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| {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{RT}};{{MS}} | | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{RT}};{{MS}} |
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| {{SK}} Hyperkalaemia.
| | ==[[Hyperkalemia overview|Overview]]== |
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| ==[[Hyperkalemia overview|Overview]]==
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| ''Hyperkalemia'' (AE) or ''Hyperkalaemia'' (BE) is an elevated blood level (above 5.0 mmol/L) of the [[electrolyte]] [[potassium]]. The prefix ''hyper-'' means high (contrast with ''hypo-'', meaning low). The middle ''kal'' refers to ''kalium'', which is [[Latin]] for potassium. The end portion of the word, ''-emia'', means "in the blood". Extreme degrees of hyperkalemia are considered a [[medical emergency]] due to the risk of potentially fatal [[arrhythmia]]s
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| ==[[Hyperkalemia pathophysiology|Pathophysiology]]== | | ==[[Hyperkalemia pathophysiology|Pathophysiology]]== |
| Potassium is the most abundant [[intracellular]] [[cation]]. It is critically important for many physiologic processes, including maintenance of cellular [[membrane potential]], [[homeostasis]] of cell volume, and transmission of [[action potential]]s in [[nerve cell]]s. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the [[gastrointestinal tract]] and the [[kidney]].
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| The renal elimination of potassium is passive (through the [[glomeruli]]), and resorption is active in the [[proximal tubule]] and the ascending limb of the [[loop of Henle]]. There is active excretion of potassium in the [[distal tubule]] and the [[collecting duct]]; both are controlled by [[aldosterone]].
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| Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in[[aldosterone]] deficiency) or due to causes in the renal parenchyma that impair excretion.
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| Increased extracellular potassium levels result in [[depolarization]] of the membrane potentials of cells. This depolarization opens some [[sodium channel|voltage-gated sodium channel]]s, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become [[refractory period|refractory]], increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, [[cardiac]], and [[gastrointestinal]] organ systems. Of most concern is the impairment of cardiac conduction which can result in [[ventricular fibrillation]] or [[asystole]].
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| Patients with the rare hereditary condition of [[hyperkalemic periodic paralysis]] appear to have a heightened sensitivity of muscular symptoms that are associated with transient elevation of potassium levels. Episodes of muscle weakness and spasms can be precipitated by exercise or fasting in these subjects.==[[Hyperkalemia
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| ==[[risk factors|Risk factors]]
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| ==Risk Factors==
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| The kidneys normally remove excess potassium from the body. Most cases of [[hyperkalemia]] are caused by disorders that reduce the kidneys' ability to get rid of potassium. This may result from disorders such as:
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| * [[Acute kidney failure]]
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| * [[Chronic kidney failure]]
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| * [[Glomerulonephritis]]
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| * Obstructive uropathy
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| * Rejection of a [[kidney transplant]]
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| The hormone [[aldosterone]] regulates kidney removal of sodium and potassium. Lack of aldosterone can result in hyperkalemia with an increase in total body potassium.[[Addison's]] disease is one disorder that causes reduced aldosterone production.
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| Any time potassium is released from the cells, it may build up in the fluid outside the cells and in the bloodstream. Acidosis leads to the movement of potassium from inside the cells to the fluid outside the cells. Tissue injury can cause the cells to release potassium. Such injury includes:
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| * [[Burns]]
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| * Disorders that cause blood cells to burst ([[hemolytic conditions]])
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| * Gastrointestinal [[bleeding]]
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| * [[Rhabdomyolysis]] from drugs, alcoholism, coma, or certain infections
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| * Surgery
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| * Traumatic injury
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| * Tumors
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| If the kidney is working properly, and there is enough aldosterone, tissue trauma alone rarely leads to hyperkalemia. A normally functioning kidney will remove the excess potassium that has been released from the cells.
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| Increased intake of potassium can cause hyperkalemia if kidney function is poor. Salt substitutes often contain potassium, as do many "low-salt" packaged foods.
