ppt of siadh

1. PROF.DR.P.VASANTHII’S UNIT
DR.V.GIRIDHARAN
A CASE OF HYPONATREMIA

2. • 68 yr old lady known diabetic and hypertensive for the
past 2 years presented to zerodelay with h/o
• chest pain,breathlessness -3 hrs duration
• No h/o palpitation
• No h/o sweating
• No h/o decreased urine output
• No h/o cough or expectoration
• No h/o fever
• No h/o head ache
• No h/o myalgia

3. • No h/o abdomen pain
• No h/o loose stools
• No h/o vomiting
• No h/o weakness of limbs
• No h/o any visual distrubances
• No h/o seizure
• No h/o syncope
• No h/o dizziness
• No h/o bladder /bowel distrubances
• No h/o loss of conciousness
• No h/o altered behaviour

4. ON EXAMINATION
• Pt concious,oriented
• Anxious
• Dyspnoeic/tachypnoeic (28/min)
• Afebrile
• No pallor
• Not cyanosed
• No clubbing
• No icterus
• No pedal edema
• Jvp not elevated
• No lymphadenopathy

5. • S1 s2 –present,no murmur
• RS-nvbs present, no crepitations
• P/A- soft,
no tenderness
no organomegally
bowel sounds +
• CNS-nfnd

6. • Known diabetic,hypertensive for past two
years–chest pain for 4 hrs ,
• Vitals stable,
• ECG-ST elevation 1,Avl,v2-v4,
• Echo-hypokinesia distal 2/3 of ivs, aw,apex.
• EF-45./.
• Thrombolysed with streptokinase.
• In ICCU with cardiac drugs

7. • No other positive history .
• Prior h/o right hemiparesis 2 yrs ago but
recovered
• Pt was concious ,well oriented at admission and
after lysis.
• Pt was dyspnoeic ,tachypnoeic (rate 28/min)
• Not febrile
• No pallor
• Not cyanosed,no clubbing,no icterus
• Jvp –not elevated

8. DAY 1
• S1 s2 +,no murmur.
• S3,s4 not heared.
• Rs-nvbs ,no crepitations
• P/A-soft
• CNS-NFND

9. DAY 1
• BP-156/90
• Pulse-106/min
• SPO2-96./. With 4 lit/min o2 (mask)
• ECG- ST elevation lead 1,aVL ,v2-v4

10. DAY 1
BLOOD SUGAR 268 mg/dl
UREA 26 mg/dl
S.CREATININE 0.8 mg/dl
Na+ 139 mg/dl
K+ 3.9 mg/dl
CPK MB 32 UNITS/L
URINE KETONES NEGATIVE

11. DAY 1
PARAMETER RESULT
HB ./. 10.2 g/dl
TOTAL COUNT 8,600
DIFFERENTIAL COUNT 65/30/5
ESR 8/16
PLATELET COUNT 2.4 lakhs
RBC 3 million
PCV 30

12. DAY 1
• Pt was thrombolysed with streptokinase
• Pt doing well till that afternoon
• After 5 pm on that day pt developed altered
sensorium
• Neurological examination shows paucity of
movement on right side
• Pt was drowsy,disoriented
• Suspected ICH ( complication of lysis)

13. DAY 1
• Emergency CT taken –didn,t show any
haemorrhage
• Infarct seen in left cerebellar hemesphire
• MRI was planned next day
• Neuro opinion was obtained
• Advised MRI/electrolytes
• Mean while pt was on cardiac drugs

14. DAY 1
BLOOD SUGAR 256 mg/dl
UREA 31 mg/dl
S.CREATININE 1.1 mg/dl
Na+ 107 mg/dl
K+ 4.2 mg/dl

15. • Pt was treated cautiously with iv fluid normal
saline 50-75 ml/hr ,while monitoring signs for
volume overload and urine output

16. DAY 2
TIMING Na+ LEVELS
MORNING LOW RANGE
AN 111 meq/l
EVENING 108 meq/l
MRI BRAIN ACUTE LEFT CEREBELLAR INFARCT
CHRONIC INFARCT LEFT TEMPARO-
PARIETAL REGION

17. 1
•SHT /T2DM
2
•ACS/AWMI
3
•CVA/CEREBELLAR INFARCT

18. SHT/T2DM ACS/AWMI
CVA/ACUTE
CEREBELLAR INFARCT
HYPONATREMIA
?

19. What next?
• In the back ground of
SHT
DM2
OLD CVA
ACS/AWMI
ACUTE LT CEREBELLAR
INFARCT
HYPONATREMIA

20. • Hypo or hypernatremia is primarily is a
disorder of water balance

21. hyponatremia
• Na+ <135 meq/l
• Subdivided diagnostically into three
groups,depending upon clinical history and
volume status.
hyponatremia
hypovolemic
euvolemic
hypervolemic

23. ASSESS THE VOLUME STATUS
Urine osmoality
>100 mosm/l
Plasma osmolality
<275 mosm/l

24. Hyponatremia is classified according to
volume status, as follows
• Hypovolemic hyponatremia: decrease in total
body water with greater decrease in total
body sodium
• Euvolemic hyponatremia: normal body
sodium with increase in total body water
• Hypervolemic hyponatremia: increase in total
body sodium with greater increase in total
body water

26. IN OUR PATIENT
HYPONATREMIA
1)ACS
2)AWMI
3)MILD PEDAL EDEMA
4)NO JVP
1)SHT
2)T2DM/HYPERGLYCEMIA
3)CREATININE-
1.2/INTERSTITIAL
NEPHRITIS
1)OLD CVA
2)RECURRENT CVA
3)ACUTE CEREBELLAR
INFARCT
HYPERVOLEMIA? HYPOVOLEMIC? EUVOLEMIC/HYPOV
OLEMIC?

