Hyperkalemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2] Syed Ahsan Hussain, M.D.[3]

Potassium was discovered in 1807 by Sir Humphry Davy in 1807 in England. He discovered potassium by means of electrolysis from potash. It was the first alkali metal to be discovered. Hyperkalemia develops when blood potassium levels are more than 5.1meq/L. Hyperkalemia can be classified based on the potassium levels, duration of onset and the cause of hyperkalemia. Potassium is the most abundant intracellular cation and is critically important for many physiologic processes. Hyperkalemia can be caused by reasons that include increased uptake, extracellular shift, tissue breakdown and impaired excretion from the body. The incidence of hyperkalemia is approximately 11000 per 100,000 individuals in hospitalized and 1000-2000 per 100,000 of outpatients.The exact prevalence of hyperkalemia is unknown. Extreme degrees of hyperkalemia are considered a medical emergency. If left untreated hyperkalemia can cause cardiac rhythm disorders and eventually cardiac arrest leading to death. Hyperkalemia can be asymptomatic, or present with irregular heartbeat, nausea, slow, weak, or absent pulse. Serum potassium is the gold standard test for the diagnosis of hyperkalemia. When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower potassium levels.

Potassium was discovered in 1807 by Sir Humphry Davy in 1807 in England. He discovered potassium by means of electrolysis from potash. It was the first alkali metal to be discovered.

Hyperkalemia develops when blood potassium levels are more than 5.1meq/L. Hyperkalemia can be classified based on the potassium levels, duration of onset and the cause of hyperkalemia.

Potassium is the most abundant intracellular cation and is critically important for many physiologic processes. The normal range of potassium in blood is 3.5-5.1mEq/L . Hyperkalemia develops when the level of potassium exceeds 5.5 meq/L in blood which can be due to an increase in intake of potassium, excessive production as seen in tissue breakdown, ineffective elimination of potassium or some drugs. The potassium levels in the body are highly regulated mainly by kidneys. The gut excretes a minimal amount of dietary potassium (approximately 10%) . Hyperkalemia is very common in patients with chronic kidney disease as potassium is not effectively excreted from the bod y.Potassium is involved in maintaining transmembrane potentials of cells, so imbalance in potassium levels can lead to disruption of cell membrane potentials and can cause hyperexcitablity leading to fatal cardiac arrhythmias and effecting nervous system.

Hyperkalemia is an elevated blood level (above 5.1 mmol/L) of the electrolyte potassium. Hyperkalemia can be caused by reasons that include increased uptake, extracellular shift, tissue breakdown and impaired excretion from the body.

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia.

The incidence of hyperkalemia is approximately 11000 per 100,000 individuals in hospitalized and 1000-2000 per 100,000 of outpatients.The exact prevalence of hyperkalemia is unknown. It changes between inpatient and outpatient cases. In one study in USA, the prevalence was 1.57. Hypekalemia occurs more in females compared to males. It is more common in older age group. African American have higher chances of developing hyperkalemia compared to non-African-Americans.

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 acute kidney failure, chronic kidney failure and glomerulonephritis.

There is insufficient evidence to recommend routine screening for hyperkalemia. However, potassium levels are routinely monitored in patients with chronic kidney diseases.

Extreme degrees of hyperkalemia are considered a medical emergency. If left untreated hyperkalemia can cause cardiac rhythm disorders and eventually cardiac arrest leading to death. Complications that can develop as a result of hyperkalemia are arrhythmia, cardiac arrest, and neuromuscular weakness. The outcome with this condition varies. In some people, the disorder causes deadly complications, while others tolerate it well.

Serum potassium is the gold standard test for the diagnosis of hyperkalemia. Pseudohyperkalemia needs to be ruled out whenever hyperkalemia is diagnosed. Pseudohyperkalemia is defined when serum potassium concentration exceeds that of plasma. Different etiologies of hyperkalemia can be assessed by using the diagnostic criteria.

Hyperkalemia often has no symptoms. Occasionally, people may have the following symptoms: 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. A detailed history taking is very helpful in diagnosing the cause of hyperkalemia.

In patients with hyperkalemia, physical examination may vary from normal to bradycardia (heart block), tachypnea due to respiratory muscle weakness and absent tendon reflexes. Evaluation of vital signs plays a key role in determining hemodynamic stability and identifying the presence of cardiac arrhythmias due to the hyperkalemia.

