Transcript Hyperkalaemia talk and a little hypokalaemia

HYPERKALAEMIA TALK
AND A LITTLE
HYPOKALAEMIA
BY
DR NIHAL ABOSAIF
CONSULTANT ACUTE PHYSICIAN
OBJECTIVES OF THE TALK
• 1- TO UNDERSTAND THE CAUSES OF HYPERKALAEMIA
• 2- TO KNOW HOW TO DIFFERENTIATE BETWEEN THE SEVERITY OF CASES OF HYPERKALAEMIA
• 3- TO KNOW HOW TO MANAGE HYPERKALAEMIA AND HYPOKALAEMIA
• 4- TO UNDERSTAND SOME OF THE PATHOPHYSIOLOGY BEHIND DIFFERENT SCENARIOS
• 5- IDENTIFY SOME CAUSES OF HYPOKALAEMIA AND HOW TO DEAL WITH THEM.
PHYSIOLOGY
 POTASSIUM IS ONE OF THE BODY'S MAJOR IONS.
 NEARLY 98% OF THE BODY’S POTASSIUM IS INTRACELLULAR.
 THE RATIO OF INTRACELLULAR TO EXTRACELLULAR POTASSIUM IS
IMPORTANT IN DETERMINING THE CELLULAR MEMBRANE POTENTIAL.
 SMALL CHANGES IN THE EXTRACELLULAR POTASSIUM LEVEL CAN HAVE
PROFOUND EFFECTS ON THE FUNCTION OF THE CARDIOVASCULAR AND
NEUROMUSCULAR SYSTEMS.
 THE KIDNEY DETERMINES POTASSIUM HOMEOSTASIS, AND EXCESS
POTASSIUM IS EXCRETED IN THE URINE.
INTRODUCTION
potassium is necessary for the maintenance
of normal charge difference between
intracellular and extracellular environments.
potassium homeostasis is tightly regulated by
specific ion-exchange pumps (primarily by a
cellular, membrane-bound, sodium-potassium
ATP-ase).
Derangements of potassium regulation often
lead to neuromuscular, gastrointestinal, and
cardiac conduction abnormalities.
CASE 1 SCENARIO
• 55 YR OLD MALE WITH KNOWN TYPE 2 DM, HTN, HYPERCHOLESTEROLAEMIA AND IHD
PRESENTED WITH INCREASED SOB, CHEST TIGHTNESS, MILD CONFUSION AND TACHYCARDIA.
• HE DEVELOPED URINARY FREQUENCY, DYSURIA AND CLOUDY URINE FOR THE LAST COUPLE OF
DAYS.
• HE NORMALLY TAKES PERINDOPRIL 5MG OD, ASPIRIN 75MG OD, FUROSEMIDE 40MG OD,
SIMVASTATIN 40MG NOCT, BISOPROLOL 5MG OD AND AMLODIPINE 5MG OD.
CASE 1 SCENARIO
• EXAMINATION; BP 170/100, HR 95/M, RR 26/M, SATS 95% AND T 36.7C
• CHEST; BILATERAL FINE BASAL CRACKLES
• HEART AND ABDOMEN
NAD
• BLOODS: S.CREAT 250MMOL/L, S.BUN 20, S.K 6.5, S.NA 140
• LFTS, FBC NAD
• CRP 25
• ABG; PH 7.25, PCO2 3.5, PO2 10, HCO3 15, BE -7, LACT 1.5
ECG
MANAGEMENT
• WHAT’S WRONG WITH THIS PATIENT
• WHAT’S YOUR FIRST PRIORITY
• FIRST LINE THERAPY
• 2ND LINE
• MAINTENANCE TREATMENT
MANAGEMENT- CASE 1
• 1-ACUTE ON CHRONIC RENAL FAILURE
• CORRECT POTASSIUM LEVEL BY GIVING ONE DOSE OF CALCIUM GLUCONATE 10MG
AMPOULE
• INSULIN DEXTROSE
• STOP NEPHROTOXIC MEDICATIONS
• IVI (BE WARE OF LV FUNCTION)
• TREAT UNDERLYING CAUSE; UTI, RENAL ACIDOSIS, REFER TO RENAL PHYSICIANS FOR F/U
CASE 2 SCENARIO
• 75 ELDERLY GENTLEMAN WITH KNOWN BPH AND MILD HTN
• PREVIOUSLY FIT AND WELL
• BECAME VERY CONFUSED OVER LAST 3 DAYS THEN WAS UNABLE TO PASS URINE FOR THE
LAST 12 HOURS WITH DULL ACHING PAIN IN THE SUPRAPUBIC REGION
• WIFE CALLED GP TO SEE PATIENT BUT SUDDENLY HE BECAME UNRESPONSIVE AND VERY
BREATHLESS.
