mia and hypernatremia-deepak madhu
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8/3/2019 mia and Hypernatremia-Deepak Madhu
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Hyponatremia andhypernatremia
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… are disorders of waterbalance
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Hyponatremia
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Hyponatremia is a common clinicalproblem developing in around2.5% of hospitalized patients.
The case fatality rate was 60 timeshigher in patients in whomhyponatremia was present.
Problem statement
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Sodium is the main extracellular osmole,
A reduction in serum sodium is associated with areduction in osmolarity.
The clinical approach to hyponatremia begins byexcluding conditions in which osmolarity is not reduced.
Deepak Madhu
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All conditions in which hyponatremia does
not result in hypo-osmolarity is called“pseudohyponatremia”
There are two conditions in which
pseudohyponatremia is really alaboratory artifact namely hyperlipidemiaand hyperproteinemia. Serum osmolarityis normal in such cases.
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Conditions in which an osmoticallyactive substance such as glucoseor mannitol accumulates in theserum and draws water out of the
intracellular space also is referredto as a kind of “pseudohyponatremia”. Serum
osmolarity is increased hereDeepak Madhu
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Once pseudohyponatremia isexcluded, hyponatremia may beclassified on the basis of ECFvolume status.
Deepak Madhu
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Hyponatremia
Serum OSM
Low Normal High
HypotonicHyponatremia
ECFv *
Low Normal
High
HyperglycemiaMannitol
Marked hyperlipidemia(lipemia, TG >35mM)Hyperproteinemia(Multiple myeloma)
•CHF•Cirrhosis• Nephrosis
•Hypothyroidism•AI•SIADH•Reset Osmostat•Water Intoxication
1° PolydipsiaTURP post-op
Renal loss (UNa > 20)• Diuretics
• Thiazide• K-sparing
• ACE-I, ARB• IV RTA, Hypoaldo• Cerebral salt
wastin
Extra-renal loss (UNa <10)• Bleeding• Burns• GI (N/V, diarrhea)• Pancreatitis
* Note: all have ↑ADH•SIADH: inappropriate•Rest: appropriate
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Depend on magnitude of thehyponatremia and rapidity of
its development.Acute (< 48 hrs): Symptoms at[Na+] of ≤ 125 mEq/L. Seizures
and coma at ≤ 115 mEq/L.Chronic: often asymptomatic
Hyponatremia:
Clinical Manifestations
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Symptoms - mainly CNSEarly: nausea, malaise,headache, muscle twitching,
lethargyLate/Severe: obtundation,seizures, coma, respiratory
arrestDeepak Madhu
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Patients with ECF volume depletion
and hyponatremia have a deficit intotal body Na that is more than thedeficit in water.
Hyponatremia withextracellular volume depletion
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There is depletion of body solutesand a concomitant failure toexcrete water as the osmoreceptorand volume receptor receive
opposing stimuli and the osmoticset-point is lowered.
Hyponatremia with
extracellular fluid volumedepletion (cont)
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Clinical:
Orthostasis,
Flat neck veins
Decreased skin turgor
Dry mucous membranes
Tachycardia
Hyponatremia with
extracellular fluid volumedepletion
Deepak Madhu
● U● R● E● U● R● E
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● U Na
>20
● Rena
l los
s
● Extr
arena
l
● U
● Rena
l los
s
● Extr
arena
l
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Diuretic excess
Mineralocorticoid deficiency
Salt losing nephropathy
Bicarbonaturia with RTA and metabolic
alkalosis
Cerebral salt wasting
Renal loss
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Vomiting
Diarrhoea
Third spacing
Burns
Pancreatitis
Trauma
Extra renal loss
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Here total body water increases
Total body sodium also increases The rise in total body waterexceeds the rise in total body
sodium
Hyponatremia with excess ECFvolume
Deepak Madhu
● U● N● C● C● A● U● N● C● C● A
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● U Na
<20
● Neph
rotic
● Cirr
hosis
● Card
iac F
ailu
re
● Acut
e or
Chro
nic r
e
● U Na
>20
● Neph
rotic
● Cirr
hosis
● Card
iac F
ailu
re
● Acut
e or
Chro
nic r
e
Hypervolemic hyponatremia
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Decreased cardiac outputresults in limited delivery of tubule fluid to the distalnephron.
Decrement in arterial filling aresensed by aortic and carotidsinus baroreceptors andstimulate AVP release.
Congestive Cardiac Failure
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Patients with advanced cirrhosis develop
hyponatremia due to their inability toexcrete a water load.
Effective arterial blood volume is contracteddue to decreased osmolality as a result of
hypoalbuminemia and due to splanchnicpooling of blood.
This results in a high AVP state
Hepatic failure
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Hypoalbuminemia results inintravascular volume contractionand a high AVP state that results inan inability to excrete a water
load.
