hypo kale mia

HYPOKALEMIA

Rima Abou Arkoub

Nephrology and Hypertension (F2)

July,29,2013

Normal serum potassium levels are

considered to lie between 3.6 and 5.0 mmol/L

pathophysiology and management of hypokalemia: a clinical perspective Unwin, R. J. et al. Nat. Rev. Nephrol. 2011

The daily minimum requirement of potassium

is considered to be approximately 1600 to

2000 mg (40-50 mmol or mEq)

Young adults may consume up to 3400 mg (85

mmol) of potassium per day.

Physiological facts

(K +) Cellular shifts

Cellular shifts in K+ levels occur because cell membranes are permeable to K+ via a family of K+ channels.

Cellular uptake of K+ is promoted by:

1-Alkalemia

2- Insulin

3- adrenergic stimulation

4- xanthines such as caffeine

Gennari.FJ,hypokalemia,NEJM.1998


Mineralocorticoid secretion and distal sodium

delivery.

Increased flow rate stimulates K+ secretion by two mechanisms:

1- Stimulating reabsorption of some of the extra

Na+ in the tubular fluid, thereby further

depolarizing the apical membrane

2- By rapidly sweeping the secreted K+

downstream, thereby maintaining the

concentration gradient for further K+ efflux.

Regulation of potassium (K) handling in the renal collecting duct. Pflgers Arch. (2009).

HYPOKALEMIA

Mild hypokalemia : potassium (3-3.5 mmol/L)

Severe hypokalemia : potassium

Prevalence

More than 20% of hospitalized patients have

hypokalemia, widely defined as a serum

potassium level of less than 3.5 mmol/L.

Low serum (or plasma) concentrations of

potassium may occur in up to 40% of outpatients

treated with thiazide diuretics

National Council on Potassium in Clinical Practice review and consensus guidelines on potassium replacement can be found in Arch Intern Med 2000

Manifestations of hypokalemia

Generalized muscle weakness& paralytic ileus.

Cardiac arrhythmias (atrial tachycardia with or without block,

atrioventricular dissociation, ventricular tachycardia, and ventricular

fibrillation).

Typical electrocardiographic changes include flat or inverted T

waves, ST-segment depression, and prominent U waves.

Hypokalemia predisposes to cardiac arrhythmias by several

mechanisms, including increased cardiac automaticity, slowed

conduction, and delayed ventricular repolarization.

These effects are accentuated in patients with ischemic heart

disease or on digitalis therapy.

The risk of arrhythmias is increased with serum potassium

concentration 3.9 mEq/L.


Manifestations of hypokalemia

Chronic hypokalemia results in hypokalemic nephropathy: a

tubulointerstitial disease characterized by nephrogenic diabetes insipidus,

alkalosis, and progressive GFR loss.

Hypokalemia also has been associated with worsening hypertension.

Increased mortality in patients with heart disease, and cerebrovascular

disease.

In severe hypokalemia :rhabdomyolysis and acute renal failure

Weiner ID,Wingo CS. Hypokalemiaconsequences, causes, and correction. J Am Soc Nephrol. 1997 Khaw KT, Barrett-Connor E. Dietary potassium and strokeassociated mortality.A12-year prospective population study. N Engl J Med. 1987

Causes of Hypokalemia

Hypokalemia

Total-body potassium depletion

Excessive potassium

loss.

Renal losses. Extra renal

losses.

Inadequate intake

Transient cell shift

A Physiologic-Based Approach to the Evaluation of a Patient With Hypokalemia, Am J Kidney Dis . 2010

A standard dose of nebulized albuterol reduces serum

potassium by 0.2 to 0.4 mmol/L. A second dose

administered within 1 hour reduces it by approximately

1 mmol/L.

The caffeine in a few cups of coffee can decrease

serum potassium by as much as 0.4 mmol per liter.


Dietary K+ restriction alone is rarely a cause of

hypokalemia, as renal K+ excretion can decrease to


These anions escape reabsorption in the distal nephron,,So a more lumen negative voltage develops and the driving force for potassium excretion into the tubular fluid is enhanced

aminoglycoside, cisplatin, and the

antiviral drug foscarnet all cause

renal potassium wasting by inducing

depletion of magnesium

diuretics block chloride-associated

sodium reabsorption and,

as a result, increase delivery of sodium

to the collecting tubules, where its

reabsorption creates a favorable

electrochemical gradient for potassium secretion.

Glucocorticoids, such as prednisone have no direct effect

on renal potassium secretion, but they increase potassium

excretion nonspecifically through their effect on the

filtration rate and distal sodium delivery.

When given over the long term, these drugs reduce serum

potassium only slightly (by 0.2 to 0.4 mmol per liter).


Investigations

Renal potassium handling can be assessed using a 24-hour

urine collection OR

spot urine sample for potassium/Cr ratio.

24 hr potassium excretion of 15-20 mEq or

a spot urine potassium/Cr ratio 1-1.5 suggests an extrarenal

cause of hypokalemia.

