome. and creatinine concentrations should be measured before feeding and repeated daily for four days after feeding is started. normal renal function.50 mmol/l or more after four days. and a phosphate concentration of less than 0. No randomised controlled trials of treatment for refeeding syndrome have been performed. Ideally a treatment regimen for refeeding syndrome would not require monitoring blood tests more often than daily. Although this study is uncontrolled. hypotension.6 However. magnesium. with frequent monitoring of serum phosphate. all patients were managed on general wards. Importantly. and would provide an adequate dose of phosphate.50 mmol. Randomised controlled trials of the treatment of refeeding syndrome. United Kingdom). although most experts on nutrition would recommend treatment of hypophosphataemia with measurements of 0. Importantly. Understanding of refeeding syndrome and its treatment is limited among general physicians and surgeons. such as patients with neurological dysphagia who are being fed through nasogastric or percutaneous endoscopic gastrostomy tubes. Feeding can be continued. leucocyte dysfunction.4 5 Importantly. may also be at risk. The other barrier is a lack of consensus on treatment. Many patients at risk of refeeding syndrome are not treated on specialist nutrition units. Previously recommended regimens for treatment of severe hypophosphataemia have been developed mainly from experience in treating small numbers of patients in intensive care settings. five patients required further phosphate as severe hypophosphataemia recurred after initial correction. Intravenous phosphate is required as oral supplementation is inadequate. Results of such a regimen have recently been published. seizures. cardiac failure. respiratory failure.50 mmol/l were treated with 50 mmol intravenous phosphate over 24 hours (500 ml Phosphates Polyfusor. urea. no patient developed renal failure.32-0. potassium. and sudden death. although three patients developed mild transient hyperphosphataemia and four asymptomatic hypocalcaemia.3 This phenomenon usually occurs within four days of starting to feed again.85-1. Dieticians and nutrition nurses can help in identifying malnourished patients at risk of developing refeeding syndrome. Refeeding syndrome can occur with parenteral as well as enteral feeding.8 Thirty patients with refeeding syndrome. Phosphate is necessary for the generation of adenosine triphosphate from adenosine diphosphate and adenosine monophosphate and other crucial phosphorylation reactions.

17: 632-7. Reid D.[Medline] Diazepam termasuk obat dengan kelas terapi antiansietas. Weston Road. Staffordshire General Hospital.295: 490-1. Efficacy and safety of intravenous phosphate replacement in critically ill patients. konvulsi akibat keracunan. Crit Care 1997. Stephen D Hearing. et al.nhs. Crook M. Paraesthesias. Silvis SE.33: 376-96. 6. dan sedatif.points such as survival.[CrossRef][ISI][Medline] 3. Mattman PE. Hearing SD. Nutrition 2001. weakness.31: 683-8. kejang demam. Crook MA. McCullagh E. Diazepam 10 . Bliss TL. Gastroenterology 1972. The current priority is to improve awareness of refeeding syndrome among general physicians and surgeons and to convince them of its importance.62: 513-20. ansietas atau insomnia. seizures. while in contrast accepting the need to treat other electrolyte deficiencies such as hypokalaemia and hypomagnesaemia. antikonvulsan. Refeeding hypophosphataemia in anorexia nervosa and alcoholism. With further liaison between hospital nutrition teams and ward staff and the use of an adequate treatment regimen. Schnitker MA.uk ) Competing interests: None declared References 1. Stafford ST16 3SA (stephen. are therefore needed. Refeeding syndrome: effective and safe treatment with phosphates polyfusor.wmids. Farquhar JR. 7. Paragas PD Jr. 2. Bouchier IAD. Am J Clin Nutr 1980.17: 1325-9. Perreault MM. Ann Intern Med 1951. Many doctors remain unconvinced of the importance of treating hypophosphataemia. Hally V.35: 69-96. 4. Disorders of plasma phosphate and indications for its measurement.[ISI][Medline] 5.hearing@msgh-tr. A clinical study of malnutrition in Japanese prisoners of war. Terlevich A. Panteli JV. Aliment Pharmacol Ther 2003. Krumdieck CL. Diazepam berikatan dengan reseptorreseptor stereospesifik benzodiazepin di neuron postsinaptik GABA pada beberapa sisi di dalam Sistem Syaraf Pusat (SSP). Smyth C. Indikasi dari diazepam adalah untuk status epileptikus. consultant gastroenterologist Department of Gastroenterology.34: 393-9. it may be possible to improve the prognosis of this currently underecognised and undertreated group substantially. BMJ 1987. The importance of the refeeding syndrome. Weinster RL. Ostrop NJ. Cumming AD. 8. and hypophosphataemia in patients receiving hyperalimentation. Death resulting from overzealous total parenteral nutrition: The refeeding syndrome revisited. Swaminathan R. Tierney MG. Woltersdorf WW. dan untuk spasme otot. Ann Clin Biochem 1996.