In a patient who does not have a risk for hyperkalemia, repeating the blood test is indicated before taking any actions unless changes are present on electrocardiography.

Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of potentially fatal arrhythmias. The EKG is an important tool in evaluating a patient who has hyperkalemia as well as in diagnosing hyperkalemia. However, EKG changes do not always correlate with the degree of hyperkalemia. Some of the EKG changes that can be seen associated with hyperkalemia include peaked T waves, PR interval prolongation, QRS complex widening, absence of P waves, sine wave pattern and sinus arrest.

There are no x-ray findings associated with hyperkalemia.

There are no echocardiography/ultrasound findings associated with hyperkalemia. However depending on the cause of hyperkalemia ultrasound findings of the particular cause might be present.

There are no CT scan findings associated with hyperkalemia.

There are no MRI findings associated with hyperkalemia

There are no other imaging findings associated with hyperkalemia

There are no other diagnostic studies associated with hyperkalemia

When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower _-p6 levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient’s condition.

Surgical intervention is not recommended for the management of hyperkalemia.

Hyperkalemia can be prevented by limiting the intake of potassium in diet and avoiding renal damage.

Stabilizing the heart membrane in hyperkalemia is very important in preventing fatal cardiac arrhythmias. Effective elimination of potassium from the body also prevents complications.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Potassium was discovered in 1807 in England by Sir Humphry Davy.

• Potassium was discovered in 1807 by Sir Humphry Davy in 1807 in England^[1].
• He discovered potassium by means of electrolysis from potash.
• It was the first alkali metal to be discovered.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2]; Huda A. Karman, M.D.

Hyperkalemia develops when blood potassium levels are more than 5.1 meq/L. Hyperkalemia can be classified based on the potassium levels, duration of onset and the cause of hyperkalemia.

• Hyperkalemia may be classified according to the potassium levels as : ^[1][2]
  • Mild- potassium levels between 5.1-6.0 mEq/L.
  • Moderate- potassium levels between 6.1-7.0 mEq/L.
  • Severe- potassium levels more than 7.0 mEq/L.
• Hyperkalemia can be classified on the basis of duration as ^[3] :
  • Hyperacute- develops in a few hours, usually in tissue breakdown or parenteral potassium supplement.
  • Acute-develops within 48 hours, could be due to acute kidney injury.
  • Chronic-develops gradually, usually due to chronic diseases such as chronic kidney disease.^[4]

Hyperkalemia classification type	Characterestics
Based on potassium levels	Mild
Potassium levels between 5.1-6.0 mEq/L.
Moderate
Potassium levels between 6.1-7.0 mEq/L.
Severe
Potassium levels more than 7.0 mEq/L.
Based on the duration	Hyperacute
Develops in a few hours Usually due to tissue breakdown Or due to parenteral potassium supplement.
Acute
Develops within 48 hours, Could be due to acute kidney injury.
Chronic
Develops gradually, Usually due to chronic diseases such as chronic kidney disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Jogeet Singh Sekhon

Potassium is the most abundant intracellular cation and is critically important for many physiologic processes. The normal range of potassium in blood is 3.5-5.1mEq/L. Hyperkalemia develops when the level of potassium exceeds 5.5 mEq/L in blood which can be due to an increase in intake of potassium, excessive production as seen in tissue breakdown, transcellular shift of potassium, ineffective elimination of potassium or due to some drugs. The potassium levels in the body are highly regulated mainly by renal excretion. The gut excretes a minimal amount of dietary potassium (approximately 10%). Hyperkalemia is very common in patients with chronic kidney disease as potassium is not effectively excreted from the body. Potassium is involved in maintaining transmembrane potential of the cells, so imbalance in potassium levels can lead to disruption of cell membrane potentials and can cause hyperexcitablity leading to fatal cardiac arrhythmias and may affect the nervous system.

• Potassium is the major intracellular cation and sodium is the major extracellular cation ^[1]
• Almost all cells possess an Na⁺-K⁺-ATPase, which pumps Na⁺ out of the cell and K⁺ into the cell and leads to a K⁺ gradient across the cell membrane (K⁺in>K⁺out) that is partially responsible for maintaining the potential difference across the membrane.
• This potential difference called the transmembrane potential is responsible for the excitability of the cells ^[2]

The distribution of potassium inside and outside the cells is maintained by various pumps, osmolarity, pH and the hormones including insulin, aldosterone, catecholamines and prostaglandins.

