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Medical decision-making and treatment
Appendix- ECG changes in hypokalemia
- causes of abnormal potassium loss in the urine ("renal wasting" diseases)
- causes of abnormal potassium loss in the stools
- causes of drug-induced hypokalemia
- algorithm to determine the cause of the hypokalemia
- diagnostic approach to metabolic alkalosis based on the urinary chloride and potassium levels
- foods with a high potassium content
- potassium supplements
| Introduction |
- the clinical effects of hypokalemia are dependent on the severity and chronicity of the hypokalemia
- chronic hypokalemia causes renal tubular damage (kaliopenic nephropathy) => decreased ability of the kidney to concentrate urine => vasopressin-resistant hyposthenuria => polyuria and worsening potassium loss
- chronic hypokalemia can also contribute to worsening hypertension in a hypertensive patient and increase the hypertensive effect of sodium loading
(* also, the hypotensive effect of diuretics is reduced in potassium-depleted patients, and enhanced in potassium-repleted patients)
- hypokalemia produces a carbohydrate-intolerance (? due to impaired insulin release and ? impaired insulin resistance) => worsening hyperglycemia in diabetics
- hypokalemia also produces a metabolic alkalosis (by ? stimulation of bicarb absorption by the proximal tubule and ? renal ammoniagenesis)
- hypokalemia can contribute to the development, or worsen the symptoms, of hepatic encephalopthy (? due to renal ammoniagenesis)
- severe (or rapidly occurring) hypokalemia can cause muscle weakness and paralysis
(* the paralysis mainly affects the proximal lower extremities => progressing to affect the upper extremities; dysphagia and dysarthria are uncommon and cranial nerve palsies are exceedingly rare)
- rhabdomyolysis can occur in severely potassium-depleted patients - especially following vigorous exercise - and muscle necrosis can rarely occur
- atrial/ventricular arrhythmias are more common in patients with underlying heart disease (especially CAD) and in patients taking digoxin
- life-threatening cardiac arrhythmias can occur when the serum potassium is very low (< 2 meq/L), or when the serum potassium is relatively low (2 - 3 meq/L) in patients with underlying heart disease, or when the patient is digoxin-toxic
| Risk factors |
- risk factors for the development of hypokalemia can be divided into four major categories - inadequate potassium intake, excessive gastro-intestinal loss, excessive renal loss or redistributional
Inadequate intake
- diet very low in potassium
- geophagia - potassium-binding clay soil ingestion
Excessive gastro-intestinal loss
- secretory diarrhea
- GIT fistula or small bowel enterostomy
- malabsorption syndrome
- excessive, voluminous vomiting
- laxative abuse
Excessive urinary loss
- hyperaldosteronism - primary or secondary
- osmotic diuresis
- diuretic drugs
- renal tubular diseases
- high urinary concentrations of anions eg. penicillin
- renal toxins eg. amphotericin B, gentamicin, toluene
- post-obstructive diuresis
- intrinsic renal transport defects (Bartter's, Liddle's and Gitelman's syndrome)
- acute insulin administration during DKA => rapid potassium uptake by the cells
- beta-sympathomimetic therapy
- hypokalemic periodic paralysis - familial or associated with thyrotoxicosis
- rapid cell growth in acute anabolic states (acute leukemia, high-grade lymphoma, following administration of granulocyte-macrophage colony-stimulating factor to a patient with refractory anemia and excess blast cells, or administration of vitamin B12 to a patient with pernicious anemia)
- transfusion of large amounts of refrigerated red cells, which "sponge-up" plasma potassium when infused
- soluble barium salt ingestion ("Ping-pang" disease - more common in China) => the barium salt blocks the potassium channels and traps potassium inside cells and prevents potassium from entering the plasma
- excessive sweating or skin loss secondary to extensive burns
- "pseudohypokalemia" occurs in acute myelogenous leukemia when the large number of leucocytes in the blood specimen (stored at room temperature) sponge-up the extracellular potassium => artefactually low serum potassium reading
| Clinical presentation |
- most patients are asymptomatic and hypokalemia is incidently found on serum electrolyte testing
