HYPONATREMIA IN CLINICAL PRACTICE

BYDR.ROHAN PATTANAIK2010 INTERNS BATCH

SODIUM-Few uses in human body.

Plays key role in regulating B.P. Maintains PH balance. Nerve impulse conduction by Na+-K+

pumps. Helps in muscle contraction. Maintains chlorine and potassium

levels.

Sodium in Human Body

RDA:3-5g per day in normal adults.Na+ should be restricted to about 1.5g

per day in Hypertensives.Table salt contains 40% sodium.1tsp of salt contains 2.3g sodium.Human body contains approx. 1.3g of

Na+(1/3rd in bones and rest in body fluids.

SOME FOODS RICH IN SODIUM

SMOKED MEATS BEET CELERY PICKLES CEREALS CHEESE MILK

What is Hyponatremia????

Definition:-Hyponatremia is generally defined as a serum sodium level below 135 meq/L, the normal range of serum sodium being 135-145 meq/L.

Severe hyponatremia is serum sodium levels below 125 meq/L.

INCIDENCE

It is the most common electrolyte disorder encountered in clinical practice.

15-20% of hospitalized patients develop hyponatremia Affects 7% of ambulatory patients. Causes approx. 1 million hospitalizations per year. Common in geriatric populations. 30% of Depressed Patients in psychiatric practice

develop hyponatremia 0.5-32% of psychiatric patients on SSRIs develop

hyponatremia.

PATHOPHYSIOLOGY

MOST OFTEN HYPONATREMIA IS A/W A LOW SERUM OSMOLALITY CAUSED BY EITHER RETENTION OF WATER OR LOSS OF SODIUM.

EXCESSIVE INGESTION OF WATER LEADING TO DILUTION OF SODIUM LEVELS.

REDUCED EXCRETION OF WATER BY THE KIDNEYS DUE TO RENAL FAILURE OR SIADH

REDUCED RENAL EXCRETION OF WATER DUE TO SLOW URINE FLOW IN COLLECTING TUBULES( DUE TO ENHANCED PROXIMAL TUBULAR REABSORPTION OF SALT AND WATER AS IN CHF AND CIRRHOSIS)

TYPES

TYPE 1:-Euvolemic Hyponatremia-In this the total body water increases but the body’s sodium content stays the same

TYPE 2:-Hypervolemic Hyponatremia-In this type sodium and water level both increase but water is increased more comparatively.

TYPE 3:-Hypovolemic Hyponatremia-In this type sodium and water both decreases or is lost but loss of sodium is comparatively more.

TYPES-A GRAPHICAL REPRESENTATION

DIFFERENTIAL DIAGNOSIS OF DIFFERENT TYPES OF

HYPONATREMIA

ETIOLOGY

Most common cause of hyponatremia is Syndrome of Inappropriate Secretion of Anti Diuretic Hormone (SIADH).

Other causes:-1. CHF2. Liver cirrhosis3. Nephrotic syndrome4. Renal failure5. Diuretics6. Ketonuria7. Addison’s Disease8. Sweating9. Vomitting10. Diarrhoea11. Hyperglycemia12. Mannitol administration13. Hypothyroidism14. Adrenal insufficiency15. Drugs

ETIOLOGY ACCORDING TO TYPES

SOME KNOWN DRUGS CAUSING HYPONATREMIA

FEW MECHANISMS OF DRUG INDUCED HYPONATREMIA

SIADH

CARDINAL FEATURES:-1. HYPONATREMIA DUE TO EXCESSIVE WATER

RETENTION.2. URINE OSMOLALITY EXCEEDS PLASMA OSMOLALITY.3. PLASMA UREA AND CREATININE ARE NORMAL OR

LOW.4. CONTINUED URINARY SODIUM EXCRETION.

SIADH

COMMON CAUSES OF HYPONATREMIA ENCOUNTERED IN

PSYCHIATRIC PATIENTS1. Primary polydipsia as in Schizophrenics with psychosis2. Psychotropic drugs causing dryness of mouth and increased

thirst.3. SSRIs intake4. Anti-epileptics and Mood stabilizers (such carbamazepine and

oxcarbezapine commonly)5. Anti-psychotics and anti-depressants 6. MMDA drug(“Ecstasy”) addiction7. Beer potomania 8. Nicotine abuse

WHAT IS PSEUDOHYPONATREMIA?

It is when serum sodium levels in the body is within normal limits but there is increased levels of other solutes.

Causes-1)Hyperglycemia 2)Hyperlipidemia

3)Hyperproteinemia 4)Mannitol administration

CLINICAL FEATURES

MUSCLE CRAMPS EASY FATIGUABILITY AND WEAKNESS MENTAL CONFUSION IRRITABILITY AND DISTURBED SLEEP DROWSINESS AND DISORIENTATION CONVULSIONS AND COMA LETHARGY AND SOMNOLENCE SHORT TERM MEMORY LOSS DECORTICATE OR DECEREBRATE POSTURING NAUSEA AND VOMITTING HEADACHE AND BLURRED VISIONS LOSS OF APPETITE

NEUROLOGICAL S/S OF HYPONATREMIA

S/S AT A GLANCE

COMPLICATIONS

HYPONATREMIC ENCEPHALOPATHY(S. Na+ <115 meq/L)-Brain herniation with seizures and cardiac and respiratory arrest.

