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DYSELECTROLYTEMIA
PRESENTER:DR. SUJAN BIKRAM DHAKAL(INTERN)
MODERATOR: DR. PARAS BHATTA(RESIDENT, INTERNAL
MEDICINE)
HYPONATREMIA
PLASMA NA+: <135 MEQ/L (NORMAL PLASMA NA+:135-145 MEQ/L)
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
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)
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
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
• 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)
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
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
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)
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
• 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
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
*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
Source – Internet
(www.Researchgate.net
HYPERNATREMIA
• PLASMA SODIUM :>145 MMOL/L (NORMAL PLASMA NA+: 135-145
MMOL/L)
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
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
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
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
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
• 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)
• 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.
Source:Internet
(www.Researchg
ate.nResearchgat
e.net
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
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
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
• 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
• INVESTIGATION:
SERUM K+:
ECG:
• 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
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
-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
HYPERKALEMIA
• SERUM K+:>4.5 MEQ/L (NORMAL SERUM K+:3.45-4.45)
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
• 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
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)
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
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
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
Reference;
• HARRISON’S PRINCIPLE OF INTERNAL MEDICINE 19 EDITION
• DAVIDSON’S PRINCIPLE OF INTERNAL MEDICINE 22 EDITION
• IM PLATINUM 3rd EDITION
• INTERNET
THANK YOU

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Electrolyte Disorders: Hyponatremia, Hypernatremia, Hypokalemia

  • 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
  • 16.
  • 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.
  • 26.
  • 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
  • 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
  • 35.
  • 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
  • 43.
  • 44. Reference; • HARRISON’S PRINCIPLE OF INTERNAL MEDICINE 19 EDITION • DAVIDSON’S PRINCIPLE OF INTERNAL MEDICINE 22 EDITION • IM PLATINUM 3rd EDITION • INTERNET