CME - Hypokalemia

APPROACH TO HYPOKALEMIA

Dr.M.EDWIN FERNANDOAssociate Professor & Head Department of NephrologyChengalpattu Medical College

Goals of this talk . . .

SESSION OBJECTIVES Learn to effectively assess & manage hypokalemia Apply your knowledge to real cases!

LEARNING METHODS Lecture/material review Interactive case scenarios Practical approach to handling hypokalemia in MOST

hospitalized patients

Guideline for supplementing K based on some evidence-based medical recommendations

Big head - Think big

Big ears - listen

patiently

Narrow eyes - Watch deeply

Long nose - Poke around

inquisitively

Small mouth - Speak less &

listen more

POTASSIUM. . .

Most abundant cation in the human body Atomic no.:19 Molecular weight : 39 Maintenance of k balance –

essential for a variety of cellular functions & neuromuscular transmission

Total body stores : 3000 – 4000mEq 98% - located in the cells

POTASSIUM. . .

Intracellular K+ concentration : 140 meq/l Extracellular concentration : 4-5 meq/l Difference is maintained by the Na+-

K+-ATPase Ratio of K+ concentration inside cell &

outside - major determinant of resting membrane potential

Participates – protein & glycogen synthesis

POTASSIUM METABOLISM

K HOMEOSTASIS – KEY HORMONES

Gennari FJ,NEJM,339:451-458:1998

Na & K transport in P cell in CCD

www.uptodate.com

ALDOSTERONE ACTION IN PRINCIPAL CELLS

Hypokalemia Overview

Plasma K < 3.5 mEq/L Occurs in > 20% of hospitalized

patients May be asymptomatic Usually does not require emergency

supplementation over minutes to hours

Can be dangerous - arrhythmias, rhabdomyolysis, paralysis

HYPOKALEMIA

Clinical manifestations determine urgency & magnititude of treatment, not laboratory values

Frequent reassessment of K required

ABG - useful

HYPOKALEMIA – CLINICAL MANIFESTATIONS

CVS : ECG changes,atrial/ventricular arrhythmias,digitoxicity

SKELETAL MUSCLE : Weakness,cramps,tetany,paralysis, rhabdomyolysis

SMOOTH MUSCLE : Constipation,Ileus,urinary retention

ENDOCRINE : Carbohydrate intolerance

HYPOKALEMIA – RENAL EFFECTS

Impaired concentrating ability – polyuria & polydipsia – Nephrogenic DI

Impaired ammonia production – hepatic failure

Impaired urinary acidification Renal insufficiency - RBF,GFR Cl wasting/Metabolic alkalosis Renal cyst formation Tubular vacuolization Interstitial nephritis

PSEUDOHYPOKALEMIA

Abnormal WBCs – in large numbers(AML) – can take up extracellular K when stored at room temp

Apparent hypokalemia – artefact of storage procedure

Rapid separation of plasma/storing at 4 deg C – confirms diagnosis, avoids this artefact & inappropriate Rx Kamel KS,1996

HYPOKALEMIA - CAUSES

DRUGS GI LOSS : Vomiting,NG suction,diarrohea SKIN :Profuse sweating,extensive burns HORMONES : Aldosterone,Steroids, RVH

Malignant HT,Renin secreting tumors,CAH BICARBONATURIA : d

RTA,Rx of p RTA,Rx of met. Alkalosis MAGNESIUM DEFICIENCY INTRINSIC RENAL TRANSPORT DEFECTS :

Bartter´s,Gitelman´s,Liddle´s syndromes

HYPOKALEMIA – DRUG INDUCED

TRANSCELLULAR K SHIFT

RENAL K LOSS

K LOSS IN STOOL

EpinephrinePseudoephedrineSalbutomolTheophyllineRitodrineVerapamilChloroquineInsulin overdose

AcetazolamideThiazidesLoop diureticsFludrocortisonePencillinAminoglycosideAmphotericin BCisplatin