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| Hyperkalemia may be caused by medications, including medications that affect kidney function (potassium sparing diuretics, such as [[spironolactone]], [[amiloride]], or[[triamterene]]) and potassium supplements (especially intravenous potassium).
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| ==[[causes|Causes]]==
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| ===Common Causes===
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| * [[ACE inhibitors]]
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| * [[Acidosis]]
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| * [[Addisonian crisis]]
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| * [[Beta blockers]]
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| * [[Blood transfusion]] and complications
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| * [[Cirrhosis]]
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| * [[Diabetic nephropathy]]
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| * [[Increased ingestion of high potassium foods]]
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| * [[Malnutrition]]
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| * [[Renal tubular acidosis]]
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| * [[Renal failure]]
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| ===Causes by Organ System===
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| {|style="width:80%; height:100px" border="1"
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| |style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
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| |style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Heart failure]], [[Volume depletion]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Chemical / poisoning'''
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| |bgcolor="Beige"| [[Ammonium Bifluoride]], [[Arsenicals]], [[Fluoride]] toxicity, [[Foxglove]] [[Poisoning]], [[Oleander]] [[Poisoning]], [[Tungsten]], [[White Chameleon]][[Poisoning]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Dermatologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Drug Side Effect'''
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| |bgcolor="Beige"| [[ACE inhibitors]], [[Acetylsalicylic Acid]], [[Aldosterone antagonists]], [[Amiloride]], [[Angiotensin receptor blockers]], [[Beta blockers]],[[Celecoxib]], [[Cyclosporine]], [[Diazoxide]], [[Digoxin]], [[Eplerenone]], [[Epsilon amino caproic acid]] ([[EACA]]), [[Erythropoietin]], [[Heparin]], [[Ibuprofen]],[[Indomethacin]], [[Isoflurane]], [[Ketoprofen]], [[Low-molecular weight heparin]], [[Mannitol]], [[Melarsoprol]], [[Methotrexate]], [[Minoxidil]], [[Naproxen]],[[Pancuronium bromide]], [[Pimecrolimus]], [[Potassium chloride]], [[Potassium citrate]], [[Propofol infusion syndrome]], [[Sodium thiopental]], [[Somatostatin]] therapy,[[Spironolactone]], [[Succinylcholine]], [[Suxamethonium]], [[Tacrolimus]], [[Triamterene]], [[Trimethoprim]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Ear Nose Throat'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Endocrine'''
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| |bgcolor="Beige"| [[ACTH Deficiency]], [[Addisonian crisis]], [[Addison's disease]], [[Adrenal gland disorders]], [[Adrenal hyperplasia, congenital type 3]], [[Autoimmune adrenalitis]], [[Congenital adrenal hyperplasia]] -- sodium-wasting form, [[Diabetes]], [[Diabetic ketoacidosis]], [[Hyperglycemia]], Hypoadrenocorticism --[[hypoparathyroidism]] -- [[moniliasis]], [[Hyporeninemic hypoaldosteronism]], [[Isolated aldosterone synthase deficiency]], [[Lipoid congenital adrenal hyperplasia]],[[Pseudohypoaldosteronism]] type 1, [[Pseudohypoaldosteronism]] type 2
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Environmental'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Gastroenterologic'''
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| |bgcolor="Beige"| [[Cirrhosis]], [[Gastrointestinal bleeding]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Genetic'''
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| |bgcolor="Beige"| [[18-Hydroxylase deficiency]], [[Congenital adrenal hyperplasia]] type 3, [[Congenital adrenal hyperplasia]] -- sodium-wasting form, [[Isolated aldosterone synthase deficiency]], [[Lipoid congenital adrenal hyperplasia]], [[Pseudohypoaldosteronism]] type 1, [[Pseudohypoaldosteronism]] type 2
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Hematologic'''
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| |bgcolor="Beige"| [[Hemolytic anemia]], [[Leukaemia]], [[Leukocytosis]], [[Sickle cell disease]], [[Thrombotic thrombocytopenic purpura]], congenital
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Iatrogenic'''
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| |bgcolor="Beige"| [[Oxalate blood sample]], [[Blood transfusion and complications]], [[Cuffed blood sample]], [[Delayed separation blood sample]], [[Drip arm sample]],[[EDTA blood sample]], [[Hemolysed blood sample]], [[IV fluids containing potassium]], [[Using clenched fist while collection of blood]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Infectious Disease'''
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| |bgcolor="Beige"| [[HIV infection]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Musculoskeletal / Ortho'''
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| |bgcolor="Beige"| [[Muscle damage]], [[Muscle wasting]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Neurologic'''
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| |bgcolor="Beige"| [[Amelo-cerebro-hypohidrotic syndrome]], [[Kohlschutter-Tonz syndrome]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Nutritional / Metabolic'''