Nephrotic syndrome
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A decrement in GFR and anincrease in thirst underlies thehyponatremia of renal failure
Renal failure
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Not orthostatic
Not dehydrated
Not edematous .
Hyponatremia with normalECF volume
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Glucocorticoid deficiency
Hypothyroidism
Psychosis- primary polydipsia
Postoperative hyponatremia
Strenuous exercise
Pharmacologic agents
SIADH
Causes
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Isolated glucocorticoiddeficiency occurs withsecondary adrenalinsufficiency caused bypituitary disorders that impairnormal ACTH secretion butleave other stimuli to
Glucocorticoid deficiency
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Hyponatremia occurs relativelyfrequently in patients with pituitaryinsufficiency who do not havediabetes insipidus
Glucocorticoid deficiency
(cont)
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The exact mechanism by which
hypothyroidism causes hyponatremia isnot known
Impaired water excretion is often presentand diminished distal fluid delivery andpersistent avp release mediate theimpaired water excretion in this disorder.
Hypothyroidism
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Defects in osmoregulation that results in
AVP secretion at plasma osmolalities lowerthan normal
Psychotic exacerbations are also associatedwith increased vasopressin levels in
schizophrenic patients with hyponatremia.
Thirst perception is also increased.
Psychosis – Primary
polydipsia
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Primarily as a cosequence of hypotonic fluid administration,hyponatremia can also occur inthis high AVP state even when
isotonic fluids are given
Post-operative
hyponatremia
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Military training, marathons,triathlons…
Associated with weight gainrelated to excessive fluid intake
Symptomatic hyponatremia canresult
Strenuous excercise
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ADH analogues
Drugs that enhance AVP
Drugs that potentiate renal action
renal action of AVPDrugs that cause hyponatremia byunknown mechanism
Drugs
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Desmopressin acetate
Oxytocin
ADH hormone analogues
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Chlorpropamide
Clofibrate
Carbamazepine
Vincristine
Nicotine
Narcotics
Antipsychotics, antidepressants
Ifosfamide
Drugs that enhance AVP
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Chlorpropamide
Cyclophosphamide
NSAIDs
Acetaminophen
Drugs that potentiate renalaction of AVP
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Haloperidol
Fluphenazine
Amitryptiline
Thioridazine
SSRI
Ecstacy
Drugs that causehyponatremia by unknown
mechanisms
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SIADH
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SIADH is the most common cause of
euvolemic hyponatremia
The criteria was defined by Bartter
and Schwartz in 1967 in the originalclassic article that described thesyndrome
SIADH
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1. True ECF hypo-osmolarity must be present.
Pseudohyponatremia and hyperglycemia must beexcluded.
2. Urinary osmolality must be inappropriate. Withserum hypo-osmolarity, urine should be less than
maximally dilute (Uosm >100)
SIADH - Criteria
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3. Clinical euvolemia must be
present.
4. Urine sodium >20 the presenceor absence of this, does not,
however diagnose or excludeSIADH.
5. Other causes should be
excluded.
SIADH – Criteria (cont)
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Carcinomas
Pulmonary disorders
CNS disorders
Other
SIADH - Causes
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Bronchogenic carcinoma
Carcinoma of the duodenum
Carcinoma of the pancreas
Thymoma
Carcinoma of the stomach
Lymphoma
Ewing sarcoma
SIADH causing carcinomas
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Carcinoma of the bladder
Prostatic carcinoma
Oropharyngeal tumor
SIADH causing carcinomas(cont)
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Encephalitis
Meningitis
Head trauma
Brain abscess
GBS
Acute intermittent porphyria
SAH
Neurological disorders
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Cerebellar and cerebral atrophy
Cavernous sinus thrombosis
Neonatal hypoxia
Shy – Drager syndrome
Rocky mountain spotted fever
Delirium tremens
CVA
Neurologic disorders (cont)
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Acute psychosis
Peripheral neuropathy
Multiple sclerosis
Neurologic disorders (cont)
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Nephrogenic syndrome of
inappropriate antidiuresis.
Gain of function mutations in the
V2R results in antidiuresis in theabsence of AVP.
NSIAD
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Management of
hyponatremia
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Overly rapid correction of
hyponatremia can result in osmoticdemyelination
This can occur irrespective of the
etiology of hyponatremia or themethod used to correct it
Rate of correction
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Limits for the correction of hyponatremia:
<10-12mEq/L in 24 hrs and upto
<18 mEq/L in 48 hrs
Rate limits
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Subgroups at increased risk for ODS:
Severe malnutrition
Alcoholism
Advanced liver disease
In these patients, correction rate should bewell below the ‘normal’ correction limits.
