This document provides information on dyselectrolytemias including hyponatremia, hypernatremia, hypokalemia, and hyperkalemia. It discusses the causes, clinical features, investigations, and management of each condition. Key points covered include definitions of normal electrolyte ranges, classifications of hyponatremia and hypokalemia based on volume status, common causes, symptoms to watch for, appropriate tests, and guidelines for correcting electrolyte imbalances while avoiding dangerous overcorrections.

1. DYSELECTROLYTEMIA
PRESENTER:DR. SUJAN BIKRAM DHAKAL(INTERN)
MODERATOR: DR. PARAS BHATTA(RESIDENT, INTERNAL
MEDICINE)

2. HYPONATREMIA
PLASMA NA+: <135 MEQ/L (NORMAL PLASMA NA+:135-145 MEQ/L)

3. HYPONATREMIA CAN BE
-ACUTE( <48 HOURS)
-CHRONIC(>48 HOURS)
• BASED ON SEVERITY
- MILD: 130-134 MEQ/L
-MODERATE:120-129MEQ/L
- SEVERE:<120 MEQ/L

4. CAUSES/CLASSIFICATION:
HYPOTONIC HYPONATREMIA:
1.HYPOVOLEMIC HYPONATREMIA(NA H20 ):BOTH SODUIM AND
WATER DECREASES BUT SODIUM LOSS IS MORE THAN WATER LOSS.
• ALSO KNOWN AS DEPLETIONAL HYPONATREMIA
• LOW URINE SODIUM(<10MEQ/L):IT IMPLIES INCREASED SODIUM RETANTION BY KIDNEY TO
COMPENSATE EXTRARENAL LOSS.
Eg: DIARRHOEA ,VOMITING,NG SUCTION,THIRD SPACE LOSS,BURNS ,PANCREATITIS
• HIGH URINE SODIUM(>20MEQ/L):RENAL LOSS IS LIKELY.
Eg: EXCESS USE OF DIURETICS,ATN,DECREASED ALDESTERONE(ACE INHIBOTORS)

5. 2.EUVOLEMIC HYPONATREMIA:
• OVERALL BODY SODIUM DOESN’T CHANGE BUT CONC. OF NA+
DECREASES.
• ALSO CALLED AS DILUTIONAL HYPONATREMIA.
- SIADH
- PSYCHOGENIC POLYDIPSIA
-HYPOTHYROIDISM
-OXYTOCIN USE
-ADMINISTRATION/INTAKE OF A RELATIVE EXCESS OF WATER
-DRUGS LIKE HALOPERIDOL

6. 3.HYPERVOLEMIC HYPONATREMIA:
BOTH NA+ AND WATER INCREASES BUT INCREASE IN WATER IS MORE
THAN SODIUM SO OVERALL CONCENTRATION DECREASES CAUSING
HYPONATREMIA
Eg: CHF
NEPHROTIC SYNDROME
LIVER FAILURE
RENAL FAILURE

7. • ISOTONIC HYPONATREMIA: DUE TO ANY CONDITIONS THAT LEADS TO ELEVATED
PROTEIN AND LIPID LEVELS
AS INCREASE IN PLASMA SOLIDS LOWERS SODIUM CONCENTRATION BUT AMOUNT OF SODIUM IN
PLASMA REMAINS NORMAL;HENCE PSEUDONATREMIA
• HYPERTONIC HYPONATREMIA:DUE TO PRESENCE OF OSMOTIC
SUBSTANCES(GLUCOSE,MANNITOL,SORBITOL,RADIOCONTRAST AGENTS)

8. CLINICAL FEATURES:
ACUTE
• SODIUM LEVEL 121-130 MEQ/L: NAUSEA,HICCOUGHS,MALAISE,HEADACHE, LETHARGY, MUSCLE
CRAMPS,DISORIENTATION,RESTLESSNESS.
• SODIUM LEVEL:<120 MEQ/L: OBTUNDATION ,SEIZURES,RESPIRATORY ARREST,COMA ,DEATH
CHRONIC
• USUALLY ASYMPTOMATIC/ NON SPECIFIC
• NAUSEA,MUSCLE CRAMPS,GAIT DISTURBANCES,FORGETFULLNESS,CONFUSION,LETHARGY,FATIGUE