• Insulin regulates potassium uptake into the cells through GLUT receptors on the cell membranes by increasing the activity of Na⁺-K⁺-ATPase pump^[4]

• Catecholamines regulate potassium uptake into the cells through β2-Receptor–induced stimulation of Na⁺K⁺ATPase pump
• Increased osmolarity as in hyperglycemia causes water efflux from the cells that drags potassium along.
• In acidosis, the decreased extracellular pH decreases the rate of Na+-H⁺ exchange (NHE1) and inhibit the inward rate of sodium bicarbonate (NaHCO3) cotransport,thus decreasing intracellular Na⁺ levels which in turn decreases the activity of Na^+-K⁺–ATPase pump and decreasing intracellular K⁺ levels.
• In alkalosis, the increased extracellular pH increases the rate of NHE1 and increases the inward rate of NaHCO3 cotransport, Thus increasing intracellular Na⁺ levels which in turn increases the activity of Na^+-K^+-ATPase pump and increasing intracellular K⁺ levels.

• The potassium levels in the body are dependent on dietary intake, tissue breakdown, gastrointestinal absorption and losses and most important is renal regulation via absorption and secretion. Kidneys play an important role in keeping the balance of potassium.

• At the glomerulus, potassium is freely filtered and then largely reabsorbed in the proximal tubule and thick ascending loop of Henle (>60 % of filtered potassium).
• The cortical collecting duct receives 10–15% of filtered potassium and constitutes the kidney’s major site of potassium excretion.
• Potassium excretion at the cortical collecting duct depends on the amount of sodium delivered there and the activity of aldosterone. It does so by the following ways.^[5][6][7]
  • Increases intracellular K⁺ concentration by stimulating the activity of the Na^+-K^+-ATPase at the basolateral membrane.
  • Stimulates Na⁺ reabsorption across the luminal membrane, which increases the electronegativity of the lumen, thereby increasing the electrical gradient favoring K⁺ secretion. If the rate of delivery of sodium and water is very high in the distal tubules then it will cause more Na⁺ reabsorption and more K⁺ secretion.
• Has a direct effect on the luminal membrane to increase K⁺ permeability.^[8]

• Alteration in the levels of potassium occur due to disruption in the above mentioned mechanisms that regulate potassium homeostasis.

• Hyperkalemia means excessive potassium in the blood(>5.1 meq/L).
• It can result from excessive potassium intake, increased tissue breakdown, increased transcellular shift or impaired excretion from the body ^[9].

• The only source of potassium to our body is by diet. If potassium rich diet is consumed or given parenterally, it can lead to hyperkalemia. However, in individuals with normal renal function, potassium levels are regulated and excess potassium is excreted

• Change in extracellular pH-decrease in pH as in mineral acidosis leads to increased shift of potassium from intracellular to extracellular space.
• Decrease in insulin as in diabetes mellitus, can lead to increased extracellular accumulation of potassium.
• Increase in osmolarity as in hyperglycemia, will cause extracellular shift of potassium.
• Decreased catecholamines or reduced function as with beta blockers use will lead to decreased uptake by cells resulting in extracellular accumulation of potassium.

• Increased tissue breakdown can occur as in rhabdomylosis, burns, haemolytic conditions or chemotherapy induced tissue breakdown.^[10]

• Pseudohyperkalemia referred to as increased serum potassium levels but plasma potassium levels are within range.This usually occurs invitro while collecting a blood sample, thrombocytosis or in myeloproliferative diseases.^[11]

.

• Potassium levels in body are regulated by the kidneys. Any impairment in the excretion mechanisms can result in hyperkalemia.
• Reduced GFR(<15ml/min) results in decreased urine flow and hence decreased sodium and water delivery to the distal tubules resulting in decreased secretion of potassium.
• Decrease in the levels of aldosterone as in primary hypoaldosteronism and secondary hypoaldosteronism results in impaired excretion of potassium.
• Pseudohypoaldostrenism- the levels of aldosterone are within normal limits but there is resistance to aldosterone in the kidneys and is not able to exert its function.
• Chronic kidney disease– the overall renal function is impaired resulting in decreased secretion of potassium as in various nephropathies.
• Renal parenchymal damage- this can occur in obstructive uropathy or AKI in which the renal parenchyma would not be able to effectively excrete potassium.^[12][13][14]
• Constipation-minor amount of potassium is also excreted by stools,so chronic constipation can lead to hyperkalemia however it is very rare.^[15]