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| |bgcolor="Beige"| [[Arginine hydrochloride]], Increased ingestion of high [[Potassium]] foods, Increased ingestion of [[Potassium]] containing drugs, [[Malnutrition]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Obstetric/Gynecologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Oncologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Opthalmologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Overdose / Toxicity'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Psychiatric'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Pulmonary'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Renal / Electrolyte'''
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| |bgcolor="Beige"| [[Acidosis]], [[Acute glomerulonephritis]], [[Acute renal failure]], Chronic [[Interstitial nephritis]], [[Chronic renal failure]], [[Diabetic nephropathy]], [[Distal chloride shunt]], Distal [[renal tubular acidosis]] type IV, [[Gordon's syndrome]], [[Hemolytic uremic syndrome]], [[Hyperkalemic periodic paralysis]], Hyperkalemic [[Renal tubular acidosis]], [[Hypernatremia]], [[Hyperosmolality]], [[Hyperphosphataemia]], [[Lupus nephritis]], [[Obstructive uropathy]],[[Polycystic kidney disease]], Familial [[Pseudohyperkalemia]]-due to red cell leak, Distal [[Renal tubular acidosis]] type 1, [[Transplanted kidneys]], [[Tubulointerstitial disease]], [[Urinary tract obstruction]], [[Urolithiasis]], [[Hyporeninemic hypoaldosteronism]], [[Amyloidosis]] - Renal
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Rheum / Immune / Allergy'''
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| |bgcolor="Beige"| [[Systemic lupus erythematosus]], [[Autoimmune adrenalitis]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Sexual'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Trauma'''
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| |bgcolor="Beige"| [[Crush syndrome]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Urologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Dental'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Miscellaneous'''
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| |bgcolor="Beige"| [[Amyloidosis]] - Renal, [[Burns]], [[Dehydration]], [[Fasting]], [[Hypothermia]], [[Internal bleeding]], [[Intravenous infusion]], [[Malignant |hyperpyrexia]], [[Phlebotomy]] complication, [[Rhabdomyolysis]], [[Sea snake poisoning]], [[Selective impairment of potassium excretion]], [[Strenuous |exercise]],[[Transplant rejection]], [[Tumor lysis syndrome]], Ureterojejunostomy
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| |-
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| |}
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|
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| ===Causes in Alphabetical Order===
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| {{MultiCol}}
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| * [[Acidosis]]
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| * [[ACTH Deficiency]]
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| * [[Acute glomerulonephritis]]
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| * [[Acute renal failure]]
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| * [[Addisonian crisis]]
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| * [[Addison's disease]]
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| * [[Adrenal gland disorders]]
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| * [[Adrenal hyperplasia]], congenital-type 3
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| * [[Aldosterone antagonists]]
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| * [[Amelo-cerebro-hypohidrotic syndrome]]
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| * [[Amiloride]]
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| * [[Ammonium Bifluoride]]
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| * [[Amyloidosis]] - Renal
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| * [[Angiotensin receptor blockers]]
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| * [[Arginine hydrochloride]]
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| * [[Arsenicals]]
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| * [[Autoimmune adrenalitis]]
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| * [[Beta blockers]]
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| * [[Blood transfusion and complications]]
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| * [[Burns]]
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| * [[Celecoxib]]
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| * [[Chronic interstitial nephritis]]
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| * [[Chronic renal failure]]
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| * [[Cirrhosis]]
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| * [[Congenital adrenal hyperplasia]] -- sodium-wasting form
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| * [[Crush syndrome]]
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| * [[Cuffed blood sample]]
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| * [[Cyclosporine]]
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| * [[Dehydration]]
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| * [[Delayed separation blood sample]]
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| * [[Diabetes]]
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| * [[Diabetic ketoacidosis]]
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| * [[Diabetic nephropathy]]
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| * [[Diazoxide]]
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| * [[Digoxin]]
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| * [[Distal chloride shunt]]
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| * [[Drip arm sample]]
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| * [[EDTA blood sample]]