PhenolphthaleinNa polystrene sulfonate

HYPOKALEMIA - ECG ST depressions with prominent U waves &

prolonged repolarization

HYPOKALEMIA - ECG Prominent U wave in V3 & V4 giving the conjoined T- U

wave the appearance of "camel's hump" "apparently" prolonged QT interval in S2 & AVF - due to

the T wave is actually a U wave with a flattened T wave merging into the following U wave – "roller coaster effect "

HYPOKALEMIA - STEPWISE APPROACH

Transtubular Potassium Gradient

TTKG = Uk x Posm Sk x Uosm

During hypokalemia -TTKG should fall <3 - indicating appropriately reduced urinary excretion of K

TTKG > 4 – indicates renal K loss is due to increased distal K secretion Ethier JH, Am. J. Kidney Dis. 15 (4): 309–15,1990

Approach to Hypokalemia

Step 1: Redistribution or depletion? Redistribution causes

Insulin therapy - DKA Beta 2 agonists - Salbutomol Metabolic alkalosis Beta 2 adrenergic stimulation – AMI cell proliferation – Rx of megaloblastic anemia Barium poisoining

Replacement of potassium in these settings may lead to overshoot & hyperkalemia


Step 1: Redistribution or depletion? Depletion causes (common)

GI tract losses (diarrhea, vomiting) Loop/thiazide diuretic therapy Other medications (e.g. amphotericin B) Osmotic diuresis (DKA) Refeeding syndrome (NEVER underestimate!) Endocrinopathies (mineralocorticoid excess) Salt wasting nephropathies/RTA’s Magnesium deficiency (NEVER overlook!)


Step 2: Estimate the deficit For every 100 mEq below normal,

serum K+ usually drops by 0.3 mEq/L Highly variable from patient to patient,

however!!

S.K(mEq/L)

3.5 3 2 <2

TOTALK deficit (mEq/L,70 kg)

125 -250 150-400 300-600 500 -750

HYPOKALEMIA & TOTAL K DEFICIT

Sterns RH, Medicine 60:339-354:1981


Step 3: Choose route to replace K+

In nearly all situations, ORAL replacement is PREFERRED over IV replacement

Oral is quicker Oral has less side effects (IV burns!) Oral is less dangerous

Choose IV therapy ONLY in patients who are NPO (for whatever reason) or who have severe depletion

Approach to Hypokalemia Step 4: Choose K+ preparation

Oral therapy Potassium Chloride is PREFERRED AGENT

Especially useful in Cl-responsive metabolic alkalosis

in ECF K quicker with KCl compared to other salts Potassium Phosphate useful when coexistant

phosphorus deficiency Often useful in DKA patients

Potassium bicarbonate, acetate, gluconate, or citrate useful in metabolic acidosis

ORAL POTTASIUM CHLORIDE SOLUTION

15 ML 20 mEq/L


Step 4 (con’t): Choose K+ prep IV therapy

Adjunct to maintenance fluids (10-20 mEq/L) “The surgical intern’s way” Try to avoid using it!!!

you often forget it’s there hyperkalemia can then develop, especially in

patients that get ARF in the hospital IV rider/”piggyback”

Generally 40-60 mEq KCl is PREFERRED AGENT again Avoid dextrose solution (trigger insulin, shift K+)

IV 15%POTTASIUM CHLORIDE 1ml 2 mEq/L 10 ml 20 mEq/L


Step 5: Choose dose/timing Mild/moderate hypokalemia

3.0 to 3.5 mEq/L 60-80 mEq PO (or IV) QDay divided doses Sometimes will require up to 160 mEq per day

(refeeders, lots of diarrhea, IV diuretics) Avoid too much PO at once

GI upset or just poor response Usually divide as BID or TID dosing


Step 5 (con’t): Choose dose/timing Severe hypokalemia (< 3.0 mEq/L)

Can use combination of IV and PO, again with PO preferred if at all possible

Avoid more than 60-80 mEq PO in a single dose

Avoid IV infusion rates faster than 20 mEq/hour—can cause arrhythmia!!!