Trans-cellular shifts	Renal secretion impairment		GI cause	Increased tissue breakdown	Increased intake of potassium
Metabolic acidosis (K+/H+ exchanger) Diabetic ketoacidosis (Insulin activates Na+/K+ ATPase) Beta blockers (catecholamines activate Na+/K+ ATPase) Hyperkalemic thyrotoxic periodic paralysis Hyperosmolarity Hypothermia	Renal parenchymal damage Nephropathies Acute kidney injury Obstructive uropathy[16] Amyloidosis[17] Glomerulonephritis Polycystic kidney disease Tubulointerstitial disease	Defect in Potassium secretion Primary hypoaldosteronism Addison’s disease Autoimmune adrenalitis Congenital adrenal hyperplasia ACTH deficiency Secondary hypoaldosteronism Renal tubular acidosis Hyporenimin hypoaldosteronism ACE inhibitors Pseudohypoaldosteronism Dehydration, Heart failure	Constipation	Rhabdomyolysis Tumor lysis syndrome Snake bite	Potasium rich diet-Spinach,green leafy vegetables,lettuce Potassium supplements Parenteral potassium citrate or potassium chloride

A lot of drugs are responsible for causing hyperkalemia. They do so by multiple mechanisms which are listed below^[18][19]:

Drug	Mechanism causing hyperkalemia
Amiloride	Blocking sodium channels of luminal membrane of principal cells
Spironolactone	Mineralocorticoid receptor antagonist (competing with aldosterone)
Beta Blockers	Decrease in cellular potassium uptake
Calcium channel blockers	Inhibition of adrenal aldosterone biosynthesis
Succinylcholine	Leakage of potassium out of cells through depolarization of cell membranes
Mannitol	*Potassium shifts out of cells due to the body’s attempt to maintain isotonicity while undergoing a hypertonic infusion
Heparin	Inhibition of adrenal aldosterone biosynthesis
Digoxin	Inhibition of Na+/K+-ATPase
ACE inhibitors	Reduction in adrenal aldosterone biosynthesis through interrupting renin-aldosterone axis and reduction in effective GFR
Angiotensin receptor-II antagonists	Reduction in adrenal aldosterone biosynthesis through interrupting renin-aldosterone axis and reduction in effective GFR
NSAIDs	Reduction in adrenal aldosterone biosynthesis through interrupting renin-aldosterone axis and reduction in effective GFR
Cyclosporine,tacrolimus	Inhibition of adrenal aldosterone biosynthesis
Trimethoprim	Blocking of sodium channels in the luminal membrane of principal cells

• Potassium is vital for maintaining the membrane potential difference of cells. Increase in blood potassium levels lead to disruption in transmemebrane potential difference.^[20]

• Hyperkalemia will depolarize the cells, thus the cells will remain excited initially.
• However, persistent depolarization will deactivate the sodium channels and sodium would not move inside the cells.
• Inability of sodium to move inside the cells will cause them to become refractory to the stimulation.
• The cells would not respond to the electric signal and will remain in a depolarized state.

• Hyperkalemia can cause fatal cardiac arrhythmias in the form of ventricular fibrillation or even cardiac arrest.
• It effects the cardiac muscle by:
  • Prolongation of membrane depolarization
  • Slower myocardial conduction
  • Shortening of the repolarization time
• This will result in peaked T waves, loss of P wave, PR interval prolongation, sine wave pattern and widening of QRS complex.^[21]

• Nervous system and muscle are effected in the same manner resulting in muscle weakness and fatigue.

Genetic conditions associated with hyperkalemia include:^[22]

• Hyperkalemic periodic paralysis
  • Hyperkalemic PP is an autosomal dominant condition with complete penetrance. The cause of hyperkalemic PP is a change in a gene that regulates the production of a protein (SCN4A) in the sodium channel of skeletal muscle. The gene is located in chromosome 17q23, and is known as SCN4A.
  • There is a defect in the sodium channels and sodium continues to leak out resulting in paralysis of the muscle.
  • During the episode of muscle paralysis,potassium leaks out into the bloodstream causing hyperkalemia.