High risk groups for ODS
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Correction by <3-4 mEq/L in 24hrs maybe
associated with excess mortality
But correction in excess of 10mmol/L in 24hrs or 18 mEq/L in 48hrs have not beenshown to improve outcome.
Rate of correction shouldneither be too slow nor too
fast…
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If volume depletion is present, the
volume deficit has to be corrected.And the relative water excess willcorrect itself
Correction of hypovolemichyponatremia
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Voulme resuscitation has to be
done with isotonic fluid until thepatient has attained clinicaleuvolemia.
Correction of hypovolemichyponatremia (cont)
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When the initial volume estimate is
equivocal, a fluid challenge with0.5 to 1 L of isotonic saline can beboth therapeutic and diagnostic.
Correction of hypovolemichyponatremia (cont)
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Isotonic saline is the mainstay of
treatment
KCl should be added if hypokalemia andmetabolic alkalosis are present due to
vomitingAn isonatric mixture of NaCl andNaHCO3 may be used if metabolicacidosis is present due to diarrhoea
Hypovolemic hyponatremiaassociated with excess
gastrointestinal loss
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Specific therapy for the underlying
disorder should be initiated, andantiemetics and antidiarrhoealsused as appropriate
Deepak Madhu
l i h i
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Obvious signs of dehydration and
volume depletion to be treatedpromptly with rehydration usingisotonic saline.
Hypovolemic hyponatremiaassociated with excess
sweating
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In the absence of obvious
dehydration, if hyponatremia ispresent, guidelines for EAH to befollowed. Isotonic saline should not
be started.
Deepak Madhu
H l i h i
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All diuretics to be withheld
The patient has to be repleted with isotonicfluid if the CNS abnormalities are mild
Hypertonic saline maybe used to raise theserum sodium level 4-5 mEq/L whenseizures or significant altered sensorium ispresent
Hypovolemic hyponatremiaassociated with diuretic
therapy
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Patients with thiazide induced
hyponatremia are at high risk of recurrence and should not berechallenged with a thiazide.
Deepak Madhu
C b l lt ti
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Patients with volume depletion from CSW
should be resuscitated by administrationof isotonic saline until they are euvolemicand maintained in neutral fluid balance
Hypertonic saline to be used if altered
sensorium believed to be due tohyponatremia is present.
Cerebral salt wasting
Deepak Madhu
C 1
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83 year old lady presented with a 3 week
history of memory disturbances. She has ahistory of hypertension and has recentlystarted antihypertensive medication,hydrochlorothiazide tablets. Otherwise she ishealthy and does not take any othermedications.
Case 1
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C 1 ( t)
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She also reports no nausea, vomiting or diarrhoea,
and the rest of her systems review is normal. Herheart rate is 100bpm and her BP is 110/70 mm Hg.When standing her pulse rate increases to 110/minand BP decreases to 90/60 mm Hg. RR – 12 bpm
Case 1 (cont)
Deepak Madhu
C 1 ( t)
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The physical examination reveals an elderly
woman in no acute distress. She is alert andoriented. The patient has dry mucous membranesand poor skin turgor. The rest of her examinationis within normal limits. Laboratory data show thatthe patient has dry mucous membranes and poor
skin turgor.
Case 1 (cont)
Deepak Madhu
C 1 ( t)
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The rest of her examination is within normal
limits. Laboratory data show that the patienthas Na -125Meq/L, a K-3.4 Meq/L, a plasmaosmolality of 270 mOsm/Kg H2O, UNa – 23MEq/Kg; BUN – 48mg/dl, S.Cr – 1.2mg/dl and aUrine osmolality of 400 mOsm/Kg of water.
Case 1 (cont)
Deepak Madhu
Q C 1
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What is the likely diagnosis for the
patient?
a) SIADH
b)
Thiazide induced hyponatremiac) Hypertonic hyponatremia
d) Renal insufficiency
Q: Case1
Deepak Madhu
A Q1
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What is the likely diagnosis for the
patient?
a) SIADH
b)
Thiazide induced hyponatremiac) Hypertonic hyponatremia
d) Renal insufficiency
Ans Q1
Deepak Madhu
Q2
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What is the next step in management?
a) Start IV normal saline
b) Start aggressive oral hydration
c) Start 3% saline to reach a 5% increase
in Na for the next 24 hours.d) Discontinue thiazide and continue
hydration using IV normal saline.
Q2
Deepak Madhu
A Q2
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What is the next step in management?
a) Start IV normal saline
b) Start aggressive oral hydration
c) Start 3% saline to reach a 5% increase
in Na for the next 24 hours.d) Discontinue thiazide and continue
hydration using IV normal saline.