Most protocols won’t allow more than 10 mEq/hour rates on the floors (ICU’s too?)


Step 6: Monitor/reassess Severe hypokalemia, DKA patients

Reassess labs Q4-6 hours Moderate hypokalemia, IV diuresis

patients Reassess labs BID to TID as needed

Mild hypokalemia Reassess labs QDay or less as needed

IV Fluid Iso M Iso P Iso G Iso E RL

K(mEq/L) 35 20 17 10 4

K CONCENTRATION OF IV FLUIDS


Step 7: Housekeeping/follow up BE AGGRESSIVE in DKA patients & IV diuresis

patients May want to keep K+ over 4.0 or even 4.5

mEQ/L in cardiac patients, especially in those with arrhythmias

BE GENTLE in patients with acute or chronic renal failure

May wish to cut doses in half, double intervals, or not replace at all

May need to monitor very closely NEVER forget to check for & treat

hypomagnesemia in refractory hypokalemia!!!

Hypokalemia – TAKE CARE . . .

Monitor IV K – ECG & S.K levels Never give IV push Never add KCl to Iso M

DON’T GIVE MORE THAN10-20mEq/hr40 mEq/L240 mEq/L/day

REMEMBER – THAT HYPOKALEMIA IS SAFER THAN HYPERKALEMIA

AVOID OVERENTHUSIASM in Rx

K RICH FOOD

Fruit juices Tender coconut

water Banana Juicy fruits

Dry fruits Chocolate Coffee Soups Salt substitutes

ACID – BASE DISORDERS IN HYPOKALEMIA

Metabolic acidosis

Metabolic alkalosis

DKA Diuretic therapy

RTA Vomiting, NG

LGI loss( diarrhea, laxative abuse

Mineralocorticoid excess

Salt-wasing nephropathy

Penicillin derivatives

Liddle, Bartter, Gitelman syndromes

HYPOKALEMIA & ABG

HYPOKALEMIA & CONTRACTION ALKALOSIS

UCl IN METABOLIC ALKALOSIS & K

HYPOKALEMIA,HT,METABOLIC ALKALOSIS - DIFFERENTIALS

HYPOKALEMIC METABOLIC ALKALOSIS WITHOUT HT

HYPOKALEMIA & PARALYSIS

Ok, You Think You Got It???

Let’s try it out on some cases Real cases from real patients

Figure out what you would do...

Case 1

30,F Diarrohea,muscle weakness ECG – s/o hypokalemia LABS – Na 140,K 2.1,Cl 117,

bicarb 10,Ph 7.26,Pco2 23 What is your diagnosis? Which would you correct first?

Case1 - discussion

Hypokalemic metabolic acidosis due to diarrohea

Correct hypokalemia first Correction of acidemia pushes K

into cells - further worsening K!

Case 2

36 F Diuretics – twice weekly HT,JVP – 5cm,skin turgor LABS – Na 136,K 3,Cl 98,Bicarb

29,Ph 7.47,UNa 60,UK 45,UCl 48 NS 2L in 1hr,UNa 20 What is your diagnosis &

differentials

Case 2 - discussion

HT,Hypokalemic Metabolic Alkalosis & kaliuresis – PRIMARY HYPERALDOSTERONISM

Diuretic Rx for HT – can mimic Hypovolemia, slight Na,

UNa after NS – BEST EXPLAINS UCl – accurate indicator of volume

depletion in metabolic alkalosis

Case 3

22,F Weakness – persistent O/E – NAD LABS – Na 136,K 2.7,Cl 108,bicarb

17,Ph 7.3,U Na 7,U K 12 What is your diagnosis?