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| * [[Eplerenone]]
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| * [[Epsilon amino caproic acid (EACA)]]
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| * [[Erythropoietin]]
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| * [[Fasting]]
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| * [[Fluoride toxicity]]
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| * [[Foxglove poisoning]]
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| * [[Gastrointestinal bleeding]]
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| * [[Gordon's syndrome]]
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| * [[Heart failure]]
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| * [[Hemolysed blood sample]]<ref>Sevastos N et al. (2006) Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude. J Lab Clin Med, 147(3):139-44; PMID 16503244.</ref>
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| * [[Hemolytic anemia]]
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| * [[Hemolytic uremic syndrome]]
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| * [[Heparin]]
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| * [[HIV infection]]
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| * [[Hyperglycemia]]
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| * [[Hyperkalemic periodic paralysis]]
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| * Hyperkalemic [[Renal tubular acidosis]]
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| * [[Hypernatremia]]
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| * [[Hyperosmolality]]
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| * [[Hyperphosphataemia]]
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| * [[Hypoadrenocorticism]] -- [[hypoparathyroidism]] -- [[moniliasis]]
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| * [[Hyporeninemic hypoaldosteronism]]
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| * [[Hypothermia]]
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| * [[Ibuprofen]]
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| * [[Increased ingestion of high potassium foods]]
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| * [[Increased ingestion of potassium containing drugs]]
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| {{ColBreak}}
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| * [[Indomethacin]]
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| * [[Internal bleeding]]
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| * [[Intravenous infusion]]
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| * [[Isoflurane]]
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| * [[Isolated aldosterone synthase deficiency]]
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| * IV fluids containing [[Potassium]]
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| * [[Ketoprofen]]
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| * [[Kohlschutter-Tonz syndrome]]
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| * [[Leukaemia]]
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| * [[Leukocytosis]]
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| * [[Lipoid congenital adrenal hyperplasia]]
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| * [[Low-molecular weight heparin]]
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| * [[Lupus nephritis]]
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| * [[Malignant hyperpyrexia]]
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| * [[Malnutrition]]
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| * [[Mannitol]]
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| * [[Melarsoprol]]
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| * [[Methotrexate]]
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| * [[Minoxidil]]
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| * [[Muscle damage]]
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| * [[Muscle wasting]]
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| * [[Naproxen]]
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| * [[Obstructive uropathy]]
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| * [[Oleander]] [[Poisoning]]
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| * [[Oxalate blood sample]]
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| * [[Pancuronium bromide]]
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| * [[Phlebotomy]] complication<ref>Don BR et al. (1990) Pseudohyperkalemia caused by fist clenching during phlebotomy. N Engl J Med, 322(18):1290-2; PMID 2325722.</ref>
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| * [[Pimecrolimus]]
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| * [[Polycystic kidney disease]]
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| * [[Potassium chloride]]
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| * [[Potassium citrate]]
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| * [[Propofol infusion syndrome]]
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| * [[Pseudohyperkalaemia, familial, due to red cell leak]] <ref>Iolascon A et al. (1999) Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis. Blood, 93(9):3120-3; PMID 10216110.</ref>
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| * [[Pseudohypoaldosteronism]] type 1
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| * [[Pseudohypoaldosteronism]] type II
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| * [[Pyrimidifen]]
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| * [[Renal tubular acidosis]], distal-type 1
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| * [[Renal tubular acidosis]], distal-type 4
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| * [[Rhabdomyolysis]]
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| * [[Sea snake poisoning]]