9. INVESTIGATION
• PLASMA SODIUM COC.<135 MMOL/L
• BLOOD UREA,URIC ACID ,BUN/CREATININE RATIO : INCRESED IN
HYPOVOLEMIC HYPONATREMIA
• PLASMA OSMOLALITY :DECREASED
• URINE SODIUM CONC
• URINE OSMOLALITY :
<100 mOSm/L IN PSYCHOGENIC POLYDYPSIA
>200 mOSm/L IN SIADH AND VOLUME DEPLETION

10. MANAGEMENT:
• CALCULATE SODIUM DEFICIT:
SODIUM DEFICIT= (DESIRED Na-PATIENT Na) x TBW
TBW=TOTAL BODY WATER =BODY WT *0.6 FOR MALE (0.5 FOR FEMALE)
ESTIMATION OF EFFECT OF INFUSATE:
CHANGE IN SERUM Na = ((INFUSATE Na + INFUSATE K) –SERUM Na)/(TBW +1)

11. CALCULATE DRIP RATE:
• AMOUNT OF FLUID=CHANGE IN SERUM Na DESIRED/ESTIMATED
EFFECT OF 1 L INFUSTAE
• DRIP RATE=AMOUNT OF FLUID/TARGET NO. OF HOURS
*NOTE:
-0.9%NS CONTAINS 154MEQ/L SODIUM
-3%NS CONTAINS 513 MEQ/L SODIUM
-0.45% NS CONTAINS 77 MEQ/L SODIUM
- RL CONTAINS 130 MEQ/l SODIUM

12. • ACUTE HYPONATREMIA
SEVERE SYMPTOMATIC : 100 ML OF 3 % NORMAL SALINE GIVEN BOLUS IN 1O MINS
-IF NO RELIEF OF SYMPTOMS AGAIN 100 ML 3% NS GIVEN
AFTER 10 MINS AND ( AGAIN REPEATED MAX 300 ML)
-AFTER RELIEF OF SYMPTOMS SWITCH TO ISOTONIC SALINE
MILD TO MODERATE SYNPTOMS: 3% NACL @0.5-2ML/KG/HR
ACUTE HYPONATREMIA -CORRECTED QUICKLY - TO REDUCE RISK OF CEREBRAL
SWELLING

13. CHRONIC HYPONATREMIA
• IF PATIENT PRESENTS WITH NEUROLOGICAL SYMPTOMS- TREATMENT GIVEN ACCORDING
TO AS SVERE ACUTE HYPONATREMIA
• CHRONIC HYPONTREMIA PATIENT. ARE AT RISK OF OSMOTIC DEMYLENATION SYNDROME
IF PLASMA NA+ CONCONCENTRATION IS CORRECTED BY >8-1O MMOL/L WITHIN 24 HRS
OR 18 MMOL /L WITHIN 1ST 48 HRS
• TREATMENT DONE ACCORDING TO VOLUME STATUS:
*HYPOVOLEMIC -CONTROL SOURCE OF SODIUM LOSS
-ORAL SODIUM SUPPLEMENTATION OR ISOTONIC SALINE INFUSION

14. *HYPERVOLEMIC -WATER AND SALT RESTRICTION
-CAUTIOUS USE OF LOOP DIURETICS
-IN CHF AND LIVER CHIRRHOSIS , VAPTANS ARE
FOUND TO BE HIGHLY EFFECTIVE
WATEER RESTRICTION
-IF RATIO OF (URINE Na +URINE K) AND SERUM NA IS <0.5 RESTRICT TO 1L/DAY
-IF RATIO IS 0.5-1, RESTRICT TO 500-700 ML/DAY
-IF RATIO IS >1 ,RESTRICT TO <500ML/DAY
*EUVOLEMIC:
SIADH-WATER RESTRICTION
-USE OF VAPTONS
ADISSION DZ – WATER RESTRICTION TO 500-1000ML/DAY
HYPOTHYROIDISM –THYROXINE
OTHERS CAUSE SHOULD BE TREATED ACCORDINGLY