• Congenital adrenal hyperplasia
  • Congenital adrenal hyperplasia consists of several disorders resulting from defective enzymes and proteins involved in steroid and cortisol synthesis pathways. Defects in steroid biosynthesis are caused by several genetic mutations and may lead to delayed puberty, precocious puberty or ambiguous genitalia in specific disorders.
  • In 21 hydroxylase deficiency there is decreased production of aldosterone and hence hyperkalemia occurs.
  • In 3 beta hydroxysteroid dehydrogenase deficiency decreased production of aldosterone causes hyperkalemia.

• There is as such no gross changes in pathology in hyperkalemia. It usually depends on the underlying condition causing hyperkalemia.

• There is as such no microscopic changes in pathology in hyperkalemia. It usually depends on the underlying condition causing hyperkalemia.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Raviteja Guddeti, M.B.B.S. [3], Mahmoud Sakr, M.D. [4]

Hyperkalemia is an elevated blood level (above 5.1 mmol/L) of the electrolyte potassium. “. Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of potentially fatal arrhythmias. Hyperkalemia can be caused by reasons that include increased uptake, extracellular shift, tissue breakdown and impaired excretion from the body.

• Hyperkalemia can become a life-threatening condition if potassium levels are too high and body is not able to remove it effectively.
• AKI and chronic renal failure^[1]
• Addisonian crisis
• Diabetic ketoacidosis
• Intravenous potassium supplement
• Digoxin toxicity
• Tumor lysis syndrome

The most common causes of hyperkalemia include:^[2][3]

• ACE inhibitors
• Acidosis
• Addisonian crisis
• Beta blockers
• Blood transfusion
• Cirrhosis
• Diabetic nephropathy
• High potassium diet
• Malnutrition
• Renal tubular acidosis

• Fasting
• Exercise
• Fluoride toxicity
• Hypoparathyroidism

• Congenital adrenal hypoplasia
• Hyperkalemic periodic paralysis
• Pseudohypoaldosteronism type1 and type 2

Cardiovascular	Heart failure, volume depletion
Chemical / poisoning	Ammonium Bifluoride, arsenicals, fluoride toxicity, foxglove poisoning, oleander poisoning, tungsten, white chameleon poisoning
Dermatologic	No underlying causes
Drug Side Effect	ACE inhibitors, Acetaminophen and Oxycodone, acetylsalicylic Acid, aldosterone antagonists, amiloride, Amlodipine besylate and Valsartan, angiotensin receptor blockers, Basiliximab, beta blockers, Cefepime, Cefpodoxime, celecoxib, Cidofovir, cyclosporine, diazoxide, digoxin, Drospirenone and Ethinyl estradiol, eplerenone, epsilon amino caproic acid, (EACA), erythropoietin, heparin, ibuprofen, indomethacin, isoflurane, ketoprofen, low-molecular weight heparin, Lisinopril and Hydrochlorothiazide, mannitol, melarsoprol, methotrexate, minoxidil, naproxen, Nivolumab, Nilotinib, pancuronium bromide, pimecrolimus, potassium chloride, Potassium bicarbonate, potassium citrate, pomalidomide,propofol infusion syndrome, rifaximin, sodium thiopental, somatostatin therapy, spironolactone, succinylcholine, sulindac, suxamethonium, tacrolimus, thalidomide, triamterene, trimethoprim
Ear Nose Throat	No underlying causes
Endocrine	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
Environmental	No underlying causes
Gastroenterologic	Cirrhosis, gastrointestinal bleeding
Genetic	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
Hematologic	Hemolytic anemia, leukaemia, leukocytosis, sickle cell disease, thrombotic thrombocytopenic purpura
Iatrogenic	blood transfusion , 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
Infectious Disease	HIV infection
Musculoskeletal / Ortho	Muscle damage, muscle wasting
Neurologic	Amelo-cerebro-hypohidrotic syndrome, Kohlschutter-Tonz syndrome
Nutritional / Metabolic	hydrochloride Arginine, high Potassium diet, Malnutrition
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Opthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal / Electrolyte	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
Rheum / Immune / Allergy	systemic lupus erythematosus, autoimmune adrenalitis
Sexual	No underlying causes
Trauma	crush syndrome
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	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

