dyskalemias

8/14/2019 dyskalemias

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MANAGEMENT OF DYSKALEMIASAuthors

Martin Ortemberg,Lautaro Albarracin,

Ingrid Kolland,


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INTRODUCTION Potassium is the major intracellular fluid cation (ICF, 150 mEq/l), 98% of the total body

potassium (TBK) being found in the ICF. Its serum concentration varies from 3.5 to 5.0 mEq/l.

Unlike sodium, potassium can shift from intracellular to extracellular f luid (ECF) without

altering the TBK; any changes to the latter, however, are capable of altering the potassium

concentration in the ICF and ECF. The maintenance of the potassium homeostasis depends on

the balance between the ICF and ECF and between intake and excretion.

The factors that regulate the transcellular potassium shift are: diet, acid-base status, cell injury,

intense exercise, osmolaritychanges, insulin, aldosterone and -adrenergic receptors.

Under normal conditions, the fractional excretion of potassium is 10 to 15%.

The serum potassium is filtered at glomerular level, reabsorbed along the proximal tubule

(67%) and loop of Henle (20%). At distal level it is secreted (or reabsorbed), as necessary.


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RATIONALE AND ADAPTABILITYOF THE DIAGNOSTIC AND

THERAPEUTICRECOMMENDATIONS FOR

DYSKALEMIAS


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HYPERKALEMIA: DIAGNOSIS If the hyperkalemia is non critical, or once the emergency has

been handled.A. Assess the risk: Arrhythmias Background Diseases (DM, CRD,

etc.) Medication (NSAID, ACEI, ARA, calcineurin inhibitors,

collecting duct diuretics, etc.) Eating disorderB. Physical examination: Vital signs Hydration level Diuresis Search for hyper K+ symptoms (muscular weakness, flaccid paralysis,

vomiting, abdominal pain, ileum)C. Basic laboratory tests: Ionogram, urea, creatinine, serum and

urine osmolality, gasometry, glucose level and complete urine test

(isolated sample and 24-hour urine test)Attention!*Potassium in an isolated sample: may lead to interpretation errors.* Quantification of the urinary K+ excretion over 24 hours: its interpretation depends on thediet and the bodys K+ balance. Expected value in hyperkalemia > 40 mmol/l. In general, it isnot very useful.


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CALCULATION OF:1)K+/creatinine ratio in an

isolated urine sample:

This is a more reliable

measurement of the K+

excretion rate, as compared to the

K+ content in an isolated

sample.

Preferably collected in the

morning, due to the dailyvariations

in the excretion.

Expected value: in hyperkalemia>15 mmol/mmol or >150 mmol/g.

2) Transtubular potassiumgradient (TTKG):Semi-quantitative determination of theK+ secretion showing demineralcorticoid activity within thedistal nephron. The formula for thecalculation of TKKG is as follows:

TTKG = [(UK+/PK+) /(UOsmol/POsmol)] 100U being the urine concentration, Pbeing the plasma concentration andOsmol being the osmolalityExpected value: in hyperkalemia > 7.Even though the measured osmolalityis to be used for the calculation, theresults obtained using the calculatedosmolality may be comparable, as far asthe absence of other osmotically activesolutes in the urine is assumed.Requirements for interpretation: Urinary Na >25 mEq/l Osmolal U/P (urinaryosmolality/plasmatic osmolalityrelationship) > 1 (indicating thepresence of AVP effect)

3) Fractional excretion ofpotassium (FEK+):Shows the excreted potassium amountwith respect to the filtered quantity. Theformula for the calculation of FEK+ is asfollows:

FEK+ = [(U/P K) / (U/P creatinine)] 100

Normal values: with a normal GFR, 10-20%

Use: useful for evaluating hyperkalemiaina context of CRD, as it adjusts itself to theglomerularfiltration rate (GFR). As theGFR decreases, the excreted potassium

fraction rises exponentially, which allowsto maintain a proper potassium balance,up to a GFR of 15-20 ml/min.

It enables to reveal the decrease in theGFR related secretion, while the absoluteexcretion may be the same as that from anormal-kalemic patient with the sameGFR decrease.


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DIAGNOSTIC APPROACH Once the alteration in the renal potassium excretion has been confirmed, thediagnostic tools should be used, according to the renal function.

Important: patients with GFR 20 ml/min or with oliguric ARF do not require anyfurther studies.