OSTEOPOROSIS CEREBRAL EDEMA SEIZURES COMA/STUPOR RESPIRATORY OR CARDIAC ARREST DEATH

INVESTIGATIONS

SERUM SODIUM AND POTASSIUM URINARY SODIUM EXCRETION ESTIMATION THYROID PROFILE (T3,T4 AND TSH) CORTISOL LEVEL ESTIMATION (URINARY FREE CORTISOL AND PLASMA CORTISOL LEVELS) BLOOD UREA AND SERUM CREATININE LIPID PROFILE (TG AND HDL LEVEL) FBS AND PPBS SERUM ALBUMIN CBC ECG AND ECHO LFT, KFT AND PFT CHEST X-RAY MRI BRAIN DEXA SCAN FOR BONE MINERAL DENSITY ESTIMATION NERVE CONDUCTION STUDIES

TREATMENT

NON-MEDICAL MANAGEMENT:-1. RESTRICTING WATER INTAKE2. INCREASING SALT INTAKE3. TAKING FOODS RICH IN SODIUM4. AVOIDING STRENOUS WORK

TREATMENT

MEDICAL MANAGEMENT ACCORDING TO PRIMARY CAUSES:-

IN ACUTE SIADH:-1. RESTRICT TOTAL FLUID INTAKE TO ATLEAST 500ML LESS

THAN URINE OUTPUT.2. IV INFUSION OF HYPERTONIC SALINE(3%) AT A RATE OF

<0.05ML/KG/MIN AND CHECKING SERUM SODIUM LEVEL 2 HOURLY AND STOP WHEN S.Na+ LEVEL REACHES 130meq/L.

TREATMENT

IN CHRONIC SIADH:-1. DEMECLOCYCLINE(A TETRACYCLINE) 150-300mg P.O T.I.D FOR 1 TO 2 WEEKS OR

FLUDROCORTISONE 0.05-0.2MG P.O B.I.D FOR 1 TO 2 WEEKS.2. FOR SHORT TERM HOSPITAL MANAGEMENT:- V2 OR V1a RECEPTOR ANTAGONISTS

LIKE CONIVAPTAN I.V OR TOLVAPTAN ORALLY CAN BE GIVEN. IN TYPE 1 HYPONATREMIA:-1. FLUID RESTRICTION2. V2 RECEPTOR ANTAGONISTS CAN BE USED IN TYPE 2 HYPONATREMIA:-1. SLOW REPLACEMENT OF SODIUM ORALLY OR BY I.V INFUSION OF N.S OR HYPERTONIC

SALINE.

TREATMENT

IN TYPE 3 HYPONATREMIA:-1. STRESS DOSES OF HYDROCORTISONE2. LOOP DIURETICS3. HYPERTONIC SALINE I.V INFUSION IN PSYCHIATRIC PATIENTS:-1. STOP SSRIs OR ANTI-PSYCHOTICS OR MOOD STABILIZERS2. FLUID RESTRICTION AND SALT INTAKE3. I.V INFUSION OF HYPERTONIC SALINE4. IF REQUIRED V2 RECEPTOR ANTAGONISTS5. FREQUENT SERUM SODIUM MONITORING

PRECAUTIONS IN TREATMENT

1. HYPERTONIC I.V INFUSION FOR CORRECTION OF SODIUM LEVELS SHOULD NOT EXCEED 1-2meq/L/hr IN ACUTE CASES AND NOT MORE THAN 0.6meq/L/hr IN GENERAL CASES.

2. 1.2ml/kg OF HYPERTONIC SALINE INCREASES SERUM SODIUM BY 1meq/L.

3. RAPID CORRECTION WITH HYPERTONIC SALINE LEADS TO A CONDITION-CENTRAL PONTINE MYELINOSIS (i.e CHARACTERIZED BY QUADRIPARESIS,ATAXIA,ABNORMAL EXTRAOCULAR MOVEMENTS,DYSARTHRIA,DYSPHAGIA AND LOSS OF CONCIOUSNESS).

4. RAPID CORRECTION ALSO LEADS TO OSMOTIC DEMYELINATION OF NEURONS OR EVEN HERNIATION OF BRAIN WHICH ARE LIFE THREATENING CONDITIONS.

NOW A SHORT PSYCHIATRIC CASE DISCUSSION AFFECTED WITH HYPONATREMIA

GENERAL HISTORY

MY PATIENT SACHIN PANDA,A 18 YEAR OLD MALE PATIENT ADMITTED TO PSYCHIATRIC WARD ON 16.11.15 WITH H/O AGRRESIVE BEHAVIOUR,ANGER OUTBURSTS,IRRITBILITY,IMPULSIVENESS, MAKING GRANDIOUS CLAIMS,RESTLESSNESS AND DECREASED SLEEP AND APPETITE AND WEAKNESS,LETHARGY AND DROWSINESS SINCE 14 YEARS AS INFORMED BY HER MOTHER.