Case 3 discussion

Low UK – extra renal loss Low UNa – volume depletion Metabolic acidosis – diarrohea SUSPECT LAXATIVE ABUSE

Case 4

22,F Easy fatigability & weakness LABS – Na 141,K 2.1,Cl 85,

Bicarb 45,UNa 80,UK 170 What are your differentials ? What further testing you will order ?

Case 4 - discussion

Unexplained K, UK wasting & metabolic alkalosis – diuretic use, vomiting, primary hyperaldosteronism

Urinary Cl – helps further differentials

Case 5

S.K 2.7 Bicarb 27 PH 7.43 UK 10 Uosm 102 – Primary waterloadPRIMARY POLYDIPSIA

Case 6

S.K 2.7 Bicarb 27 Ca 7.3 Alb 4.1 Ph 7.46 UK 45HYPOMAGNESEMIA

Case 7

S.K 2.7 Bicarb 14 Ph 7.28 UK 52 Urine Ph 6 UAG + 25RENAL TUBULAR ACIDOSIS

ODUVANTHALAI leaves - Cleistanthus collinus is an extremely toxic plant poison

Cleistanthin A & B, the toxins of Cleistanthus collinus,are diphyllin glycosides which produce cardiac arrhythmias, urinary potassium wasting, hypoxia, metabolic acidosis & hypotension

We report ARDS, distal renal tubular acidosis and distributive shock secondary to inappropriate vasodilatation in a case following ingestion of its leaves J Assoc Physicians India. 2006 Sep;54:742-4

Cleistanthus Collinus PoisoningSPE Benjamin, M Edwin Fernando, J Jerene Jayanth, B Preetha

Primary Sjögrens Syndrome Presenting with DistalRenal Tubular Acidosis & RhabdomyolysisEBS Prakash, M.Edwin Fernando, Malathi Sathiyasekaran, RM Bhoopathy, JJ Jayanth

Primary Sjögrens syndrome (PSS) is rare in India Clinically manifest renal disease in PSS is

uncommon & is usually an autoimmune tubulointerstitial nephritis presenting with distal renal tubular acidosis (dRTA) or a urinary concentrating defect.

Hypokalemic paralysis due to dRTA in PSS is rare but well documented in medical literature

Rhabdomyolysis as a consequence of hypokalemia in PSS is exceptional

We report a case of PSS with dRTA & rhabdomyolysis causing prolonged respiratory failure and quadriparesis

J Assoc Physicians India. 2006 Dec;54:949 - 50

CASE 10

GITELMAN SYNDROME

HYPOKALEMIA IN LEPTOSPIROSIS

Hypokalemia – 26 to 40% Seguro AC,Nephron 55:146-151,1990

Kaliureis – inhibition of Na reabsorption in PCT with ↑ Na delivery to CD for Na-K exchange Abdulkader RC,Am J Trop Hyg 54:1-6,1996

OMP of leptospires – inhibit Na – K ATP ase – secondary effects on Na transport at luminal sites Younes-Ibrahim M,CR Acad Sci III 318:619-625,1995

Inhibition of Na –K - Cl cotransport in m TAHL Yang CW J Am Soc Nephrol 11;2017-2026,2000

Urinary concentrating ability Respiratory alkalosis - hyperkaliuria Leptospirosis - current scenario in

India,S. Shivakumar Medicine Update 2008

HYPOKALEMIA Recap of Major Learning Points Minimise hypokalemia – adequate intake PO almost always preferred over IV KCl is preferred preparation Don’t give too much too quickly Be aggressive in DKA & IV diuresis

patients,arrhythmia,musular paralysis Be gentle in renal failure patients Don’t forget to check magnesium levels in

refractory hypokalemic patients Remember genetic & endocrine causes galore –

deligent work up essential

Dr.M.A. MuthusethupathiDr.M.JayakumarDr.R.VijayakumarDr.N.Gopalakrishnan

THANKS . . .

CME - Hypokalemia

Health & Medicine

Transcript of CME - Hypokalemia