HYPONATREMIA IN
CLINICAL PRACTICE
BY
DR.ROHAN PATTANAIK
2010 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. CHF
2. Liver cirrhosis
3. Nephrotic syndrome
4. Renal failure
5. Diuretics
6. Ketonuria
7. Addison’s Disease
8. Sweating
9. Vomitting
10. Diarrhoea
11. Hyperglycemia
12. Mannitol administration
13. Hypothyroidism
14. Adrenal insufficiency
15. 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
PATIENTS
1. Primary polydipsia as in Schizophrenics with psychosis
2. Psychotropic drugs causing dryness of mouth and increased thirst.
3. SSRIs intake
4. Anti-epileptics and Mood stabilizers (such carbamazepine and
oxcarbezapine commonly)
5. Anti-psychotics and anti-depressants
6. MMDA drug(“Ecstasy”) addiction
7. 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 INTAKE
2. INCREASING SALT INTAKE
3. TAKING FOODS RICH IN SODIUM
4. 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 RESTRICTION
2. 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 HYDROCORTISONE
2. LOOP DIURETICS
3. HYPERTONIC SALINE I.V INFUSION
 IN PSYCHIATRIC PATIENTS:-
1. STOP SSRIs OR ANTI-PSYCHOTICS OR MOOD STABILIZERS
2. FLUID RESTRICTION AND SALT INTAKE
3. I.V INFUSION OF HYPERTONIC SALINE
4. IF REQUIRED V2 RECEPTOR ANTAGONISTS
5. 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
Hyponatremia in Clinical Practice

Hyponatremia in Clinical Practice

  • 1.
  • 2.
    SODIUM-Few uses in humanbody.  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.
  • 3.
    Sodium in HumanBody 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.
  • 4.
    SOME FOODS RICHIN SODIUM  SMOKED MEATS  BEET  CELERY  PICKLES  CEREALS  CHEESE  MILK
  • 5.
    What is Hyponatremia???? Definition:-Hyponatremiais 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.
  • 6.
    INCIDENCE  It isthe 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.
  • 7.
    PATHOPHYSIOLOGY  MOST OFTENHYPONATREMIA 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)
  • 8.
    TYPES  TYPE 1:-EuvolemicHyponatremia-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.
  • 9.
  • 10.
    DIFFERENTIAL DIAGNOSIS OFDIFFERENT TYPES OF HYPONATREMIA
  • 11.
    ETIOLOGY  Most commoncause of hyponatremia is Syndrome of Inappropriate Secretion of Anti Diuretic Hormone (SIADH).  Other causes:- 1. CHF 2. Liver cirrhosis 3. Nephrotic syndrome 4. Renal failure 5. Diuretics 6. Ketonuria 7. Addison’s Disease 8. Sweating 9. Vomitting 10. Diarrhoea 11. Hyperglycemia 12. Mannitol administration 13. Hypothyroidism 14. Adrenal insufficiency 15. Drugs
  • 12.
  • 13.
    SOME KNOWN DRUGSCAUSING HYPONATREMIA
  • 14.
    FEW MECHANISMS OFDRUG INDUCED HYPONATREMIA
  • 15.
    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.
  • 16.
  • 17.
    COMMON CAUSES OFHYPONATREMIA ENCOUNTERED IN PSYCHIATRIC PATIENTS 1. Primary polydipsia as in Schizophrenics with psychosis 2. Psychotropic drugs causing dryness of mouth and increased thirst. 3. SSRIs intake 4. Anti-epileptics and Mood stabilizers (such carbamazepine and oxcarbezapine commonly) 5. Anti-psychotics and anti-depressants 6. MMDA drug(“Ecstasy”) addiction 7. Beer potomania 8. Nicotine abuse
  • 18.
    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
  • 19.
    CLINICAL FEATURES  MUSCLECRAMPS  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
  • 20.
    NEUROLOGICAL S/S OFHYPONATREMIA
  • 21.
    S/S AT AGLANCE
  • 22.
    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
  • 23.
    INVESTIGATIONS  SERUM SODIUMAND 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
  • 24.
    TREATMENT NON-MEDICAL MANAGEMENT:- 1. RESTRICTINGWATER INTAKE 2. INCREASING SALT INTAKE 3. TAKING FOODS RICH IN SODIUM 4. AVOIDING STRENOUS WORK
  • 25.
    TREATMENT  MEDICAL MANAGEMENTACCORDING 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.
  • 26.
    TREATMENT  IN CHRONICSIADH:- 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 RESTRICTION 2. 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.
  • 27.
    TREATMENT  IN TYPE3 HYPONATREMIA:- 1. STRESS DOSES OF HYDROCORTISONE 2. LOOP DIURETICS 3. HYPERTONIC SALINE I.V INFUSION  IN PSYCHIATRIC PATIENTS:- 1. STOP SSRIs OR ANTI-PSYCHOTICS OR MOOD STABILIZERS 2. FLUID RESTRICTION AND SALT INTAKE 3. I.V INFUSION OF HYPERTONIC SALINE 4. IF REQUIRED V2 RECEPTOR ANTAGONISTS 5. FREQUENT SERUM SODIUM MONITORING
  • 28.
    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.
  • 30.
    NOW A SHORTPSYCHIATRIC CASE DISCUSSION AFFECTED WITH HYPONATREMIA
  • 31.
    GENERAL HISTORY  MYPATIENT 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.
  • 32.
    MSE  GENERAL APPEARANCE-18YR 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
  • 33.
    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.
  • 34.
    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
  • 35.
    FINDINGS AND COURSEOF 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.
  • 36.
    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