Acidosis ACTH Deficiency Acute glomerulonephritis Acute renal failure Addisonian crisis Addison’s disease Adrenal gland disorders Congenital adrenal hyperplasia due to 21-hydroxylase deficiency Aldosterone antagonists Amelo-cerebro-hypohidrotic syndrome Amiloride Ammonium Bifluoride Amyloidosis Angiotensin receptor blockers Arginine hydrochloride Arsenicals Autoimmune adrenalitis Beta blockers Blood transfusion Burns Celecoxib Cefepime Interstitial nephritis Chronic renal failure Cidofovir Cirrhosis Crush syndrome Cuffed blood sample Cyclosporine Dehydration Delayed separation blood sample Diabetes Diabetic ketoacidosis Diabetic nephropathy Diazoxide Digoxin Distal chloride shunt Drip arm sample EDTA blood sample Eplerenone Epsilon amino caproic acid (EACA) Erythropoietin Fasting Fluoride toxicity

Foxglove poisoning Gastrointestinal bleeding Gordon’s syndrome Heart failure Hemolysed blood sample[4] Hemolytic anemia Hemolytic uremic syndrome Heparin HIV infection Hyperglycemia Hyperkalemic periodic paralysis Hyperkalemic Renal tubular acidosis Hypernatremia Hyperosmolality Hyperphosphataemia Hypoadrenocorticism– hypoparathyroidism — moniliasis Hyporeninemic hypoaldosteronism Hypothermia Ibuprofen Indomethacin Internal bleeding Intravenous infusion Isoflurane Isolated aldosterone synthase deficiency IV fluids containing Potassium Ketoprofen Kohlschutter-Tonz syndrome Leukaemia Leukocytosis Lipoid congenital adrenal hyperplasia Lisinopril and Hydrochlorothiazide Low-molecular weight heparin Lupus nephritis Malignant hyperpyrexia Malnutrition Mannitol Melarsoprol Methotrexate Minoxidil Muscle damage Muscle wasting Naproxen Obstructive uropathy

Oleander Poisoning Oxalate blood sample Pancuronium bromide Phlebotomy complication[5] Pimecrolimus Polycystic kidney disease Potassium chloride Potassium citrate Propofol infusion syndrome Pseudohyperkalemia familial, due to red cell leak [6] Pseudohypoaldosteronism type 1 Pseudohypoaldosteronism type II Pyrimidifen Renal tubular acidosis, distal-type 1 Renal tubular acidosis, distal-type 4 Rhabdomyolysis Sea snake poisoning Selective impairment of potassium excretion Sickle cell disease Sodium thiopental Somatostatin therapy Spironolactone Strenuous exercise Succinylcholine Suxamethonium Systemic lupus erythematosus Tacrolimus Thrombotic thrombocytopenic purpura-congenital Thrombocytosis Transplant rejection Triamterene Trimethoprim Tubulointerstitial disease Tumor lysis syndrome Tungsten Ureterojejunostomy Urinary tract obstruction Urolithiasis Using clenched fist while collection of blood Volume depletion White Chameleon poisoning

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia.

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia

Organ system Conditions Distinguishing features Additional findings Symptoms Signs Labs Renal Acute kidney injury[1] Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema Tremor, confusion, edema Hyperkalemia, increased BUN and Cr, metabolic acidosis Recently developed symptoms Chronic kidney disease[2] Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema Tremor, confusion, edema Hyperkalemia, increased BUN and Cr, metabolic acidosis, hypocalcemia, hyperphosphatemia Chronic underlying disease (DM, HTN), duration of symptoms ≥ 3 months Renal tubular acidosis type-4[3] Usually asyptomatic Signs of underlying disease Hyperkalemia, normal anion gap metabolic acidosis, urine PH< 5.5 History of diabetes mellitus Endocrine DKA[4] Change in mental status, abdominal pain Decreased skin turgor, dry oral mucosa, tachycardia Hyperglycemia, increased anion gap metabolic acidosis, ketonemia Rapidly developing polyuria, polydipsia, and weight loss HHS[5] Change in mental status, abdominal pain Decreased skin turgor, dry oral mucosa, tachycardia Severe hyperglycemia, normal anion gap, increased serum osmolality Polyuria, polydipsia, and weight loss develop more insidious Congenital adrenal hyperplasia (CAH)[6][7] Poor feeding, failure to thrive, precocious puberty, short statue, hirsutism, weight loss Ambiguous genitalia, hypotension Hyperkalemia, increased 17 hydroxyprogestrone, hyponatremia Salt wasting Addison’s disease Skin hyperpigmentation, fatigue, salt craving, nausea and vomiting, amenorrhea, depression Hyperpigmentation, hypotension, pubic and axillary hair loss Hyperkalemia, decreased serum cortisol level Diagnosis by cosyntropin test Tissue break down Tumor lysis syndrome[8] Fever, weight loss, symptoms related to underlying malignancy Altered mental status, lymphadenopathy, muscle weakness Hyperkalemia, hyperphosphatemia, hypocalcemia History of underlying malignancy Rhabdomyolysis[9] Myalgia, fatigue Altered mental status, hypotension Hyperkalemia, increased muscle enzymes (CK, aldolase) History of seizure, drug overdose, or trauma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2]