CASE 2 SCENARIO
• EXAMINATION; BP 70/40, HR 35/M, RR 30/M, SATS 85% AND T 36.7C
• CHEST; NAD
• HEART AND ABDOMEN
NAD
• BLOODS: S.CREAT 800MMOL/L, S.BUN 50, S.K 8.5, S.NA 140
• LFTS, FBC NAD
• CRP 45
• ABG; PH 7.05, PCO2 2.5, PO2 20, HCO3 5, BE -17, LACT 9
ECG-1
ECG 2
MANAGEMENT
• WHAT’S WRONG WITH THIS PATIENT
• WHAT’S YOUR FIRST PRIORITY
• FIRST LINE THERAPY
• 2ND LINE
• MAINTENANCE TREATMENT
MANAGEMENT- CASE 2
• IMMEDIATE MANAGEMENT OF HYPERKALAEMIA AS LIFE THREATENING
• GET ITU IMMEDIATELY
• IV CALCIUM CHLORIDE OR CALCIUM GLUCONATE UP TO 50 MG INSTANTEOUSLY UNTIL ECG
CHANGES
• IV INSULIN DEXTROSE
• IV SODIUM BICARBONATE
• NEBS WHEN SLIGHTLY BETTER
• URGENT DIALYSIS AFTER STABILISATION
MANAGEMENT- CASE 2
• POSSIBLE CAUSE IS RENAL OBSTRUCTION, ? STONE, MASS OR ENLARGED PROSTATE
• URGENT USS KUB TO R/O HYDRONEPHROSIS
• NEPHROSTOMY
• RENAL AND UROLOGY RV
CASE 3 SCENARIO
• 25 YEAR OLD FEMALE WITH IDDM PRESENTED WITH DIARRHOEA AND VOMITING. SHE WAS
UNABLE TO KEEP ANY FLUIDS IN AND BECAME VERY DEHYDRATED.
• SHE DIDN’T HAVE HER INSULIN DOSES FOR THE LAST 24HOURS AS SHE FELT VERY TIRED AND
LETHARGIC.
• ON ARRIVAL TO A&E, SHE LOOKED VERY DEHYDRATED, SOB AND VOMITED TWICE IN RESUS.
CASE 3 SCENARIO
• EXAMINATION; BP 80/50, HR 125/M, RR 26/M, SATS 95% OA AND T 36.7C
• CHEST; CLEAR
• HEART AND ABDOMEN
NAD
• BLOODS: S.CREAT 110MMOL/L, S.BUN 20, S.K 7.0, S.NA 120
• LFTS, FBC WBCS 15, N 13, HB 15
• CRP 35
• ABG; PH 7.02, PCO2 2.5, PO2 11, HCO3 15, BE -8, LACT 5
MANAGEMENT
• WHAT’S WRONG WITH THIS PATIENT
• WHAT’S YOUR FIRST PRIORITY
• FIRST LINE THERAPY
• 2ND LINE
• MAINTENANCE TREATMENT
MANAGEMENT- CASE 3
• HYPERKALAEMIA IS SECONDARY TO DKA
• INSULIN DEFICIENCY CAUSED SHIFT OF K FROM IC COMPARTMENT TO EC COMPARTMENT
• TREATMENT IS BY CORRECTING DKA AS IN PROTOCOL
• IVI 1,2,4, 6 HOURLY BAGS OF IV N SALINE
• FIXED RATE INSULIN
• CHECK ABG HOURLY
• IF K STARTS TO BE LOW THEN START GLUCOSE 5% AND K INFUSION
CASE 4 SCENARIO
• 43 YEAR OLD WOMAN RETURNED FROM A TRIP TO CYPRUS WITH SEVERE D&V.