THE PATIENT WAS APPARENTLY ALRIGHT 16 YEARS BACK WHEN HE DEVELOPED FITS AT THE AGE OF 2 YEARS AND HAD SEVERAL ATTACKS FROM THEN ON ONWARDS ALONG WITH EPISODES OF ANGER OUTBURSTS,FIGHTING WITH HER MOTHER,THINKING ABOUT OTHERS CONSPIRING AGAINST HIM AND MAKING TALL CLAIMS AND LEAVING HIS HOUSE IN ANGER.THERE WAS NO REPORTED DELAY IN DEVELOPMENTAL MILESTONES AS PER HER MOTHER.

THE PATIENT HAS F/H/O SEIZURES AFFECTING HIS PATERNAL UNCLE. THE PATIENT WAS BEING TREATED WITH

OXCARBEMAZAPINE,RESPERIDONE,TRIHEXYPHENIDYL AND CLOBAZAM FOR MORE THAN 10 YEARS AND HAS A SEIZURE FREE PERIOD OF 4-5 YEARS NOW.

MSE

GENERAL APPEARANCE-18 YR OLD MALE,MAKES EYE CONTACT,WELL KEPT,RAPPORT COULD BE ESTABLISHED,COOPERATIVE,NON-HOSTILE.

SPEECH-RATE AND FLOW NORMAL,REACTION TIME IS NORMAL,GOAL DIRECTED ACTIVITY HIGHER MENTAL FUNCTIONS-WAS ATTENTIVE BUT NOT ABLE TO CONCENTRATE MEMORY-IMMEDIATE AND RECENT MEMORY INTACT BUT REMOTE MEMORY WAS

IMPAIRED. MOOD-SUBJECTIVE-THE PATIENT FEELS FINE -OBJECTIVE-IRRITABLE AND ANXIOUS AFFECT THOUGHT CONTENT-DELUSION OF REFERENCE NO PERCEPTUAL ABNORMALITIES INSIGHT-ABSENT

CLINICAL PSYCHOLOGIST EVALUATION

COMPLETE ADMINISTRATION OF ADULT IQ WAS NOT FEASIBLE PATIENT WAS ATTENTIVE AND COMPREHENSION WAS ADEQUATE SOCIO-OCCUPATIONAL FUNCTIONING WAS 2+ PATIENT WAS ABLE TO PERFORM MILD MONETARY TRANSACTIONS AND

SELFCARE ACTIVITIES. IMPRESSION-MILD MR WITH PSYCHOSIS WITH

BEHAVIOURAL ABNORMALITIES.

INVESTIGATIONS DONE

CBC FBS LFT SERUM ALBUMIN AND GLOBULIN SERUM SODIUM AND POTASSIUM T3,T4 AND TSH AND FREE T4 SERUM CALCIUM,PHOSPHORUS SERUM CREATININE AND BLOOD UREA

FINDINGS AND COURSE OF MANAGEMENT

THE PATIENT HAD LOW SODIUM IN THE RANGE OF SEVERE HYPONATREMIA THE PATIENT HAD S. Na+ LEVEL OF 122meq/L AT THE TIME OF INITIAL TESTING WHICH WAS THEN

REPEATED AFTER 2 DAYS AFTER DECREASING THE DOSAGE OF CABAMAZEPINE WHICH AGAIN CAME TO BE 123meq/L

ALL OTHER PARAMETERS WERE WITHIN NORMAL LIMITS. AFTER ADJUSTING THE DOSAGE OF DRUGS AND SUPPLEMENTING HIS DIET WITH HIGH SALT

CONTENT AND RESTRICTING WATER INTAKE THE SERUM SODIUM LEVEL WAS REPEATED WHICH CAME TO BE 126meq/L

NOW AFTER CONSULTATION WITH A ENDOCRINOLOGIST HE WAS ADMINISTERED NORMAL SALINE AT 100ML/HR ON ONE OCASSION AND WAS ADVISED TO CONTINUE SALT RICH DIET.

AFTER THESE COLLECTIVE STEPS HIS SERUM SODIUM LEVEL WAS FOUND TO BE 133meq/L ON 22.11.15 AND IS NOW FEELING BETTER AND MAINTAINING WELL

HIS S/S HAVE SUBSIDED AND HE IS NOW CALM AND HAPPY AND COOPERATIVE AND IN RECOVERY PHASE.

THOUGH THERE IS RISK OF REAPPEARANCE OF SEIZURES DUE TO DECREASED DOSAGE OF CARBAMAZEPINE.

PRESENT ONGOING MEDICATIONS

TAB CPZ 50MG H.S TAB. DEPAKOT XR 250 MG BD TAB DAXID 50MG BD TAB PACITANE 2MG BD TAB FRISIUM 5MG BD TAB SERENACE 10MG BD TAB ZONEGRON 100 BD TAB PAN 40 OD