Investigations

The transtubular potassium gradient (TTKG) has been proposed as a useful tool to assess

renal potassium handling because the equation takes into consideration the effect of renal

water handling on urine potassium concentration: TTKG*K urine (Osm urine Osm serum)+

K serum

In a healthy individual ,TTKG ranges from 8-9 and will increase to 11 with increased

potassium intake.

In patients with hypokalemia caused by extra renal potassium losses, TTKG should decrease

to 3.

it should be obtained when the cause for hypokalemia is not readily apparent.


Simply think of the TTKG as a rough measurement of aldosterone activity in the kidney.

As aldosterone's action is retention of Na with excretion of K, tubular fluid

K concentration is high if there is aldosterone action, and so is TTKG. Division by (urine osmo/plasma osmo ) is to adjust the urinary potassium

for the concentrating effects that occur in the collecting tubule, where water is removed from the urine.

Note that this formula is valid only when Uosm >300 and UNa >25

In hypo K, if TTKG is still > 7, it means that there is inapproriately

high aldosterone activity despite the hypo K, and thus renal loss of K is the

cause of the hypo K, e.g. hyperaldosteronism

If TTKG is < 5, it means that aldosterone activity is appropriately low to

conserve K, and thus the hypo K is not due to renal loss, i.e. non-renal loss

Treatment

CONSENSUS GUIDELINES FOR THE USE OF POTASSIUM REPLACEMENT IN CLINICAL PRACTICE

1. Dietary consumption of potassium-rich foods should be

supplemented with potassium replacement therapy.

Often, increasing dietary potassium intake is not completely

effective in replacing the potassium loss associated with chloride

depletion (eg, that which occurs in diuretic therapy, vomiting, or

nasogastric drainage) because dietary potassium is almost entirely

coupled with phosphate, rather than with chloride.



2. Potassium replacement is recommended for individuals who are

subject to nausea, vomiting, diarrhea, bulimia, or diuretic/laxative

abuse. Potassium chloride has been shown to be the most effective

means of replacing acute potassium loss.

A dosage of 20 mmol/d of potassium in oral form is generally

sufficient for the prevention of hypokalemia, and 40 to 100 mmol/d

sufficient for its treatment



3.Potassium replacement should be routinely considered

in patients with CHF, even if the initial potassium

determination appears to be normal (eg, 4.0 mmol/L).

In patients with CHF or myocardial ischemia, mild-to-

moderate hypokalemia can increase the risk of cardiac

arrhythmia.



4. It is prudent to maintain optimal potassium levels in

patients at high risk for stroke (including those with a

history of atherosclerotic or hemorrhagic cerebral vascular

accidents).

prospective studies suggest that the incidence of fatal and

nonfatal stroke correlates inversely with dietary potassium

intake.


The management of hypokalemia should take into consideration the following:

(1) The amount of potassium necessary

(2) The potassium preparation and route of

administration

(3) The rate of potassium repletion.

With simple potassium depletion, it has been

conservatively estimated that :

every 0.3 mEq/L decrease in serum potassium

concentration corresponds to a 100-mEq

deficit in total-body potassium.

A Physiologic-Based Approach to the Treatment of a Patient With Hypokalemia Am J Kidney Dis. 2012

Potassium salts include: 1. potassium chloride 2. potassium phosphate 3.potassium bicarbonate.

Potassium chloride administration results in distal

nephron chloride re absorption in exchange for

bicarbonate secretion, which corrects the metabolic

alkalosis.


Potassium chloride (KCl) is available in either liquid or tablet formulations.

Although liquid forms may be less expensive,

they have a strong, unpleasant taste and often

are not well tolerated.

Be Careful

Infusion rate 10-20 mEq/hour.

Use central venous catheter for infusion rates > 10 mEq/hour.

Maximum daily dose 240-400 mEq/day .

Continuous cardiac monitoring recommended for infusion rate > 10

mEq/hour.

Maximum concentration of potassium solutions:

80 mEq/L via peripheral vein, and 120 mEq/L via central vein infusion.

In non emergent situations requiring intravenous potassium replacement,

20-40 mEq of potassium can be added to each liter of glucose-free

solution.

Glucose may predispose to arrhythmias or neuromuscular paralysis by

stimulating insulin release and potassium shift into cells.

For a patient with GFR 30 mL/min/1.73 m2 (0.5 mL/s/1.73 m2), these

rates should be decreased by 50%-80% with frequent (2- to 4-hour)

reassessment of serum potassium concentration.


Serum potassium (K) concentration generally

should not be checked until:

1-2 hour after an intravenous (IV) dose is

given and 2-4 hours after an oral dose.

Mg Deficiency

Hypokalemia can be refractory to treatment due

to a persistent increase in urinary potassium

excretion because:

intracellular magnesium normally inhibits

potassium secretion through the ROMK (renal

outer medullary K channel; channel in the distal

nephron.)


Thank you

hypo kale mia

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