• SHE WAS PREVIOUSLY FIT AND WELL WITH NO MEDICAL ILLNESSES.
• SHE WAS TRYING TO DRINK AS MUCH AS SHE CAN BUT KEPT ON HAVING RUNNING
THROUGH DIARRHOEA.
• SHE FEELING VERY TIRED AND LETHARGIC AFTER THREE DAYS THEN WASN’T ABLE TO MOVE
HER LOWER LIMBS
CASE 4 SCENARIO
• ON EXAMINATION, BP 90/60, HR 45/M, RR 12/M, SATS 95% OA AND T 37.7C
• CHEST AND HEART; CLEAR
• ABDOMEN , SOFT BUT TENDER AND DISTENDED AND SLUGGISH BOWEL SOUNDS
• NEURO: POWER 1/5 IN BOTH LL, NO SENSORY LOSS OR SPEECH CN LOSS.
• MILD DYSPHAGIA
• BLOODS: S.CREAT 120MMOL/L, S.BUN 20, S.K 2.0, S.NA 120
• LFTS, FBC WBCS 15, N 13, HB 10
• CRP 150
• ABG; PH 7.5, PCO2 5.5, PO2 9, HCO3 28, BE +3, LACT 3
•
MANAGEMENT
• WHAT’S WRONG WITH THIS PATIENT
• WHAT’S YOUR FIRST PRIORITY
• FIRST LINE THERAPY
• 2ND LINE
• MAINTENANCE TREATMENT
MANAGEMENT- CASE4
• HYPOKALAEMIA SECONDARY TO D&V
• PARALYSIS SECONDARY TO HYPOKALAEMIA
• TREATMENT;
• IV POTASSIUM INFUSION THROUGH A CENTRAL LINE
• RATE 20-40 MMOL/HOUR
• IVI
UNDERSTANDING CAUSES
• HYPERKALEMIA IS MOST OFTEN DUE TO DECREASED URINARY POTASSIUM EXCRETION
SECONDARY TO ACUTE OR CHRONIC KIDNEY DISEASE AND/OR DISORDERS OR DRUGS THAT
INHIBIT THE RAAS.
• • LESS COMMONLY, TOTAL BODY POTASSIUM CAN REMAIN THE SAME OR EVEN DECREASE
AND POTASSIUM CAN MOVE OUT OF THE CELLS SECONDARY TO VARIOUS PROCESSES (SUCH
AS HYPERGLYCEMIA). THIS RESULTS IN REDISTRIBUTIVE HYPERKALEMIA.
INDICATIONS FOR TREATMENT
• HYPERKALEMIA PER LAB RESULTS WITH ECG CHANGES PRESENT SERUM POTASSIUM GREATER
THAN 6.5 TO 7 MMOL/L
• • A SERUM POTASSIUM THAT IS RAPIDLY INCREASING
• – NOTE HERE THAT IN PATIENTS WITH SUBSTANTIAL TISSUE BREAKDOWN (EG,
RHABDOMYOLYSIS, CRUSH INJURY, TUMOR LYSIS SYNDROME) LARGE AMOUNTS OF
POTASSIUM IS RELEASED FROM THE CELLS, WHICH CAN LEAD TO RAPID AND
• SUBSTANTIAL ELEVATIONS IN SERUM POTASSIUM. SO AGGRESSIVE TREATMENT IS INDICATED
EVEN WITH ONLY SLIGHT INCREASE IN POTASSIUM PER SERUM STUDIES.
• ESSENTIALLY THE TREATMENT COMES DOWN TO ACUTELY MANAGING HYPERKALEMIA AND ITS
ADVERSE RESULTS AND THEN ULTIMATELY REMOVING
• EXCESS POTASSIUM IF THE SITUATION CALLS FOR IT.