- moderate-severe hypokalemia can produce generalized lassitude, muscle weakness and fasiculations, restless legs, paresthesias, depressed deep tendon reflexes
- profound hypokalemia can produce muscle paralysis if the hypokalemia is extreme (serum potassium < 2 meq/L) or if the decrease in serum potassium is rapid (hypokalemic periodic paralysis)
- patients can present with palpitations, weakness, syncope or sudden death due to cardiac arrhythmias
(* cardiac arrhythmias are uncommon in healthy patients with hypokalemia, but are far more common and significant in elderly patients with underlying heart disease)
| Diagnostic testing |
Blood work
- all patients should have a serum sodium, chloride, bicarbonate and BUN and creatinine performed in addition to the serum potassium
- a plasma aldosterone and plasma renin level should be performed in patients who have unexplained hypokalemia - especially if it is persistent or resistant to therapy, or if specific "renal potassium wasting" diseases are suspected
Urinalysis for potassium and chloride
- useful in differentiating renal from non-renal causes of hypokalemia when the etiology of the hypokalemia is not readily apparent
| Medical decision-making and treatment |
Potassium replacement therapy is immediately indicated for severe hypokalemia (< 2.5 meq/L) or if the hypokalemia is causing muscle paralysis or malignant cardiac arrhythmias => the patient should probably be admitted to an ICU for supervised IV administration of potassium
- patients with mild hypokalemia (serum potassium 3.0 - 3.5 mEq/L) do not necessarily need to be admitted to hospital => po potassium replacement therapy could be started in the ED if the patient has underlying cardiac disease (or takes digoxin), while outpatient therapy and follow-up in 48 - 72 hours may be acceptable for mild hypokalemia patients with no underlying heart disease
- patients with moderate hypokalemia (serum potassium 2.5 - 3.0 mEq/L) can be treated with po potassium, and discharged if they do not have underlying heart disease or serious hypokalemic symptoms
(* there are no definite criteria for admitting patients with moderate hypokalemia to hospital => a physician should use clinical judgment)
- after initiating any necessary potassium therapy => address the issue of "what is causing the hypokalemia?"
- cardiac monitoring is necessary in patients with profound hypokalemia (< 2.5 meq/L), or if cardiac arrhythmias are present, or if IV potassium is going to be rapidly administered
- rapid IV bolus administration of potassium is usually contra-indicated - the body has a limited ability to rapidly absorb potassium and lethal cardiac arrhythmias may result
- rapid IV administration of potassium (5 - 10 meq over 10 minutes) should be reserved for very rare situations of extreme hypokalemia causing respiratory muscle paralysis or hypokalemia-induced malignant arrhythmias
(* rapid IV administration of potassium should occur via a central line and should be physician-supervised, and a repeat serum potassium level should be performed q 30 minutes)
- IV potassium should normally be diluted in saline solution so that the maximum concentration is 40 meq/L (peripheral lines) or 60 meq/L (central lines) and IV potassium should be administered at 10 - 20 meq/hour (in the average-sized adult) for severe hypokalemia - if po potassium replacement therapy cannot be tolerated or if a malabsorption syndrome is suspected
(* IV administration at > 20 meq/hour is acceptable for a few hours
if the patient is profoundly hypokalemic)
| IV infusion rate for severe or symptomatic hypokalemia |
| 5 - 10 meq/hour | If heart block or renal insufficiency exists |
| 10 - 20 meq/hour | Standard IV replacement rate |
| 20 - 40 meq/hour | Serum potassium < 2.5 meq/L or moderate-severe symptoms |
| > 40 meq/hour | Serum potassium < 2.0 Meq/L or life-threatening symptoms |
- although IV potassium replacement therapy is a common practice, po administration is preferable in all patients who can tolerate po potassium (even if the hypokalemia is moderately severe) because oral administration of potassium is safer than IV administration and po potassium is very rapidly absorbed
(* 40 - 80 meq of potassium can be given orally in one hour if rapid replacement therapy is necessary)
- if the hypokalemia is mild-moderate => po administration should occur more slowly over several days at 80 - 160 meq/day in divided doses