15. Source – Internet
(www.Researchgate.net

17. HYPERNATREMIA
• PLASMA SODIUM :>145 MMOL/L (NORMAL PLASMA NA+: 135-145
MMOL/L)

18. CAUSES:
• HYPOVOLEMIC HYPERNATREMIA (SODIUM DEFECIT WITH RELATIVE
WATER DEFICIT) :
- RENAL SODIUM LOSS
-DIURETIC THERAPY (ESP OSMOTIC OR LOOP DIURETIC DURING WATER RESTRICTION
-GLYCOSURIA
-GASTROINTESTINAL SODIUM LOSS
-COLONIC DIARRHOEA
-SKIN NA+ LOSSES
-EXCESSIVE SWEATING
EUVOLEMIC HYPERNATREMIA: (WATER DEFICIT ALONE)
-DIABETES INSIPIDUS
-INSESIBLE RESPIRATORY LOSS DURING TACHYPNEA

19. HYPERVOLEMIC HYPERNATREMIA: SODIUM RETENTION WITH
RELATIVELY LESS WATER RETENTION
-ENTERAL OR PARENTERAL FEEDING
-IV OR ORAL SALT ADMINISTRATION
-CHRONIC RENAL FAILURE(DURING WATER RESTRICTION)
-PRIMARY HYPERALDOSTERONISM
-CUSHING SYNDROME
-EXOGENOUS GLUCOCORTICOIDS

20. INVESTIGATION
• PLASMA NA+ >145 MMOL/L
• PLASMA CREATININE , BLOOD UREA- RAISED DUE TO DEHYDRATION
• PLASMA OSMOLALITY RAISED >300 mOSM/L
• URINE VOLUME AND OSMOLALITY-HELPS IN ASSESSMENT OF THE
CAUSE OF HYPERNATREMIA

21. CLINICAL FEATURES
• DRY MOUTH AND MUCOUS MEMBRANE, DRY AXILLA
• EXCESSIVE THIRST
• OLIGURIA
• ORTHOSTATIC BLOOD PRESSURE CHANGES
• TACHYCARDIA
• NEUROLOGICAL-ALTERED MENTAL STATUS,RESTLESSNESS,WEAKNESS,FOCAL
NEUROLOGICAL DEFICITS
- CAN LEAD TO CONFUSION,SEIZURES,COMA,ICH

22. MANAGEMENT :
• CALCULATION OF WATER DERICIT:
WATER DEFICIT=(PLASMA Na -140)/140*TOTAL BODY WATER
TOTAL BODY WATER=APPROX 50% OF LEAN BODY WT IN MEN AND 40% IN WOMEN
REPLACE CALCULATED WATER DEFICIT ORALLY OR IV ROUTE
CONDITION ASSOCIATED FLUID TO BE USED
IF HYPERNATREMIA ONLY - 5 % DEXTROSE
HYPERNATREMIA WITH HEMODYNAMIC COMPRAMISE - INITALLY NS FOLLOWED BY 5% DEXTROSE
HYPERNATREMIA WITH VOLUME DEFICIT - HALF NS
HYPERNATREMIA WITH HYPERGLYCEMIA - DEXTROSE CONTAINING SOLUTION WITH
APPROPRIATE USE OF INSULIN