Metabolit yang ketiga adalah Temazepam dengan estimasi t1/2 antara 10-20 jam. sehingga mengakibatkan pertumbuhan embrio yang lambat. volume distribusinya 1. Di dalam tubuh embrio bahan metabolit tersebut berpotensi menginhibisi neuron. amnesia. hipotensi. Perubahan ini mengakibatkan ion klorida berada dalam bentuk terhiperpolarisasi (bentuk kurang aktif / kurang memberikan rangsangan) dan stabil. Dengan pH yang tinggi 11 . Oxazepam memiliki estimasi t1/2 antara 5-15 jam. anak-anak di bawah 6 bulan (per oral). N-Desmetildiazepam (nordiazepam) merupakan salah satu metabolit yang memiliki efek farmakologis yang sama dengan diazepam. vertigo. dimana t1/2-nya lebih panjang yaitu antara 30-200 jam. dengan tingkat pengikatan pada albumin dalam plasma sebesar (98-99%). Ketika diazepam dimetabolisme oleh enzim CYP2C19 menjadi nordiazepam. Temazepam dimetabolisme dengan bantuan enzim CYP3A4 dan CYP 3A5 serta mengalami konjugasi dengan asam glukuronat sebelum dieliminasi dari tubuh. meningkatkan pH di dalam sel. ibu hamil. JALUR METABOLISME DIAZEPAM Diazepam diabsorpsi dengan cepat secara lengkap setelah pemberian peroral dan puncak konsentrasi dalam plasmanya dicapai pada menit ke 15-90 pada dewasa dan menit ke-30 pada anakanak. menghasilkan tiga metabolit aktif. atau di bawah 30 hari (parenteral). bingung. ataksia.Metabolisme utama diazepam berada di hepar. karena itu penggunaan untuk ibu hamil dan menyusui sebisa mungkin dihindari. insufisiensi pulmonar akut depresi pernapasan. konsentrasi N-Desmetildiazepam dalam plasma lebih tinggi dari diazepam sendiri. kelemahan otot. Efek samping dari penggunaan diazepam antara lainmengantuk. ketergantungan. Range t1/2 diazepam antara 20100 jam dengan rata-rata t1/2-nya adalah 30 jam. depresi pernapasan. kondisi fobia dan obsesi. suatu metabolit aktif yang dieliminasi dari tubuh melalui proses glukuronidasi. Pada fase eliminasi baik pada terapi dosis tunggal maupun multi dosis. Diazepam secara cepat terdistribusi dalam tubuh karena bersifat lipid-soluble. kadang nyeri kepala. gangguan mental.meningkatkan penghambatan efektifitas GABA dalam menghasilkan rangsangan dengan meningkatkan permeabilitas membran terhadap ion klorida. Dengan terinhibisinya neuron maka akan terganggu pula transfer neurotransmiter untuk hormon-hormon pertumbuhan. Bioavailabilitas obat dalam bentuk sediaan tablet adalah 100%. Diazepam dikontraindikasikan pada pasien yang hipersensitifitas terhadap diazepam atau komponen lain dalam formulasi (misalnya hipersensitif terhadap benzodiazepin yang masih ada dalam formulasi). Enzim utama yang digunakan dalam metabolisme diazepam adalah CYP2C19 dan CYP3A4. terjadilah proses N-dealkilasi. N-Desmetildiazepam dengan bantuan enzim CYP3A4 diubah menjadi oxazepam. glaukoma. dapat bersifat toksik.1L/kg. Diazepam diekskresikan melalui air susu dan dapat menembus barier plasenta.

Hal ini mungkin dapat disebabkan karena t1/2 diazepam yang cukup panjang. Pada trimester pertama masa kehamilan merupakan periode kritis maka bahan teratogen yang bersifat toksik akan mempengaruhi pertumbuhan embrio. lebih sedikit daripada prosentase diazepam yang terikat protein plasma (98%-99%). 2 kali t1/2 Diazepam. untuk itu mungkin perlu dilakukan kontrol terhadap konsentrasi diazepam dan metabolitnya dalam plasm 12 . sehingga kerja hormon pertumbuhan juga terganggu yang akhirnya pertumbuhan janin juga terganggu. Oleh karena itu penggunaan diazepam dalam terapi pengobatan harus ekstra berhati-hati. Diazepam ini tidak boleh digunakan dalam jangka waktu yang panjang (tidak boleh lebih dari 3 bulan). bahkan dapat mengakibatkan kematian janin. yaitu perlu dipertimbangkan adanya efek yang ditimbulkan oleh metabolit aktif Diazepam. ditambah lagi t1/2 N-Desmetildiazepam yang lebih panjang yaitu. karena berakibat buruk bagi tubuh penderita. masih dapat dihasilkan efek bahkan sebesar 2 kalinya yang diperoleh dari N-Desmetildiazepam sebagai metabolit aktif diazepam.Efek samping ringan Diazepam dapat terjadi pada konsentrasi plasma mencapai 50-100μg/L. Ditambah lagi persentase metabolit yang terikat protein dalam plasma (97%). Hal ini berarti setelah konsentrasi diazepam dalam tubuh habis untuk menghasilkan efek.mengakibatkan sel tidak dapat tereksitasi. tetapi ini juga tergantung pada sensitivitas setiap individual. Efek anxiolitik terlihat pada penggunaan secara long-term dengan konsentrasi 300-400μg/L.

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