(* there is no direct correlation between the serum potassium and the total body potassium deficit, but a rough estimate is to assume a total body deficit of ~ 200 - 400 meq of potassium for every 1 meq/L the serum potassium is below 4 meq/L)
- always consider the possibility of associated magnesium deficiency - especially in malnourished alcoholic or terminal cancer patients - and remember that the hypokalemia cannot be successfully treated unless the magnesium deficit is concurrently corrected
- IV magnesium replacement therapy is indicated if the serum magnesium < 1 meq/L
- a loading dose of 0.5 - 1 g of magnesium can be given IV over 15 minutes, followed by ~ 0.5 g/hour by continuous IV infusion prn
- after initiating any necessary potassium replacement therapy => determine the cause of the hypokalemia
Determining the cause of the hypokalemia
Diuretic therapy is the most common cause of hypokalemia in ED patients
Alcoholism is also a common cause of hypokalemia in ED patients
(* the cause of hypokalemia in alcoholism is multi-factorial - poor intake, associated vomiting and secondary hyperaldosteronism)
- first exclude "pseudo-hyperkalemia" due to abnormal potassium uptake by a large number of leucocytes in the blood specimen sent to the laboratory
- then consider redistributional causes - acute insulin/beta sympathomimetic therapy or an associated metabolic alkalosis (or bicarbonate therapy) or rapid new cell growth or familial/thyrotoxic periodic paralysis
- if the patient is not taking any diuretics (or if you suspect multiple etiological factors) => take a careful history to first exclude an abnormally low dietary intake, and/or abnormal GIT losses (history of extensive vomiting, copious secretory-type diarrhea, enteric fistula, enterostomies), and/or an excessive intake of licorice compounds or potassium-binding compounds (certain clay soils) and/or the ingestion of other drugs that may cause hypokalemia by various mechanisms
(see the appendix for a list of causes of abnormal potassium loss in the stools and a list of drugs causing hypokalemia)
- if there are no obvious drug causes or redistributional causes or GI losses to account for the hypokalemia => go over the clinical history with the patient and search diligently for clues that could suggest occult laxative abuse (normal urinary chloride) or surreptitious diuretic use (high urinary chloride) or surreptitious vomiting (low urinary chloride)
- suspect laxative abuse in patients who are "fixated" on their degree of bowel regularity and their body image
(* phenolpthalein will cause the urine to turn pink when the urine pH is > 9; stools can also be tested for magnesium, sulfate and phosphate purgatives)
- if the cause is still not obvious after repeat careful history-taking => measure a "spot" urine potassium and chloride level and determine the acid base status of the patient
- if the urine potassium < 20 meq/L => suggests a non-renal cause of the hypokalemia => determine the acid-base status of the patient => use the algorithm to determine the likely cause of the extra-renal cause of the hypokalemia based on the acid-base status of the patient
(* a low urinary potasium + low urinary chloride suggests GIT losses eg. surreptitious vomiting; a low urinary potassium and normal urinary chloride suggests laxative abuse)
- if the urine potassium > 20 meq/L => suggests an adrenal or renal disease causing an abnormal potassium loss => use the acid-base status of the patient, the urine chloride levels and the patient's blood pressure level to determine the likely cause of the hypokalemia (see algorithm)
- precise differentiation of the different "renal wasting" diseases usually requires supplementary laboratory testing (measurement of a serum aldosterone and serum renin level) and a special expertise in sorting out the different diagnostic possibilities => many ED physicians would prefer to defer this problem to their internist colleagues
- it is perfectly reasonable to defer diagnostic testing to the appropriate specialist, but an ED physician should not simply ignore this diagnostic dilemma - because serious disease entities could be missed by a casual, disinterested approach
- certain simple combinations of clinical features and abnormal laboratory values could suggest a particular diagnosis (see the two algorithms for further details)