23. • CALCULATED WATER DEFICIT PLUS THE AMOUNT LOST THROUGH
INSENSIBLE LOSS SHOULD BE GIVEN OVER 24-48 HOURS
• ADMINISTER HALF OF REQUIRED AMOUNT OF WATER OVER 12-24 HRS AND
REMAINING OVER 24- 48 HR
• MONITOR PLASMA SODIUM EVERY 4-5 HOURS
• RATE OF CORRECTION:
ACUTE : -AGGRESSIVE CORRECTION IS POTENTIALLY DANGEROUS.
-CORRECTED @2-3MEQ/L/HR( FOR 2-3 HRS) MAX. 12MEQ/L/DAY
CHRONIC :INITIALLY LOWERED BY 0.5 MEQ/L/HR ( 8-10MEQ OVER NEXT 24 HRS)

24. • ONCE HYPONATREMIA IS CORRECTED, TREATMENT OF UNDERLYING
CAUSE DONE
• PREVENTION OF HYPERNATREMIA:
-USE OSMOTIC DIURETICS CAUTIOUSLY AND MONITOR PLASMA Na FREQUENTLY
-MONITOR PLASMA Na FREQUENTLY WHEN HYPERTONIC SALINE IS BEING USED, AS IN THE TRATNMENT
OF SEVERE HYPONATREMIA.

25. Source:Internet
(www.Researchg
ate.nResearchgat
e.net

27. HYPOKALEMIA
• PLASMA K+:<3.5 MEQ/L (NORMAL PLASMA K+:3.5-4.5 MEQ/L)
CAUSES
DECREASED INTAKE:CLAY INGESTION ,STARVATION
REDISTRIBUTATION INTO THE CELLS
ACID-BASE: METABOLIC ACIDOSIS
HORMONAL:
-INSULIN
-INCREASED BETA2 ADRENERGIC SYMPATHETIC ACTIVITY:
POST MI,HEAD INJURY
-THYROTOXIC PERIODIC PARALYSIS
ANABOLIC STATE
OTHERS : HYPOTHERMIA,BARIUM TOXICITY,DRUGS LIKE
THEOPHYLLINE,CAFFIENE,HYDROXYCHLOROQUINE,BETA
AGONIST,ALPHA ANTAGONIST

28. INCREASED LOSS:
- NON RENAL LOSS:
GI LOSS:DIARRHOEA,PROLONGED USE OF LAXATIVES,PURGATIVES ABUSE,
FISTULA,ILEOSTOMY
INTEGUMENTARY LOSS (SWEAT)
-RENAL LOSS:
INCREASED DISTAL FLOW AND DISTAL NA+ DELIVERY : DIURETICS,OSMOTIC
DIURESIS,SALT WASTING NEPHROPATHIES
INCREASED SECRETION OF POTASSIUM: MINERALOCORTICOID EXCESS,
DISTAL DELIVERY OF NON ABSORBED ANIONS(VOMITING,NG
SUCTION,PROXIMAL RTA,DKA,GLUE SNIFFING),
MAGNISIUM DEFICIENCY

29. CLINICAL FEATURES:
HISTORY-H/O MAY BE VAGUE
- OFTEN SYMPTOMATIC
- SYMPTOMS OFTEN DUE TO THE UNDERLYING CAUSE RATHER THAN THE HYPOKALEMIA ITSELF
-PATIENT MEDICATION SHOULD BE REVIEWED TO ASCERTAIN WHETHER ANY OF THEM COULD CAUSE
HYPOKALEMIA
COMMON SYMPTOMS:
PALPITATION ABDOMINAL CRAMPING
SKELETAL MUSCLE WEAKNESS OR CRAMPING PSYCHOSIS
PARALYSIS DELIRIUM
PARESTHESIA
NAUSEA OR VOMITING

30. • PHYSICAL FINDING:
SIGN IF ILEUS HYPOTENSION
VENTRICULAR ARRYTHMIAS CARDIAC ARREST
BRADYCARDIA OR TACHYCARDIA PREMATURE ATRIAL OR VENTRICULAR BEATS
HYPOVENTILATION, RESPIRATORY DISTRESS LETHARGY
DECREASED MUSCLE STRENGTH,FASCICULATION DECREASED TENDON REFLEX