Ans Q2
Deepak Madhu
Discussion Case 1
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Kindly note that it is wise to check
Na levels 1 week after startingthiazide diuretic
Discussion Case 1
Deepak Madhu
Dicsussion Case 1 ( Cont)
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The differences in the risk of hyponatremia
between thiazides and loop diuretics is due to thedifference in their mechanism of action.
With loop diuretics, the reabsorption of water dueto ADH is interfered , even though loop diureticsalso increase ADH levels by inducing volume
depletion
Dicsussion Case 1 ( Cont)
Deepak Madhu
Discussion Case 1 (cont)
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Thiazide induced hyponatremia
occurs in the first 1-2 weeks afterstarting thiazides .
Elderly women are more at risk.
Discussion Case 1 (cont)
Deepak Madhu
Euvolemic Hyponatremia
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Acute symptomatic hyponatremia -
3% saline
IV furosemide 20-40mg to be givento prevent fluid overload
Euvolemic Hyponatremia-SIADH
Management
Deepak Madhu
SIADH Management
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Infusion rate of hypertonic saline:
body wt(kg)Xrate of correctiondesired(mEq/L/hr)
For example a 70 kg man requiring
1meq/l/hr requires 70ml/hr of 3%saline.
SIADH - Management
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Acute treatment should be interrupted
once any of the three end points areachieved:
1. Patient ‘s symptoms are abolished
2. A safe serum Na+ level >120mEq/L is
achieved
3. A magnitude of correction18mEq/L isachieved
Deepak Madhu
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In SIADH with reset osmostat, no
treatment is required
Most other cases of mild-moderatehyponatremia can be managed
with fluid restriction.
Deepak Madhu
Fluid restriction measures
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1. All fluids not only water, should be included in thisrestriction.
2. The degree of restriction required depends on urineoutput plus insensible fluid loss- non food fluids restrictedto 500ml/day below the average daily urine volume.
3. Several days of restriction are necessary
4.
Only fluid, not sodium, should be restricted
Fluid restriction measures
Deepak Madhu
Fluid restriction measures
8/3/2019 mia and Hypernatremia-Deepak Madhu
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5. Because of the high negative
sodium balance, patients withSIADH need to be started on ahigh NaCl diet unless otherwise
contraindicated.7. Any drug potentially causing
SIADH should be
substituted/discontinued
Fluid restriction measures(cont)
Deepak Madhu
Pharmacologic therapy of
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Pharmacologic therapy is reserved
for cases refractory to fluidrestriction.
SIADH associated with tumors will
resolve with treatment of thelesion.
Pharmacologic therapy
Demeclocycline 600-1200 mg/day
Pharmacologic therapy of SIADH
Deepak Madhu
Pharmacologic therapy of
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Urea 30g/day PO may also be
used.
Vaptans are a new group of drugsthat have been found to be
effective.
Pharmacologic therapy of SIADH(cont)
Deepak Madhu
NSIAD
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Same as SIADH
Urea therapy has been found to beparticularly effective
Urea has to be dissolved in orange juice or any such solvent tocamouflage the taste.
NSIAD
Deepak Madhu
Glucocorticoid deficiency
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If there is suspicion of adrenal
insufficiency, glucocorticoidreplacement should be startedimmediately after a rapid ACTH
stimulation test
Glucocorticoid deficiency-management
Deepak Madhu
Glucocorticoid deficiency
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Prompt water diuresis after initiation of
glucocorticoid therapy confirms diagnosisAbsence of a quick response does notnegate this diagnosis
In such cases, primary treatment of the
hyponatremia is indicated if the patient issymptomatic
Glucocorticoid deficiency –management (cont)
Deepak Madhu
Hypothyroidism
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Hyponatremia associated with hypothyroidism
is generally mild and only modest fluidrestriction necessary
Symptomatic hyponatremia is seen in patientswith more severe hypothyroidism and alteredmental status, primary treatment of thehyponatremia is indicated
Hypothyroidism
Deepak Madhu
Exercise associated
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Can be severe and life threatening
as a result of cerebral oedema andnon-cardiogenic pulmonaryoedema.
Exercise associatedhyponatremia
Deepak Madhu
Exercise associated
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Runners are frequently fatigued, light
headed, pre-syncopal, or dizzy at theconclusion of exercise but seizures,profoundly altered level of consciousness,ataxia or focal neurological deficits should
raise suspicion of hyponatremia
Exercise associatedhyponatremia (cont)
Deepak Madhu
Exercise associated
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With significant CNS impairment,
hypertonic saline should be startedat once and continued till S. Na is>125 or symptoms resolve.
Exercise associatedhyponatremia (cont)
Deepak Madhu
Psychosis-polydipsia
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Clozapine has been found to be
useful in reducing and preventingrecurrent hyponatremia in a subsetof patients
Psychosis-polydipsiamanagement
Deepak Madhu
Case 2
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The patient is a 78 year old man who is
a cigarette smoker and presents withincreasing cough, hemoptysis, anddrowsiness. He is taking nomedications. During the last one year
he has lost approximately 8 Kg and hiscurrent weight is 72 Kg.