In patients with reduced GFR, urinary

flow < 800 ml/day and/or urinary Na < 25mEq/l, said objectives may be sought withdiuretics (furosemide 20 mg IVR or 40 mgOR) or expansion with saline solution 0.9%(15 ml/kg), depending on the hydration state.

In these cases, calculate if the FEK+agrees with the GFR.

If the FEK+ is appropriate, search forthe causes of intake and/or redistributionincrease. The FEK+ may beinappropriate; this includes the cases ofoliguricARF, CRF at GFR 20 ml/min andcertain causes for FEK+ being lower asexpected for the GFR.

In patients with normal renal function, the

TKKG must be calculated; in patients with a value> 7 the causes for the decrease in the effectivecirculating volume must be investigated.

In patients with TKKG < 6, the decreasein the distal potassium secretion is confirmedand, as for those with an alteration in the renalfunction and an FEK+ lower than expected, run afludrocortisone test (0.1-0.3 mg IV or oral) or

hydrocortisone test (100 mg IV bolus), withulterior re-evaluation (at 4) of the respectivelycorresponding parameters.

Patients who achieve the expected valuesare those with low bioactivity of aldosterone,those who do not achieve them are aldosterone-resistant patients. Studies of renin andaldosterone dosing in blood should be run, inaddition.


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HYPERKALEMIA: TREATMENT

THERAPEUTIC OPTIONS

THERAPEUTIC ALGORITHM


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THERAPEUTIC OPTIONS

4. Dialysis: either hemodialysis or peritoneal dialysis are implemented upon failure of themeasures outlined above.

2. Drugs that promote the entry to the intracellular space: they are temporary and donot eliminate the potassium from the body. They show the fastest onset of action.

Insulin -adrenergic agonists Sodium bicarbonate

1. Stabilizers of the myocardial membrane:

Calcium gluconate

3. Drugs that favor the elimination of potassium: the onset of action is slower,they tend to maintain the potassium level within an appropriate range; they are notsuitable for stabilizing in an emergency situation.

DiureticsExchange resins


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THERAPEUTIC ALGORITHM

1.K+ > 6 mEq/L and/or ECG alterations(absence of P wave, widened QRS or bradycardia),prior to the administration of glucose and insulin,and/or salbutamol, administer the following:

A. Calcium gluconate 10%Adults: 10-30 ml IV.(slow). Onset of

action within 1-2 minutes. Continuous ECG monitoringrequired during infusion. The dose may be repeated after5 minutes.

If the second dose is inefficient, this measure willprobably no longer be useful (its effects last for 1 hour),and the possibility of implanting a provisionalpacemaker should be considered. Administrate with carein patients treated with digoxin.

Children: calcium gluconate 0.5ml/kg IV slow (with electrocardiographic monitoring for5 to 10 min; apart from the bicarbonate)B. Sodium bicarbonate, 1 mole

Adults: 50-150 mEq via IV for 5minutes. Onset of action: 15-30 min. Duration of action:1-2 hours. Useful in patients with hyperkalemia

underlying acidosis (pH < 7.20 or HCO3 - < 15 mmol/L).Contraindicated in case of hypernatremia and/or cardiacfailure and usually ineffective in case of chronic renalfailure.

Children: 1 to 2 mEq/kg for 15 to 30min.*Run control ionograms and ECG every 2 hours.*Once the ECG has been normalized and/or the kalemia< 6 mEq/l, administrate resins, as calcium gluconatedoes not change the serum K+ and administratingbicarbonate (like glucose and insulin, or salbutamol)does not lower the body potassium, even though it does

lower the K+ concentration .

2. K+ higher than 6 mEq/L and normalECG Insulin and glucose IV.

Adults: the usual dose is 10 UI of regularinsulin diluted in 500 ml of dextrose 5% or in250 ml dextrose 10% for intravenousadministration during 30 minutes. The onset ofaction is 15 to 30 minutes, and the duration ofaction 2-3 hours.

Children: glucose 10% 0.5-1 g/kg insulin 0.1-0.2 U/kg.

SalbutamolAdults: 0.5 mg (1 vial), diluted in 50 ml IVsaline solution, to be administered for 10-15minutes. A dose of 0.5-1 mg can also beadministered via nebulization.