31. • INVESTIGATION:
SERUM K+:
ECG:

32. • TRANSTUBULAR POTASSIUM GRADIENT(TTKG):
TTPK>4 DURING HYPOKALEMIA POINTS TO RENAL LOSS
• TTKG=URINE K /SERUM K *SERUM OSM/URINE OSM
• URINE K+/CREATININE RATIO:
- IF VALUE<1.5 MEQ/MMOL,HYPOKALEMIA IS USUALLY FROM POOR DIET
INTAKE,TRANSCELLULAR K+ SHIFTS,GI LOSS, OR PREVIOUS USE OF DIURETRICS
-HIGHER VALUE ARE INDICATIVE OF ONGOING RENAL POTASSIUM WASTING

33. TREATMENT OF HYPOKALEMIA
• DISCONTINUE ANY DRUGS THAT MAY AGGRAVATES HYPOKALEMIA
• ORAL POTASSIUM IS SAFEST METHOD OF REPLACEMENT AND IS APPROPRIATE IN MOST OF THE INSTANCES
- USING 10 MEQ/L OF KCL INCREASES K+ LEVEL BY O.1 MEQ/L
- ORAL DOSES OF 40 MEQ/L ARE GENERALLY TOLERATED AND CAN BE GIVEN AS OFTEN AS EVERY 4 HOURS
• POTASSIUM DEFICIT=(DESIRED K-ACTUAL K )/0.27 X 100. THIS IS FOR NON –DISTRUBUTIVE HYPOKALEMIA
FOR OTHER ,K+ DEFICIT IS ESTIMATED AS 400-800 MMOL REDUCTIONFOR A 2 MMO;/L FALL IN SERUM K+
• TARGET K+ FOR CARDIAC PATIEANT IS USUALLY 4.0 ; OTHERWISE A TARGET OF 3.5 IS USED
• IV KCL GIVEN IF HYPOKALEMIA IS SEVERE (<2.5) OR IF PATIENT HAS ARRYTHMIAS SECONDARY TO
HYPOKALEMIA
- MAX. CONCENTRATION OF ADMINISTERED K+ SHOULD BE NO MORE THAN 40 MEQ/L VIA PERIPHERAL VEIN OR
100MEQ/L VIA CENTRAL VEIN
- MAX. INFUSION RATE SHOULD BE 1O MEQ/L IN PERIPHERAL LINE AND 20 MEQ/L IN CENTRAL LINE

34. -MONITER K+ CONC. AND MONITER CARDIAC RHYTHM WHEN GIVING IN POTASSIUM
-1% LIDOCAINE MAY BE ADDED TO BAG TO DECREASE PAIN(POTASSIUM BRUSTS)
• IDEALLY KCL SHOULD BE MIXED IN NS( IF MIXED WITH DEXTROSE MAY INITIALLY AXACERBATE
HYPOKALEMIA AS A RESULT OF INSULIN MEDIATED MOVEMENTS OF K+
• IF MAGNESIUM DEPLETION IS ALSO PRESENT ,REPLACEMENT OF MAGNESIUM MAY ALSO BE
REQUIRED FOR HPOKALEMIA TO BE CORRECTED(SINCE LOW Mg++ CAN ENHANCE MECHANISM
FOR TUBULAR POTASSIUM SECRETION,CAUSING URINARY LOSS)
• IDENTIFY AND TREAT THE UNDERLYING CAUSE

36. HYPERKALEMIA
• SERUM K+:>4.5 MEQ/L (NORMAL SERUM K+:3.45-4.45)

37. CAUSES OF HYPERKALEMIA
• DECREASED EXCRETION:
-RENAL FAILURE
-DRUGS:ACE INHIBITOR,ALDOSTERONE ANTAGONISTS,NSAIDS,ALPHA-
BLOCKER,DIGOXIN,CYCLOSPORIN,TRIMETHOPRIM,PENTAMIDE
-ALDESTERONE DEFICIENCY
-TYPE(A) RTA
-ADISSION DISEASE
INCREASED RELEASED FROM CELLS:
-ACIDOSIS
- DKA
-RHABDOMYOLOSIS,TUMOR LYSIS SYNDROME,HAEMOLYSIS
-VIGOROUS EXERCISE
-SUCCINYLCHOLINE