Case 2
Deepak Madhu
Case 2 (cont)
8/3/2019 mia and Hypernatremia-Deepak Madhu
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His mucous membranes are moist, skin
turgor normal and does not have anorthostatic fall in BP. Other thannicotine staining of right index andmiddle fingers, his physical
examination is normal. His chestexamination reveals a 4 cms lung massin the right.
Case 2 (cont)
Deepak Madhu
Case2 (cont)
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His S. Na is 123Meq/L , K is 4.3
Meq/L and creatinine is 1.1mg/dl.Measured osmolality is270mOsm/Kg. Uric acid level is
4.2mg/dl. And U Na – 45mEq/L. The TSH level is normal
Case2 (cont)
Deepak Madhu
Case 2: Q 1
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What is the cause of the patients
hyponatremia?a) Renal failure
b) Treatment with thiazides
c)
Hypothyroidismd) SIADH
Case 2: Q 1
Deepak Madhu
Case2:A1
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What is the cause of the patients
hypoonatremia?a) Renal failure
b) Treatment with thiazides
c)
Hypothyroidismd) SIADH
Case2:A1
Deepak Madhu
Further
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The patient insists on being
treated at home and agrees torestrict his fluid intake to 800mleach day. The next morning the
patients son brings the patientwith complaints of disorientationand unresponsiveness
Further …
Deepak Madhu
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The patient is comatose on examination and does notrespond to verbal or painful stimuli. His physical
examination, apart from mental status changes, issignificant for depressed reflexes. His repeatelectrolytes are as follows:
S.Na – 108mEq/L, K -4.0, S.Cr-4.0, S. Osm –264mOsm/Kg, Urine Osm – 600mOsm/Kg H20.
Deepak Madhu
Case2:Q2
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How sould the patient be managed?
a) Begin fluid restriction and administer NSb) Begin 3%saline and administer vasopressin
c) Begin fluid restriction and administer 3% salineinfusion.
d) Administer vasopressin and furosemide
Case2:Q2
Deepak Madhu
Case2:A1
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How sould the patient be managed?
a) Begin fluid restriction and administer NSb) Begin 3%saline and administer vasopressin
c) Begin fluid restriction and administer 3% salineinfusion.
d) Administer vasopressin and furosemide
Case2:A1
Deepak Madhu
Hypervolemic
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CHF – Fluid restriction is the
approach. Other options includedemeclocycline, Urea, and fluidrestriction.
Hypervolemichyponatremia-CHF
Deepak Madhu
Hypervolemic hyponatremia
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Cirrhosis: Fluid restriction should
be instituted. Demeclocycline –contraindicated due to the highincidence of nephrotoxicity. Urea
has not been tried often
Hypervolemic hyponatremia- Cirrhosis
Deepak Madhu
Nephrotic syndrome, ARF
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Fluid restriction is the only option
Nephrotic syndrome, ARFand CRF
Deepak Madhu
Case 3
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The patient is a 64 year old man who
presents with increasing shortness of breath, fatigue, paroxysmal nocturnaldyspnoea and marked oedema. He hasa long history of coronary artery
disease and underwent coronarybypass surgery 6 years ago.
Case 3
Deepak Madhu
Case 3 (cont)
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The patients physical examination
reveals JVD, rales and S3. His chestradiographs show B/L pleural effusions,cardiomegaly and interstitial infiltrates.His sodium levels is 121mEq/L, his K
-3.5, his urine sodium -5 mEq/L andplasma osmolality 260 mOsm/Kg of H2O
Case 3 (cont)
Deepak Madhu
Case3:Q1
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Which is the appropriate diagnosis for the patient?
a) Iso-osmotic hyponatremia
b) Isovolemic hypo-osmotic hyponatremia
c) Hypovolemic hypo-osmotic hyponatremia
d) Hypervolemic hypo-osmotic hyponatremia
Case3:Q1
Deepak Madhu
Case3:A1
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Which is the appropriate diagnosis for the patient?
a) Iso-osmotic hyponatremia
b) Isovolemic hypo-osmotic hyponatremia
c) Hypovolemic hypo-osmotic hyponatremia
d) Hypervolemic hypo-osmotic hyponatremia
Case3:A1
Deepak Madhu
Case3:Q2
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What is the reason for the
hyponatremia in this patient?a) Impairment of water excretion due to
ADH excess
b) Increased water intakec) SIADH
d) Adrenal failure
Case3:Q2
Deepak Madhu
Case3:A2
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What is the reason for the
hyponatremia in this patient?a) Impairment of water excretion due to
ADH excess
b) Increased water intakec) SIADH
d) Adrenal failure
Case3
Deepak Madhu
Case3:Q3
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How should the patient be treated?