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| * [[Selective impairment of potassium excretion]]
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| * [[Sickle cell disease]]
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| * [[Sodium thiopental]]
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| * [[Somatostatin]] therapy
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| * [[Spironolactone]]
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| * [[Strenuous exercise]]
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| * [[Succinylcholine]]
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| * [[Suxamethonium]]
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| * [[Systemic lupus erythematosus]]
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| * [[Tacrolimus]]
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| * [[Thrombotic thrombocytopenic purpura]]-congenital
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| * [[Thrombocytosis]]
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| * [[Transplant rejection]]
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| * [[Transplanted kidneys]]
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| * [[Triamterene]]
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| * [[Trimethoprim]]
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| * [[Tubulointerstitial disease]]
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| * [[Tumor lysis syndrome]]
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| * [[Tungsten]]
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| * [[Ureterojejunostomy]]
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| * [[Urinary tract obstruction]]
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| * [[Urolithiasis]]
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| * [[Using clenched fist while collection of blood]]
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| * [[Volume depletion]]
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| * [[White Chameleon poisoning]]
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| {{EndMultiCol}}
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|
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| ==Diagnosis==
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| ==History==
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| A detailed history taking is very helpful in diagnosing the cause of [[hyperkalemia]].
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| * ''Dietary history'' (diets with low [[sodium]] and rich in [[potassium]])
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| ** Diets recommended for patients with [[cardiac disease]], [[hypertension]], and [[diabetes mellitus]]
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| ** Potassium supplements in herbal supplements, salt substitutes
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| ** Fruits, dried fruits, juices, banana and vegetables
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|
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| * ''Medications history'' (drugs causing a decreased excretion of potassium)
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| ** [[Nonsteroidal anti-inflammatory drugs]]
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| ** [[Angiotensin-converting enzyme inhibitors]]
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| ** [[Angiotensin receptor blockers]] (potassium-sparing diuretics, especially popular in the treatment of [[cirrhosis]] and [[congestive heart failure]])
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| ** [[Cyclosporine]] or [[tacrolimus]]
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| ** Antibiotics, such as [[pentamidine]] or [[trimethoprim]]/[[sulfamethoxazole]]
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|
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| * ''Medical history''
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| ** [[Renal failure]]
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| ** [[Diabetes mellitus]]
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| ** [[Sickle cell disease]] or trait
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| ** [[Urinary tract obstruction]] - Type IV [[renal tubular acidosis]], also called hyperkalemic renal tubular acidosis. It can be seen with [[polycystic kidney disease]],[[amyloidosis]] and diabetes mellitus.
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| ** The combination of [[abdominal pain]], [[hypoglycemia]] and [[hyperpigmentation]], often in the context of a history of other [[Autoimmune diseases|autoimmune disorders]], may be signs of [[Addison's disease]], itself a medical emergency.
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|
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| ==Symptoms==
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| [[Hyperkalemia]] often has no symptoms and the problem may be detected during screening [[blood test]]s for another medical disorder, or it may only come to medical attention after complications have developed, such as [[cardiac arrhythmia]] or [[Cardiac arrest|sudden death]]. Patients may present with the symptoms such as, irregular heartbeat, [[nausea]], slow, weak, or absent [[pulse]]. Extreme degrees of [[hyperkalemia]] are considered a [[medical emergency]] due to the risk of potentially fatal[[arrhythmias]]. Symptoms are fairly nonspecific and may include:
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| * [[Malaise]]
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| * [[Palpitations]]
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| * [[Muscle weakness]]
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| * Mild breathlessness may indicate [[metabolic acidosis]], one of the settings in which hyperkalemia may occur.