38. • INCREASED EXTRANEOUS LOAD:
-KCL AND SALT SUBSTITUTES
-TRANSFUSION OF STORED BLOOD
• SPURIOUS:
-INCREASED INVITRO RELEASED FROM ABNORMAL CELLS(LEUKEMIA,THROMBOCYTOSIS)
-PSEUDOHYPERKALEMIA - HEMOLYSIS FROM SYRINGE,INCREASE RELEASED FROM
MUSCLE DUE TO VIREROUS FISTING DURING PHLEBOTOMY

39. CLINICAL FEATURES
• PROGRESSIVE MUSCLE WEAKNESS
• LOSS OF TENDON REFLEX
• FLACCID PARALYSIS(PARALYSIS USUALLY SPARES THE MUSCLE SUPPLIED BY CRANIAL NERVES AND PATIENT REMAINS ALERT
AND APPREHENSIVE UNTIL THR CARDIAC ARREST AND DEATH OCCURS)
• ABDOMINAL DISTENSION AND ILEUS
• SYNCOPE COLLAPSE DUE TO CARDIAC ARRYTHMIAS
• SOMETIMES THERE MAY NOT BE ANY SYMPTOMS
UNTILL CARDIAC ARREST OCCURS(HENCE IT IS CALLED
SILENT KILLER)

40. INVESTIGATION:
• SERUM ELECTROLYTES:
• RENAL FUNCTION TEST(RFT)
• ECG:
-TALL T WAVES
- PROLONGATION OF PR INTERVAL
- REEDUCED AMPLITUDE OR LOSS OF P WAVE
-PROLONGRD QRS SEGMENT
-ST ELEVATION
-SINE WAVE
-VENTRICULAR FIBRILLATION
- ASYSTOLE
-BUNDLE BRANCH BLOCK

41. MANAGEMENT:
• IMMEDIATELY, ATTACH ECG MONITOR AND OPEN IV ASCESS
• PROTECT MYOCARDIUM(MEMBRANE STABILIZATION):
- 10 ML OF 10% CALCIUM GLUCONATE IV OVER 10 MINS (CARDIAC MONITERING)
-EFFECT IS TEMPORATY BUT DOSE CAN BE REPEATED AFTER 10-15 MINS
• SHIFT K+ INTO THE CELL:
-INSULIN 10 UNIT AND 50 ML OF 50% GLUCOSE IV OVER 10-15 MINS FOLLOWED BY REGULAR
CHECKS OF BLOOD GLUCOSE AND PLASMA K+
-NEBULIZED WITH SALBUTAMOL
-INFUSE 50-100ML OF SOD. BICARBONATE

42. REMOVE K FROM BODY:
• SODIUM POLSTYRENE SULPHONATE 25-50 MG WITH 100 ML 20% SORBITAL
• POLYSTYRENE SULPHONATE RESINS: 15 MG CALCIUM RESONIUM 3 TIMES DAILY WITH
LAXATIVES
( EACH GRAM OF CALCIUM RESONIUM BINDS WITH 1 MMOL OF POTASSIUM)
• IV FUROSEMIDE 20 MG IN CASE OF INTACT RENAL FUNCTION
HEMODIALYSIS: IN SEVERE HYPERKALEMIA NOT CONTROLLED BY ABOVE
MEASURES

44. Reference;
• HARRISON’S PRINCIPLE OF INTERNAL MEDICINE 19 EDITION
• DAVIDSON’S PRINCIPLE OF INTERNAL MEDICINE 22 EDITION
• IM PLATINUM 3rd EDITION
• INTERNET

45. THANK YOU