a) Administer IV 3% saline solution
b) Start IV normal saline and loop diuretics
c) Implement fluid restriction and start
loop diureticsd) Start high doses of beta blockers
Q
Deepak Madhu
Case3:A3
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How should the patient be treated?
a) Administer IV 3% saline solution
b) Start IV normal saline and loop diuretics
c) Implement fluid restriction and start
loop diureticsd) Start high doses of beta blockers
Deepak Madhu
Infusates
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Infusate Meq/L
Normal Saline 154
3% saline 513
Deepak Madhu
Common salt
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Sodium chloride consists of 40%
w/w Na and 60% w/w Cl.One level teaspoon (US) contains5750mg salt which is 2300mg
sodium which is inturn 100mEq of Na
Deepak Madhu
Correction of Hyponatremia-
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1. Estimate total body water
2. Estimate the change in Na perlitre of infusate
3. Calculate the amount of infusaterequired
4. Calculate the rate of infusion
ypsteps
Deepak Madhu
For example
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A 70 kg man of age 45 years, with Na 0f 110mEq/L, is obtunded . The goal: his S.Na shouldincrease rapidly by 4 mEq/L over the next 2-4hours.
p
Deepak Madhu
Calculation of total body
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TBW = total body water
This is calculated by multiplyingbody weight with a correctionfactor
The correction factors vary withage and sex and is as follows…
ywater
Deepak Madhu
Correction factors
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Patient Correction factor
Pediatric 0.6
Male, non elderly 0.6
Female, non elderly 0.5
Male, elderly 0.5
Female, elderly 0.45Deepak Madhu
Formulas for calculating
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gchanges in sodium levels in
hypo/hyper-natremia
Deepak Madhu
The patient’s hyponatremia
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p ypcorrection
Deepak Madhu
Aquaretics
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Antagonists of the kidney
vasopressin V2 receptors(nicknamed vaptans) have longbeen predicted to be the ideal
agent for treatment of patientswith dilutional hyponatremia.
q
Deepak Madhu
Aquaretics (cont)
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These agents stimulate renal free
water excretion (aquaresis) andthereby lead to increased serum[Na+] in most patients with
dilutional hyponatremia due toSIADH, congestive heart failure, orcirrhosis.
q
Deepak Madhu
Conivaptan
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In 2005 the U.S. Food and DrugAdministration (FDA) approved conivaptan, acombined V1a and V2 vasopressin receptorantagonist, for treatment of euvolemichyponatremia, and in 2006 this approval wasextended to patients with hypervolemic
hyponatremia.
Deepak Madhu
Conivaptan (cont)
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Phase 3 clinical trials of conivaptan
demonstrated a prompt correctionof serum [Na+] in most treatedhyponatremic patients, averaging
6 to 8 mEq/L over a 2- to 4-daycourse of treatment.
Deepak Madhu
Conivaptan (cont)
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Conivatan is an inhibitor of the
hepatic cytochrome P450isoenzyme CYP3A4, and henceinhibits metabolism of many drugs
therefore, its use has been limitedto short-term (<4 days)intravenous administration inhospitalized patients.Deepak Madhu
Conivaptan (cont)
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Conivaptan was found to be useful
in that it corrected serum [Na+]more rapidly than fluid restrictionin patients with non–life-
threatening degrees of hyponatremia.
Deepak Madhu
Tolvaptan
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Tolvaptan, a selective V2
vasopressin receptor antagonist,was approved by the FDA in 2009for treatment of euvolemic and
hypervolemic hyponatremia.
Deepak Madhu
Tolvaptan (cont)
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Clinical trials of tolvaptan showed
normalization of serum [Na+] in mosthyponatremic patients treated, and thiseffect was sustained over a 30-daytreatment period with recurrence of the
hyponatremia by 7 days after cessationof the drug.
Deepak Madhu
Tolvaptan (cont)
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The use of tolvaptan in the United States islimited to patients with severe hyponatremia(serum [Na+] < 125 mEq/L) and those withmilder degrees of hyponatremia who aresymptomatic and for whom treatment withfluid restriction has failed.
Deepak Madhu
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Hypernatremia
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Hypernatremia is a rise in serum
sodium concentration to a valueexceeding 145 mEq/L.
Hypernatremia invariably denotes
hypertonic hyperosmolality andalways causes cellular dehydrationatleast transiently
Deepak Madhu
Hypernatremia can result
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Net water loss or hypertonic sodium
gainNet water loss accounts for themajority of cases
Net water loiss can be pure water loss(no sodium deficit) or hypotonic fluidloss.
from…
Deepak Madhu
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Hypertonic sodium gain usually
results from accidental sodiumloading.