*It is contraindicated in patients with ischemiccardiopathy or severe supraventriculararrhythmia. The onset of action is 15-30 min.

Children:weight < 25 kg, 2.5 mg. weight > 25kg, 5 mg. It i s prepared in 2.0 to 2.5 ml ofisotonic saline solution 0.9% and administeredvia nebulization for 10 minutes.

*Both procedures may reduce the K+ by 1-1.5 mEq/lwithin 30-60 minutes, the effects lasting for about 4-6hours.

*These measures do not eliminate the K+ from thebody; if a negative balance is needed, the followingprocedures should be used.

3. K+ lower than 6 mEq/Land normal ECG

Cation exchange resins(see above)

Diuretics: oral orintravenous furosemide

Adults: 20-200 mgaccording to renalfunction, onset ofaction at least onehour afteradministration.

Children: 1-1.5mg/kg IV.

Reduce potassiumintake, with a low fruitsan

Suspend any foods or drugs that cause the kalemia to rise; then if:


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ELIMINATION OF POTASSIUM

Cation exchange resins: calciumpolystyrene sulfonate

Adults. Oral, 15-60 g every 6-8 hours,diluted in water (not juice). Rectal

(retention enema), 30-60 g in glucosesolution 5%, 1-3 times/day, to beretained for 6 hours, then irrigate thecolon to eliminate the resin.Children: 1 g/kg with 3-4 ml glucose10% in enema to be retained for 15 min,or OR 0.5-1 g/kg in glucosated solution.

Note: Calcium resins (calciumpolystyrene gluconate -RIC-CALCIUM),administrated by OR eliminate 0.7 andadd 72.18 mg of calcium for every gram ofresin.

Hemodialysis:

-Especially indicated in severerenal failure.

-Hemodialysis eliminates some 25to 30 mEq per hour, corrects theacidosis but has the inconveniencethat a certain time is requiredbefore it can be started.

-Peritoneal dialysis is half asefficient.


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HYPOKALEMIA: TREATMENT

Purpose: to normalize the serum potassium. Define acting scenario.

Severe hypokalemia(medical emergency) Mild to moderate hypokalemia

Consider co-occurrence of hypomagnesemia The most frequently used potassium salt is KCl. The replacement of K+ should preferably be made in saline

solutions. Glucosated solutions cause the endogenous insulinproduction to rise, which may promote the uptake of potassium

by the cells, preventing a normalization of the plasmaconcentrations.

Acute therapy consists of intravenous administration of KClwhile monitoring the serum potassium concentrations.


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MODALITY REPLACEMENT

When ?

K+ < 2.5 or K+ < 3.5 and:

-Symptoms or changes in

ECG.

-Digitalized patients.

-Intolerance to oral

administration route.

-Congestive cardiac failure,

history of arrhythmias,

ischemia, AMI

At whatconcentration?

Peripheral route =up to 40 mEq/l.

Central route = upto 60 mEq/l.

At what infusionrhythm?

Adults: Not beyond20 mEq/hour(exceptionally up to40 mEq/hour).

Children: 0.5 to 1

mEq/kg/hour.

Ensure appropriate potassium intake throughdiet.

K+ supplements, in the form of tablets or syrup.

What potassium salt? Differentiatebetween

Hypokalemia with metabolic alkalosis: KCl.

Hypokalemia with metabolic acidosis: organic

potassium salts (potassium gluconate or citrate). At what dose?

Adults: replacement: 40-100 mEq/day;maintenance: 20-40 mEq/day.

Children: 3-4 mEq/kg/day.

Note: In chronic hypokalemia, for every 1 mEq/l of decrease

in the serum potassium, the potassium reserves will havedecreased between 200 and 400 mEq. Kalemias below 2mEq/l reveal a deficit in the body potassium of about 1,000

IV replacement indication

(emergency)

Chronic or mild-moderatehypokalemia(oral route)


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ReferencesModificado de Estrategias para el diagnostico y eltratamiento de las diskalemias. Capitulo 11, Compendiosobre las recomendaciones de la Sociedad Argentina deNefrologa. 2011.

Authors Amelia Bernasconi, Elsa Zotta, Martin Ortemberg, Lautaro Albarracin, CarlosMusso, Ingrid Kolland, Federico Ochoa, Stella M. Dieguez, Sebastin Lapman, Ricardo M.Heguilen

dyskalemias

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