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|
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| ==Physical Examination==
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| ===Vitals===
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| ====Pulse====
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| * [[Bradycardia]] (heart block)
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| ====Respiratory Rate====
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| * Tachypnea (respiratory muscle weakness)
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| ===Neurologic===
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| * Muscle weakness
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| * [[Flaccid paralysis]]
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| * Depressed or absent deep tendon reflexes
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| * Muscle tenderness associated with muscle weakness ([[rhabdomyolysis]])
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|
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| ==Laboratory Findings==
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| ''Initial''
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| * Calcium
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| * Phosphate
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| * Magnesium
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| * Blood urea nitrogen (BUN)/creatinine
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| ''Extensive Evaluation''
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| * Cortisol
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| * Renin
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| * Aldosterone levels
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| * Transtubular potassium gradient (by assessing potassium+ secretion)
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|
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| ==Electrocardiogram==
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| There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarization. Hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarization of the cardiac [[action potential]] causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the [[QRS complex]].
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|
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| ===Moderate Hyperkalemia===
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| With moderate hyperkalemia, there is reduction of the size of the [[P wave]] and development of [[tent-shaped T waves]].
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|
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| ===Severe Hyperkalemia===
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| Further hyperkalemia will lead to [[widening of the QRS complex]], and the QRS complex may ultimately become sinusoidal in shape (sine wave pattern).
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|
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| ==EKG Examples==
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| The EKG below demonstrates Peaked T waves of [[hyperkalemia]].
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| [[Image:Hyperkalemia2.jpg|center|500]]
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|
| |
| ----
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| The EKG below demonstrates characteristics of [[hyperkalemia including]]: [[Broad QRS complexes]] circled in green; fusion of the [[QRS complex]] and the [[Twave]] as circled in blue; and tall [[peaked T waves]] as circled in red.[[image:Hyperkalemia123.jpg|center|500px|thumb]]
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| ----
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|
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| ===Tall, Narrow, and Peaked T waves===
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| * Earliest sign of hyperkalemia
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| * Occurs with K > 5.5 meq/li
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| * Differential diagnosis of this EKG change includes the T wave changes of [[bradycardia]] or [[stroke]].
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| * Prominent [[U wave]]s and [[QTc]] prolongation are more consistent with [[stroke]] than hyperkalemia.
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|
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|
| Shown below is the EKG demonstrating Tall, narrow and peaked T waves:
| | ==[[Hyperkalemia causes|Causes]]== |
| [[Image:Hyperkalemia1.jpg|center|500px]]
| |
| Shown below is the EKG demonstrating Tall, narrow and peaked T waves:
| |
| [[Image:Hyperkalemia.jpg|center|500px]] | |
| <br clear="left"/>
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|
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|
| ===Intraventricular Conduction Defect=== | | ==[[Hyperkalemia differential diagnosis|Differentiating hyperkalemia from other Disorders]]== |
| * Observed when K > 6.5 meq/li
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| * There is a modest correlation of the [[QRS]] duration with serum K
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| * As the K rises, the [[QRS]] complexes may resemble sine waves