Deepak Madhu
Pure water loss
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Insensible losses
Hypodipsia
Neurogenic diabetes insipidus
Congenital nephrogenic diabetesinsipidus
Acquired nephrogenic diabetes
insipidusDeepak Madhu
Hypotonic fluid loss
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Renal causes: loop diuretics, Osmotic
diuretics, Postobstructive diuresis,polyuric phase of ATN, intrinsic renaldisease
GI causes: Vomiting, nasogastric
drainage, enterocutaneous fistula,diarrhoea, use of osmotic catharticagents
Deepak Madhu
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Cutaneous causes: excessive
sweating, burns
Deepak Madhu
Hypertonic sodium gain
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Hypertonic sodabicarb infusion
Hypertonic feeding preparation
Ingestion of sodium chloride
Ingestion of sea water
Sodium chloride – rich emetics
Hypertonic saline enemas
Deepak Madhu
Hypertonic sodium gain( )
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Intrauterine injection of hypertonic
salineHypertonic sodium chlorideinfusions
Hypertonic dialysis
Primary hyperaldosteronism
Cushing’s syndrome
(cont)
Deepak Madhu
Clinical manifestations of h i ( )
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• Symptoms may start as lethargy, weaknessand irritability
• May progress to twitching, seizures,obtundation or coma
• Cell dehydration and resulting decrease in
brain volume can lead to rupture of cerebral veins leading to hemorrhage
hypernatremia (cont)
Deepak Madhu
Clinical manifestations of h t i ( t)
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• Severe symptoms usually occur
with rapid increase of sodiumconcentration to 158 mEq ormore
•
Sodium concentration greaterthan 180 mEq are associatedwith high mortality
hypernatremia (cont)
Deepak Madhu
Management
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Two pronged apprroach which
requires management of theunderlying cause as well asmanagement of the hypernatremiaitself
Deepak Madhu
Management (cont)
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Hypernatremia that developed
over a period of hours can becorrected rapidly.
In such patients, the sodium
maybe reduced at a rate of 1mEq/L/hr
Deepak Madhu
Management (cont)
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In hypernatremia of longer or
unknown duration, a slower rate of correction is required.
The maximum rate of correction in
such patients is 0.5mEq/L/hr.
Deepak Madhu
Management (cont)
8/3/2019 mia and Hypernatremia-Deepak Madhu
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In a hypovolemic patient, volumeresuscitation for a hemodynamicallyunstable patient should be accomplished byisotonic 0.9% saline. One the patient ishemodynamically stable, intravenous fluidsshould be changed to a hypotonic 0.45%
saline.
Deepak Madhu
Management (cont)
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The euvolemic patient: pure water
replacement with iv hypotonicsaline or free water.
Dextrose containing solutions may
be used but blood sugar should bemonitored as hyperglycemia wouldcontribute to osmolarity
Deepak Madhu
Management (cont)
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For significantly hypernatremic
individuals in whom central DI isconsidered, 5-10 units of aqueousvasopressin should be givensubcutaneously every 3-4 hours.
Deepak Madhu
Management (cont)
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Sodium levels in the serum should
be checked every 4 hours.Cerebral oedema is an importantcomplication of hyponatremia
correction.
Deepak Madhu
Management (cont)
8/3/2019 mia and Hypernatremia-Deepak Madhu
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In order to avoid cerebral oedema, a
maximum decrease of 10 mEq/L per 24hour period is recommended.
The free water deficit has to becalculated first,and no more than half of
the water deficit is to be corrected in thefirst 24 hours and the remainder has tobe corrected over the next 1-2 days.
Deepak Madhu
Calculation of free waterdeficit
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deficit
Deepak Madhu
Calculation of total bodywater
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TBW = total body water
This is calculated by multiplyingbody weight with a correctionfactor
The correction factors vary withage and sex and is as follows…
water
Deepak Madhu
Correction factors
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Patient Correction factor
Pediatric 0.6
Male, non elderly 0.6
Female, non elderly 0.5
Male, elderly 0.5
Female, elderly 0.45Deepak Madhu
For example…
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Deepak Madhu
How is the free water deficitcorrected?
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The free water deficit maybe
corrected over 3 days. Total intake = (total output +insensible + 1/3 – 1/2 water
deficit) each day for the next threedays.
corrected?
Deepak Madhu
Formulas for calculatingchanges in sodium levels in
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changes in sodium levels in
hypo/hyper-natremia
Deepak Madhu
Infusate composition
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Infusate Infusate Na ECF distribution
5%D 0 40
0.2% NaCl in 5%D 34 55
0.45% NaCl inwater
77 73
Ringers lactate 130 97
0.9% NaCl in water154 100Deepak Madhu
Case 4
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A 76-year-old man presents with a severeobtundation, dry mucous membranes,decreased skin turgor, fever, tachypnea, anda blood pressure of 142/82mm Hg withoutorthostatic changes. The serum sodiumconcentration is 168 mmol per liter, and the
body weight is 68 kg. How would youmanage the patient?
