Approach to Hypokalemia

Dr Garima Aggarwal

22.09.2014

APPROACH TO HYPOKALEMIA

PATHOPHYSIOLOGY

CLINICAL APPROACH

TREATMENT

Potassium homeostasis.

The ratio of intracellular to extracellular potassium determines the cellular membrane potential.

Small changes - profound effects on the function of the cardiovascular and neuromuscular systems.

Intracellular K+ affects intra to extracellular K+

With K+ depletion , K+ loss from ECF > ICF loss

causing increased Ki + / Ke+

K+ depletion : hyperpolarization

K+ retention : depolarization

Cellular K+ Content

Na+ K+ ATPase

Acid base statusPancreatic hormones : insulin , glucagonCatecholaminesAldosteronePlasma Osmolality ExerciseCellular K+ content

Factors modifying transcellular K+ distribution

Acid Base Status

H+

K+

H+

K+

ACIDOSIS

ALKALOSIS

An oversimplification in acidosis

Alkalemia promotes K+ uptake by cells Acidemia diminishes K+ uptake by cells

Recurrent contraction increases K+ egress from muscle

Modest exercise : high K+ in ECF in local environment produces vasodilatation & thereby increased regional blood flow

Severe exercise : increase plasma K+ modestly

Physical training increases Na+K+ATPase activity in skeletal muscle which helps skeletal muscle to take up K+ again

Exercise

RENAL ADAPTATION

Kidneys adapt to both acute and chronic

alterations in potassium intake.

obligatory renal losses are 10-15 mEq/d.

Maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min.

In the presence of renal failure, the proportion of potassium excreted through the gut increases.

However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load.

Renal Handling of K+Glomerulus: freely filtered

PCT, Thick As limb LOH : reabsorbed

DCT, CNT, CCD – secreted

INTERCALATED CELLS

RENAL ADAPTATIONExcretion is increased by

(1) aldosterone,

(2) high sodium delivery to the collecting duct (eg, diuretics),

(3) high urine flow (eg, osmotic diuresis),

(4) high serum potassium level

Invitro studies

Aldosterone stimulates Na+K+ATPase and thereby activating Na + influx

Aldosterone

Defined as plasma concentration of K+ < 3.5 mEq/L

Mild Hypokalemia : 3.0 – 3.5 mEq/L : asymptomatic

Moderate Hypokalemia < 3.0 mEq/L : symptomatic

Severe Hypokalemia <2.5 mEq/L

Clinical manifestations of hypokalemia vary greatly between individual

patients &

their severity depends on degree of hypokalemia

Hypokalemia

Hypokalemia

Decreased intakeRedistribution

into cells

Increased loss

Renal Extra renal

PSEUDOHYPOKALEMIA-spurious

"pseudohypokalemia" occurs in acute myelogenous leukemia

large number of leucocytes in the blood specimen (stored at room temperature)

sponge-up the extracellular potassium => artefactually low serum potassium reading

Decrease K intakeDietary – starvation, clay ingestion

IV therapy

Redistribution into cells

Alkalosis

Insulin Excess

Beta-2 agonist

Alpha antagonist

Hypokalemic periodic paralysis

Anabolic state- vit. B 12, folic acid

•GM CSF

•Total parenteral nutrition

•Hypothermia

•Barium toxicity

•Pseudohypokalemia

GI LOSS of K+

Secretory diarrhea

GIT fistula or small bowel enterostomy

malabsorption syndrome

excessive, voluminous vomiting

laxative abuse

Transtubular potassium gradient (TTKG)

To account for the potentially confounding effect of urine concentration on the interpretation of the urine potassium

the serum-to-tubular fluid ratio of potassium at the level of the cortical collecting tubule, where potassium is secreted.

TTKG = (Urine potassium/urine osmolality : serum potassium /serum osmolality)

A value less than 3 suggests that the kidney is not wasting excessive potassium, while a value greater than 7 suggests a significant renal loss..

DISTAL K+ SECRETION (TTKG>4)

With normal or low blood pressure

1.With alkalosis – Diuretic therapy, Bartters and gitelmans syndrome

2. With acidosis – RTA type 1& 2, carbonic anhydrase inhibitor therapy

3. With variable pH – post obstructive diuresis, Recovery after ATN,Mg depletion,amphotericine B

Barrter’s SyndromeSite of lesion – TAL

Abnormal NKCC2,ROMK,Cl channel

Na wasting,volume contraction

RAASNa reabs by CT

K&H secretion,met alkalosis,hypokalemia

Gitelman’s syndromeAutosomal

recessive

Abnormal NCCT

Na wasting RAAS activation

K & H secretion metabolic alkalosis,hypokalemia

DISTAL K+ SECRETION (TTKG>4)

With Hypertension

1.Hyperaldosteronism-

Primary - Conns syndrome

Secondary - Renal ischemia, malignant HTN,hypovolemia, renin secreting tumours

2. Other forms of mineralocorticoids receptor activation - cushing syndrome, apparent min. excess

3. Liddles syndrome

Hypokalemia,Hypertension & Alkalosis

Disease S.aldosterone

PRA

S.cortisol Response to steroids

Primary aldosteronism

No

GRA Yes

AME Yes

Liddle’s synd No

Adr enz def Yes

HYPOKALEMIATREATMENT

HYPOKALEMIA-TREATMENT

(1) decreasing potassium losses,

(2) replenishing potassium stores,

(3) evaluating for potential toxicities,

(4) determining the cause in order to prevent future episodes.

HYPOKALEMIA-TREATMENTIn treating hypokalemia, the first step is to identify

and stop ongoing losses of potassium.Discontinue diuretics/laxatives. Use potassium-sparing diuretics if diuretic therapy is

required (eg, severe heart failure). Treat diarrhea or vomiting. Use H2 blockers to decrease nasogastric suction losses. Control hyperglycemia if glycosuria is present.

HYPOKALEMIA-TREATMENTRepletion of potassium losses is the second step.

As a first approximation, for every decrease in serum potassium of 1 mEq/L, the potassium deficit is approximately 200-400 mEq..

Oral potassium is absorbed readily.Relatively large doses can be given safely.

HYPOKALEMIA-TREATMENT

if the hypokalemia is mild-moderate => po administration potassium chloride should occur more slowly over several days at 80 - 160 meq/day in divided doses .

HYPOKALEMIA-TREATMENTIntravenous potassium is less well tolerated because

it can be highly irritating to veins and can be given only in relatively small doses, generally 10 mEq/h.

Under close cardiac supervision in emergent circumstances, as much as 40 mEq/h can be administered through a central line.

Oral and parenteral potassium can be used safely simultaneously.

Take ongoing potassium losses into consideration

HYPOKALEMIA-TREATMENT avoid glucose-containing parenteral fluids to

prevent an insulin-induced shift of potassium into the cells.

If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells.

Replete magnesium if low.

Digoxin , liver disease –keep at 4.0 meq/l

Potassium replacement therapy

- cardiac monitoring is necessary in patients with profound hypokalemia (< 2.5 meq/L), or if cardiac arrhythmias are present, if IV potassium is planned

- 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

Potassium replacement therapy

- IV potassium diluted in saline solution the maximum concentration is 40 meq/L (peripheral lines) or 60 meq/L (central lines)

10 - 20 meq/hour (in the average-sized adult) for hypokalemia - if po potassium replacement therapy cannot be tolerated or if a malabsorption syndrome is suspected

IV infusion rate for severe or symptomatic hypokalemia

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

Thank you for your attention