The incidence of hyperkalemia is approximately 11000 per 100,000 individuals in hospitalized and 1000-2000 per 100,000 of outpatients.The exact prevalence of hyperkalemia is unknown. It changes between inpatient and outpatient cases. In one study in USA, the prevalence was 1.57. Hypekalemia occurs more in females compared to males. It is more common in older age group. African American have higher chances of developing hyperkalemia compared to non-African-Americans.

• The incidence of hyperkalemia is approximately 11000 per 100,000 individuals in hospitalized and 1000-2000 per 100,000 of outpatients ^[1]

• The exact prevalence of hyperkalemia is unknown. It changes between inpatient and outpatient cases. In one study in USA, the prevalence was 1.57 ^[2]

• Hypekalemia occurs more in males compared to females ^[3]

• It is more common in older age group.

• African American have lower chances of developing hyperkalemia as compared to non-African-Americans ^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2],Jogeet Singh Sekhon

The kidneys normally remove excess potassium from the body. Most cases of hyperkalemia occur in disorders that reduce the kidneys’ ability to get rid of potassium. This may result from disorders such as acute kidney failure, chronic kidney failure and glomerulonephritis.

• The kidneys normally remove excess potassium from the body
• Most cases of hyperkalemia are due to disorders that reduce the kidneys‘ ability to get rid of potassium ^[1][2]

• The most common risk factors for hyperkalmeia include^[3]:
  • Acute kidney failure
  • Chronic kidney failure^[4]
  • Diabetes mellitus
  • Glomerulonephritis
  • Obstructive uropathy
  • Rejection of a kidney transplant
  • Addison’s disease

• Burns
• Disorders that cause blood cells to burst (hemolytic conditions)
• Gastrointestinal bleeding
• Rhabdomyolysis from drugs, alcoholism, coma, or certain infections
• Surgery
• Traumatic injury
• Tumors
• Acidosis
• Medications
  • spironolactone
  • amiloride
  • triamterene
  • Potassium supplements (especially intravenous potassium).

• Fasting
• Exercise
• Fluoride toxicity
• Hypoparathyroidism

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon

There is insufficient evidence to recommend routine screening for hyperkalemia. However potassium levels are routinely monitored in patients with chronic kidney diseases

• There is insufficient evidence to recommend routine screening for hyperkalemia
• However potassium levels are routinely monitored in patients with chronic kidney diseases

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] Jogeet Singh Sekhon

Extreme degrees of hyperkalemia are considered a medical emergency. If left untreated hyperkalemia can cause cardiac rhythm disorders and eventually cardiac arrest leading to death. Complications that can develop as a result of hyperkalemia are arrhythmia, cardiac arrest, and neuromuscular weakness. The outcome with this condition varies. In some people, the disorder causes deadly complications, while others tolerate it well.

• Extreme degrees of hyperkalemia are considered a medical emergency
• If left untreated hyperkalemia can cause cardiac rhythm disorders and eventually cardiac arrest leading to death.^[1][2]

• Complications that can develop as a result of hyperkalemia are ^[3][4]
  • Arrhythmias
  • Cardiac arrest
  • Changes in nerve and muscle (neuromuscular) control resulting in weakness and fatigue

• The prognosis of hyperkalemia depends on the duration and the severity of hyperkalemia. The mortality rate of patients with hyperkalemia is 14%.^[5][6]
• Hyperacute and severe hyperkalemia have poor prognosis and the mortality rate is very high as compared to mild, moderate, acute and chronic hyperkalemia
• Prognosis of mild, moderate, acute and chronic is generally good if detected in time and the cause corrected.
• The prognosis worsens as potassium levels increases.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.B.B.S. [2]; Jogeet Singh Sekhon

Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case #1

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For patient information, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.B.B.S. [2]; Jogeet Singh Sekhon

Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case #1

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