• – THIS CAN BE BROKEN DOWN IN TO THREE APPROACHES TO THE TREATMENT
• • 1) ANTAGONIZING THE MEMBRANE EFFECTS OF POTASSIUM
• – USING CALCIUM
• • 2) DRIVING EXTRACELLULAR POTASSIUM INTO THE CELLS
• – INSULIN WITH GLUCOSE, BETA-2-ADRENERGIC AGONISTS AND SODIUM
• BICARBONATE
• • 3) REMOVING EXCESS POTASSIUM FROM THE BODY
• – DIURETICS, RESINS OR DIALYSIS
MECHANISM OF ACTION OF CALCIUM
• MECHANISM: DIRECTLY ANTAGONIZES THE MEMBRANE ACTIONS OF HYPERKALEMIA.
• • HIGH LEVELS OF POTASSIUM INDUCE DEPOLARIZATION OF THE RESTING MEMBRANE POTENTIAL WHICH LEADS TO
INACTIVATION OF SODIUM CHANNELS AND DECREASED MEMBRANE EXCITABILITY. THIS LEADS TO THE CARDIOTOXICITY
OF HYPERKALEMIA. THIS IS A POTENTIALLY FATAL COMPLICATION OF HYPERKALEMIA SO CALCIUM TX IS VERY
IMPORTANT EARLY IN SEVERE CASES.
• – ONSET: EFFECT OF IV CALCIUM IS SEEN WITHIN MINUTES AND LASTS FOR 30-60 MINUTES.
• – INDICATIONS: SEVERE MANIFESTATIONS WITH WIDE QRS COMPLEXES OR LOSS OF P WAVES. ESSENTIALLY IN
PATIENTS WHERE IT IS TOO RISKY TO WAIT THE 30 MINUTES TO AN HOUR IT TAKES OF INSULIN TO PROVIDE BENEFITS.
• – EFFECT: PROTECTS HEART BUT DOES NOT CHANGE SERUM POTASSIUM LEVELS.
• – DOSE: CALCIUM GLUCONATE 1000 MG OVER 2-3 MINUTES. CALCIUM CHLORIDE 500 TO
• 1000 MG OVER 2-3 MINUTES. CENTRAL ACCESS PREFERRED WITH CALCIUM CHLORIDE DUE TO POSSIBLE PERIPHERAL
VEIN IRRITATION AND EXTRAVASATION LEADING TO TISSUE NECROSIS. REPEAT EITHER AFTER 5 MINUTES IS EKG
CHANGES PERSIST.
• – SPECIAL NOTE: IN PATIENTS BEING TREATED WITH DIGITALIS CALCIUM SHOULD BE ADMINISTERED MORE SLOWLY
AND WITH A MORE DILUTE SOLUTION. THIS IS TO AVOID CARDIOTOXIC EFFECTS OF CALCIUM THAT PATIENTS ON
DIGITALIS ARE SUSCEPTIBLE TO.
SHIFT OF K INTRACELLULARY
DEXTROSE- INSULIN
• MECHANISM: INSULIN ENHANCES THE ACTIVITY OF THE NA-K-ATPASE PUMP IN SKELETAL MUSCLE THUS DRIVING POTASSIUM IN TO THE
CELLS AND REDUCING SERUM CONCENTRATIONS.
• • GLUCOSE IS GIVEN TO PREVENT HYPOGLYCEMIA BUT IS NOT NEEDED IF BLOOD GLUCOSE IS ABOVE 20 MMOL/L
• – ONSET: EFFECT OF INSULIN BEGINS IN 10 TO 20 MINUTES BUT DOES NOT PEAK UNTIL 30 TO 60 MINUTES. THE EFFECTS LAST FOR 4-6
HOURS.
• – EFFECT: UP TO 0.85 MMOL/L DECREASE IN POTASSIUM IN ONE HOUR.
• – DOSE: EITHER DRIP OR BOLUS.
• • DRIP IS 10 UNITS OF REGULAR INSULIN IN 500 ML OF 10% DEXTROSE OVER 60 MINUTES.