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| * Generally the widening is diffuse and usually there is no resemblance of the morphology to that of either [[LBBB]] or [[RBBB]]
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| ====Intraventricular Conduction Defect on EKG Before and After Treatment for Hyperkalemia==== | |
| Shown below are the series of EKG images before, during and after treatment:
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| ; Before Treatment
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| [[Image:Ecg hyperkaliemie.jpg|500px|center]]
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| ; During Treatment
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| [[Image:Ecg hyperkaliemie2.jpg|500px|center]]
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| ; After Treatment
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| [[Image:HK3.jpg|500px|center]]
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| ----
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|
| ===Decrease of the Amplitude of the P wave or an Absent P Wave=== | | ==[[Hyperkalemia epidemiology and demographics|Epidemiology and Demographics]]== |
| * Decreased [[P wave]] amplitude occurs when the K is > 7.0 meq/li
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| * [[P wave]]s may be absent when the K is > 8.8 meq/li
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| * The impulses are still being generated in the [[SA node]] and are conducted to the ventricles through specialized atrial fibers without depolarizing the atrial muscle
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| * Moderate or sever hyperkalemia can cause [[sinus arrest]] <ref name="pmid16792034">{{cite journal |author=Bonvini RF, Hendiri T, Anwar A |title=Sinus arrest and moderate hyperkalemia |journal=[[Annales De Cardiologie Et D'angéiologie]] |volume=55 |issue=3 |pages=161–3 |year=2006 |month=June |pmid=16792034 |doi= |url= |issn=}}</ref>
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| ===ST Segment Changes Simulating Current of Injury=== | | ==[[Hyperkalemia risk factors|Risk Factors]]== |
| * Have been labeled the dialyzable current of injury
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| ===Cardiac arrhythmias: bradyarrhythmias, tachyarrhythmias, atrioventricular conduction defects===
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| * Occurs with severe hyperkalemia, not mild to moderate hyperkalemia
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| | ==[[Hyperkalemia natural history|Natural History, Complications and Prognosis]]== |
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| ==Treatment== | | == Diagnosis == |
| ==Medical Therapy==
| | [[Hyperkalemia history and symptoms|History and Symptoms]] | [[Hyperkalemia physical examination|Physical Examination]] | [[Hyperkalemia laboratory findings|Laboratory Findings]] | [[Hyperkalemia electrocardiogram|Electrocardiogram]] | [[Hyperkalemia ultrasound|Ultrasound]] |
| * [[Calcium]] supplementation (calcium gluconate 10% (10ml), preferably through a [[central venous catheter]] as the calcium may cause [[phlebitis]]) does not lower potassium but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]].
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| * [[Insulin]] (e.g. intravenous injection of 10-15u of (short acting) insulin (e.g. Actrapid) {along with 50ml of 50% dextrose to prevent hypoglycemia}) will lead to a shift of potassium ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]].
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| * [[Bicarbonate]] therapy (e.g. 1 ampule (45mEq) infused over 5 minutes) is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H<sup>+</sup> for Na<sup>+</sup>, thus leading to stimulation of the [[sodium-potassium ATPase]].
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| * [[Salbutamol]] (albuterol, Ventolin<sup>®</sup>) is a β<sub>2</sub>-selective catacholamine that is administered by nebuliser (e.g. 10-20 mg). This drug promotes movement of K into cells, lowering the blood levels.
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| * [[Polystyrene sulfonate]] (Calcium Resonium, Kayexalate) is a binding resin that binds K within the intestine and removes it from the body by defecation. Calcium Resonium (15g three times a day in water) can be given by mouth. Kayexelate can be given by mouth or as an [[enema]]. In both cases, the resin absorbs K within the intestine and carries it out of the body by [[defecation]]. This medication may cause diarrhea.
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| * Refractory or severe cases may need [[dialysis]] to remove the potassium from the circulation.
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| * Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a [[diuretic]] (such as[[furosemide]] (Lasix<sup>®</sup>) or [[hydrochlorothiazide]]).
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| ==References== | | == Treatment == |
| {{Reflist|2}}
| | [[Hyperkalemia dietary management|Dietary Management]] | [[Hyperkalemia medical therapy|Medical Therapy]] | [[Hyperkalemia surgery|Surgery]] | [[Hyperkalemia primary prevention|Primary Prevention]] |
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| | ==Case Studies== |
| | [[Hyperkalemia case study one|Case #1]] |
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