- hypertension + high serum renin + high serum aldosterone => renin secreting tumor or bilateral renal artery stenosis or malignant hypertension
- hypertension + low serum renin + high serum aldosterone => primary hyperaldosteronism (serum sodium often high)
- hypertension + low serum renin + low serum aldosterone => Liddle syndrome or congenital adrenal hyperplasia or chronic ingestion of licorice-compounds containing glycyrrhizin or ingestion of other exogenous mineralocorticoids
- hypertension + normal/high serum renin + normal serum aldosterone => Cushings syndrome
- hypotension/normotension + high serum renin + high serum aldosterone => secondary hyperaldosteronism
- normotension + hypocarbotinemia (metabolic acidosis) + hyperchloremia + urine pH > 6 => distal RTA
- normotension/hypotension + hypercarbitonemia (metabolic alkalosis) + low urinary chloride => surreptitious vomiting or prolonged naso-gastric suction and excessive gastric fluid loss
- normotension/hypotension + increased serum renin + hypercarbitonemia (metabolic aklalosis) + hypomagnesemia + hypercalciuria + increased urinary chloride (> 100 meq/L) => Bartter's syndrome
(* Gitelman's syndrome has similar features to Bartter's syndrome except that hypocalciuria is present)
| Appendix |
Flattened T waves and prominent U waves (apparent
QT prolongation)
Prominent U waves combined with depressed ST
segments and flattened T waves ("roller-coaster" effect)
Causes of hypokalemia
| Causes of abnormal potassium loss in the urine - "renal potassium wasting"diseases |
Primary hyperaldosteronism
Ectopic corticotropin syndrome Cushing's syndrome Secondary hyperaldosteronism
Renovascular hypertension Malignant hypertension Apparent mineralocorticoid excess
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| Causes of abnormal potassium loss in the stools |
Infectious diarrhea
Enteric fistula Malabsorption syndromes Tumors
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| Drug-induced hypokalemia |
Due to transcellular shifts
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Increased renal loss
Diuretics
mineralocortocoid effects
High dose antibiotics
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Excess secretion in the stools
depletion of magnesium
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Algorithm
to determine the cause of the hypokalemia
Diagnostic approach to metabolic alkalosis based on the urinary chloride and potassium levels
Potassium replacement therapy
- patients with mild hypokalemia (3.0 - 4.0 meq/L) can be simply advised to increase their dietary intake of potassium
| Foods with high potassium content |
Highest content
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Very high content
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High content
Vegetables
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- patients with mild hypokalemia (3.0 - 3.5 meq/L) should be given potassium salt supplements if they are vulnerable to cardiac arrythmias eg. elderly patients with CAD
- all patients with a serum potassium < 3.0 meq/L should receive potassium supplementation
- the standard recommended potassium supplement is potassium chloride - liquid/powders/tablets
(* the elixir is acrid in taste and disliked by most patients, but it's the cheapest form; while slow-release tablets may produce intestinal ulceration and gastro-intestinal bleeding)
- the average adult dose = 20 - 40 meq of potassium chloride bid
or qid
| Oral forms of potassium available in the USA |
Liquids
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Powders
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Tablets/capsules
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- potassium carbonate (or citrate) should only be used in patients with RTA and an associated metabolic acidosis
- potassium phosphate can be used in patients with associated phosphate deficiency (malnourished alcoholics)
- the serum potassium should rise within 72 hours of commencing potassium replacement therapy
- magnesium replacement therapy is often necessary in malnourished alcoholics with hypokalemia; and hypomagnesemia should be suspected if the serum potassium does not increase within ~ 96 hours of the commencement of potassium supplementation therapy
- magnesium can be given orally - 3g qid x 4 doses prn
Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.