• • BOLUS IS 10 UNITS OF REGULAR INSULIN FOLLOWED BY 50ML OF 50% DEXTROSE.
• • BOLUS REGIMEN PROVIDES A BETTER REDUCTION IN SERUM POTASSIUM DUE TO HIGHER INSULIN
• LEVELS ACHIEVED BY BOLUS BUT THERE IS A HIGHER INCIDENCE OF HYPOGLYCEMIA IN PATIENTS RECEIVING BOLUS THERAPY.
• – SPECIAL NOTE: GIVING GLUCOSE ALONE THEORETICALLY RAISES ENDOGENOUS INSULIN LEVELS PROVIDING A THERAPEUTIC EFFECT BUT
ENDOGENOUS RELEASE IS HIGHLY VARIABLE.
• IF ENDOGENOUS INSULIN RELEASE IS IMPAIRED, HYPERGLYCEMIA CAN RESULTS WHICH WILL ACTUALLY RAISE PLASMA OSMOLALITY
PROMOTING WATER AND POTASSIUM MOVEMENT
BETA 2 AGONISTS
• ESSENTIALLY THIS IS EITHER ALBUTEROL (OR SALBUTAMOL) OR EPINEPHRINE. ALBUTEROL IS
USED RARELY AND EPINEPHRINE SHOULD REALLY NOT BE USED AT ALL.
• EPINEPHRINE ALSO HAS ALPHA-ADRENERGIC ACTIVITY WHICH CAN ACTUALLY CAUSE
POTASSIUM MOVEMENT OUT OF CELLS, NOT INTO THEM.
• – MECHANISM: LIKE INSULIN ALBUTEROL INCREASES THE ACTIVITY OF THE NA-K-ATPASE PUMP
IN SKELETAL MUSCLE. IN ADDITION IT ALSO ACTIVATES THE NA-K-2CL COTRANSPORTER. BOTH
ACT TO DRIVE POTASSIUM INTO CELLS.
• – ONSET: PEAK EFFECT IS 90 MINUTES WITH NEBULIZATION AND 30 MINUTES WHEN GIVEN IV.
• – EFFECT: HAS BEEN SHOWN TO LOWER POTASSIUM CONCENTRATIONS BY 0.5 TO 1.5
MMOL/L.
SODIUM BICARBONATE
• MECHANISM: RAISES THE SERUM PH RESULTING IN HYDROGEN ION RELEASE FROM CELLS TO
BUFFER. THIS H RELEASE IS ACCOMPANIED BY POTASSIUM MOVEMENT INTO CELLS TO
MAINTAIN ELECTRONEUTRALITY
• – ONSET: WITHIN 15 MINUTES VIA IV WITH DURATION OF ACTION OF 1-2
• HOURS.
• – INDICATIONS: LIMITED EVIDENCE SUPPORTING THE ACUTE MANAGEMENT OF HYPERKALEMIA
WITH SODIUM BICARBOANTE. IT SHOULD NOT BE USED ALONE IN ACUTE THERAPY BUT CAN BE
BENEFICIAL IN CHRONIC KIDNEY DISEASE PATIENTS WITH METABOLIC ACIDOSIS REGARDLESS
OF POTASSIUM.
• – DOSE: IN ACUTE SETTING (AGAIN NOT AS MONOTHERAPY) SHOULD BE GIVEN AS 150
MMOL IN 1L OF D5W. IF GIVEN IN NORMAL SALINE YOU ARE GIVING INCREASED SODIUM SO
PLASMA OSMOLALITY WILL INCREASED AND SLOW THE CORRECTION OF HYPERKALEMIA
OTHER MODALITIES;
DIALYSIS
• DIALYSIS IS THE ULTIMATE TX IF ALL OTHER MODALITIES HAVE FAILED OR THE HYPERKALEMIA IS
EXTREMELY SEVERE OR INCREASING RAPIDLY.
• – HEMODIALYSIS IS PREFERRED OVER PERITONEAL DIALYSIS.