Deepak Madhu
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Deepak Madhu
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Deepak Madhu
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Deepak Madhu
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The patient’s serum glucose level also has tobe monitored regularly and insulin given at
the slightest signs of hyperglycemia
Other parameters have to be monitoredatleast every 6 hours.
Deepak Madhu
Case 5
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A 58-year-old woman with postoperativeileus is undergoing nasogastric suction. Sheis obtunded and has diminished skin turgorand mild orthostatic hypotension. The serumsodium concentration is 158 mEq per liter,the potassium concentration is 4.0 mEq per
liter, and the body weight is 63 kg. howwould she be managed?
Deepak Madhu
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She has hyponatremia due to hypotonicfluid loss and therefore an infusion of 0.45 percent NaCl maybe planned.
The initial administration of isotonicsaline is not warranted as her
hemodynamic status is not socompromised as to require it.
Deepak Madhu
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Deepak Madhu
Q continued
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The patients S.Na levels rechecked
came as 155mEq/L at the end of 12 hours and the patient continuesto be somnolent.How would youproceed?
Deepak Madhu
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More aggressive lowering of the
S.Na levels is required and thepatient maybe shifted to analternative agent, say, 0.2% saline.
Therapy maybe resumed with theaim of reducing the S.Na levels by10mmols over the next 24 hours.
Deepak Madhu
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One litre of 0.2%NaCl is expected to reducethe S.Na levels by 3.7L and thus 2.7 L of fluid
is required to achieve the goal.
With the allowance for ongoing loss + urineoutput + insensible loss, say 2L, the total fluidrequired, 4.7L, maybe given IV over 24 hours
at the rate of 200ml/hr.
Deepak Madhu
Case 6
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A 60-year-old man has received 10
ampules of sodium bicarbonateover a period of six hours duringresuscitation after recurrentcardiac arrest. He is stuporous andis undergoing mechanicalventilation..
Deepak Madhu
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His blood pressure is 138/86 mm
Hg, and peripheral edema (+++)is present. The serum sodiumconcentration is 156 mmol perliter, the body weight is 85 kg, andthe urinary output is 30 ml perhour. How will you proceed tomanage this patient?Deepak Madhu
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The patient has hyponatremia due tohypertonic sodium gain and itscorrection requires excess sodium andwater to be excreted.
The administration of furosemide along
with electrolyte free water will berequired.
The estimated TBW =0.6*85 = 51LDeepak Madhu
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The retention of 1 L of 5%D is expected todecrease S.Na levels by 3mEq/L and 2L
maybe infused over 8 hours. The patientsvolume status and clinical status should beclosely watched. The correction will beopposed by hypotonic renal and extrarenal
loss. Allowance for ongoing fluid but notsodium loss may also be taken into account.
Deepak Madhu
Complications of hypo/hypernatremia
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Rapid overcorrection of
hyponatremia and hypernatremiacan result in osmotic demyelinationand cerebral oedema respectively.
Rapid transcellular shift of water canresult in cellular damage,particularly in the CNS
hypo/hypernatremia
Deepak Madhu
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As an initial compensatory
mechanism to preserve cellvolume, there is rapid shift of sodium , potassium, chloride andwater out of the cells inhyponatremia and into the cells inhypernatremia.
Deepak Madhu
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After 48 – 72 hours, a slower
adaptive phase takes effect.Cells mobilize organic osmolytes,comprised mostly of amino acids,
to continue efforts to maintainnormal cellular volume
Deepak Madhu
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The initial and gradual flux of ions
help maintain normal cellularvolume.
Excessively rapid correction of
hypo and hypernatremia can resultin extreme cellular volumechanges and cellular damage
Deepak Madhu
Click to edit Master text stylesS d l l
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Second level●
Third level● Fourth level
● Fifth level
Deepak Madhu
Osmotic demyelinationsyndrome
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Occurs when water moves too
rapidly out of brain cells duringadministration of relativelyhypertonic saline solutions.
Classically described in the pons,this has also been described inother parts of the brain also
syndrome
Deepak Madhu
ODS
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These patients classically present
with deteriorating mental statusand progressive neurologicaldeficits, such as pseudobulbarpalsies and spastic quadriparesis,after a transient period of improvement with fluidadministration.Deepak Madhu
ODS
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ODS typically occurs 1 to 6 days
after treatment. It is associatedwith dismal prognosis and has noeffective treatment.
Chronic alcoholism andmalnutrition have also beenassoiciated with ODS.
Deepak Madhu
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Thank You