• – HEMODIALYSIS CAN REMOVE 25 TO 50 MMOL OF POTASSIUM/ HOUR
HYPOKALAEMIA
DEFINITION
• HYPOKALEMIA IS DEFINED AS A
POTASSIUM LEVEL LESS THAN 3.5 mmol/h.
• MODERATE HYPOKALEMIA IS A SERUM LEVEL
OF 2.5-3 mmol/h.
• SEVERE HYPOKALEMIA IS DEFINED AS A LEVEL
LESS THAN 2.5 mmol/h
THE REFERENCE RANGE FOR SERUM
POTASSIUM LEVEL IS 3.5-5 mmol/h
PATHOPHYSIOLOGY
Total body deficit
of potassium
chronic inadequate intake,
long-term diuretic or laxative use,
chronic diarrhea, hypomagnesemia & hyperhidrosis
Acute potassium
depletion
diabetic ketoacidosis,
severe GI losses : vomiting / diarrhea,
dialysis, and diuretic therapy
potassium shifts
from the EC
to IC space
Alkalosis & hypothermia
insulin,
catecholamines
Other causes
Distal RTA & Bartter syndrome,
Periodic hypokalemic paralysis,
Hyperaldosteronism & hyperthyroid.
ABNORMALITIES OF SERUM POTASSIUM ARE
ASSOCIATED WITH WELL DESCRIBED CLINICAL
FEATURES:
S. K+ level
Clinical features
<3.5 mmol/l
Lassitude
< 2.5 mmol/l
Possible muscle necrosis
<2 mmol/l
Flaccid paralysis with
respiratory compromise
Gennari FJ. Hypokalemia. N Engl J Med 1998; 339: 451-458
EFFECTS OF HYPOKALEMIA
• 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.
EFFECTS OF HYPOKALEMIA
• 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 POTASSIUMDEPLETED PATIENTS - ESPECIALLY FOLLOWING VIGOROUS
EXERCISE - AND MUSCLE NECROSIS CAN RARELY OCCUR
IV INFUSION RATE FOR SEVERE OR SYMPTOMATIC
HYPOKALEMIA
Standard
IV replacement rate
Serum potassium < 2.5 meq/L, or
 Moderate-severe symptoms
 Serum potassium < 2.0 Meq/L, or
 Life-threatening symptoms
 If heart block, or
 Renal insufficiency exists

10 - 20 mmol/h
20 - 40 mmol/h
> 40 mmol/h
5 - 10 mmol/h
Medical Decision-Making and Treatment
Transient, asymptomatic, or mild hypokalemia may resolve
spontaneously or may be treated with enteral potassium supplements.
Potassium replacement therapy is immediately
indicated for:
 Severe hypokalemia (< 2.5 mmol/h), or
 If the hypokalemia is causing muscle paralysis, or
 Malignant cardiac arrhythmias .
MEDICAL DECISION-MAKING AND TREATMENT
OUTPATIENT THERAPY AND FOLLOW-UP IN
48 - 72 HOURS MAY BE ACCEPTABLE FOR
MILD HYPOKALAEMIA PATIENTS WITH NO
UNDERLYING HEART DISEASE.
MEDICAL DECISION-MAKING AND TREATMENT
THE PATIENT SHOULD BE TRANSFERRED
TO ICU FOR SEVERE OR SYMPTOMATIC
HYPOKALEMIA FOR:
IV POTASSIUM SUPPLEMENTATION.
CONTINUOUS CARDIAC
MONITORING.
MAGNESIUM REPLACEMENT THERAPY
• MAGNESIUM REPLACEMENT THERAPY IS OFTEN NECESSARY IN
MALNOURISHED ALCOHOLICS WITH HYPOKALEMIA.
• HYPOMAGNESEMIA SHOULD BE SUSPECTED IF THE SERUM
POTASSIUM DOES NOT INCREASE WITHIN ~ 72 HOURS OF
THE COMMENCEMENT OF POTASSIUM SUPPLEMENTATION
THERAPY.
• MAGNESIUM CAN BE GIVEN ORALLY (3G X 4 DOSES).