27. PSEUDO HYPONATREMIA
• Hyperlipidemia
• Hyperproteinemia
• Hypertonic (or translocational) hyponatremia
occurs when osmotically active solutes
(glucose or mannitol) draw water from cells.
• For each increase of 100 mg /dl of glucose,
sodium declines by 1.6 to 2.4 meq/l

28. CONFUSED OF HYPO OR EUVOLEMIC?
• When diagnostic uncertainty remains, volume
contraction of the extracellular fluid can be ruled
out by infusing 2 liters of 0.9% saline over a
period of 24 to 48 hours.
• Even though 0.9% saline is not the preferred
treatment for SIAD, it is usually safe when the
baseline urinary osmolality < 500 mOsm /kg
• correction of the hyponatremia suggests underly
ing volume depletion of extracellular fluid.

29. SERUM OSMOLALITY 267 mOsm/kg
URINE OSMOLALITY 281 mOsm/kg
URINE SODIUM 95 meq/l
Urine chloride 83 mOsm/l
Urine spot k+ 7 meq/l

30. Thyroid function test
T4 2
TSH 4
7 AM CORTISOL
X RAY CHEST NORMAL
USG ABDOMEN NORMAL KIDNEY SIZE ,1.1 mm left
renal calculi,resr normal

31. S.URIC ACID 4 mg/dl

32. ADH
• Synthesized in hypothalamus
• Transported down to posterior pituitary
• Released in response to hyperosmolality (major stimuli,
mediated through osmoreceptors in hypothalamus) or
hypovolemia (via baroreceptors in left atrium, aortic arch, etc)

33. ADH
• Binds to V2 receptors in collecting tubules
– stimulates cyclic adenosine monophosphate
– leads to insertion of aquaporin-2 channels into apical
membranes
• The goal is to facilitate the transport of solute-free water

34. SIADH => SIAD
• A slight misnomer
• The name implies inappropriate secretion
• 1/3rd of pts do secrete AVP independent of plasma osmolality
• Others exhibit reset osmostat – AVP is fully supressed, but
serum Na level is lower than nl
• AVP levels may be undetectable in some pts
• Some aquaporin mutations lead to concentrated urine in the
absence of AVP
• Therefore, the new term, Syndrome of Inappropriate
Antidiuresis (SIAD) has been proposed

35. Patterns of plasma levels of arginine vasopressin (AVP; also known as the antidiuretic hormone), as compared with
plasma sodium levels in patients with SIAD, are shown. Type A is characterized by unregulated secretion of AVP, type B
by elevated basal secretion of AVP despite normal regulation by osmolality, type C by a "reset osmostat," and type D by
undetectable AVP. The shaded area represents normal values of plasma AVP. Adapted from Robertson

36. DOES AVP NEEDS MEASUREMENT?
• Measurement of the serum level of arginine
vasopressin is not recommended routinely,
because urinary osmolality above 100 mOsm
per kilogram of water is usually sufficient to
indicate excess of circulat- ing arginine
vasopressin.

38. Neurological adaptation
• The severity of neurologic symptoms
correlates well with the rate and degree of the
drop in serum sodium. A gradual drop in
serum sodium, even to very low levels, may be
tolerated well if it occurs over several days or
weeks, because of neuronal adaptation.

39. SIADH
Hypothalamus receives
feedback from:
• Osmoreceptors
• Aortic arch baroreceptors
• Carotid baroreceptors
• Atrial stretch receptors
Any increase in osmolality or
decrease in blood volume will
stimulate ADH secretion from
posterior pituitary.

40. SIADH - pathophysiology
 ADH-induced water retention
 Dilutional hyponatremia
 Volume expansion -> secondary natriuresis
 Sodium and water loss
 Potassium loss
 Result: Euvolemic hyponatremia
 Reduced serum osmolality
 Increased urine osmolality
 Increased urine sodium

41. SIADH - treatment
Treat the underlying cause, if known
Fluid Restriction – commonly 800-1000mL/d
Correct Na+ deficit – no more than 10mEq/L in
24 hours, 18mEq/L in 48 hours
0.9% NaCl
3% NaCl
NaCl enteral tablets – 2-3g TID
Add a loop diuretic

43. Malignant
Diseases
Pulmonary
Disorders
Disorders of CNS Drugs Other
Causes
Carcinoma
Lung
Small cell
Mesothelioma
Oropharynx
Gastrointestinal
tract
Stomach
Duodenum
Pancreas
Genitourinary
tract
Ureter
Bladder
Prostate
Endometrium
Endocrine
thymoma
Lymphomas
Sarcomas
Ewing's sarcoma
Infections
Bacterial
pneumonia
Viral pneumonia
Pulmonary
abscess
Tuberculosis
Aspergillosis
Asthma
Cystic fibrosis
Respiratory
failure associated
with positive-
pressure
breathing
Infection
Encephalitis
Meningitis
Brain abscess
Rocky Mountain spotted
fever
AIDS
Bleeding and masses
Subdural hematoma
Subarachnoid hemorrhage
Cerebrovascular accident
Brain tumors
Head trauma
Hydrocephalus
Cavernous sinus
thrombosis
Other
Multiple sclerosis
Guillain-Barré syndrome
Shy-Drager syndrome
Delerium tremens
Acute intermittent
Drugs that stimulate
release of AVP or
enhance its action
Chlorpropamide
SSRIs
Tricyclic
antidepressants
Clofibrate
Carbamazepine
Vincristine
Nicotine
Narcotics
Antipsychotic drugs
Ifosfamide
Cyclophosphamide
Nonsteroidal anti-
inflammatory drugs
MDMA (ecstasy)
AVP analogues
Desmopressin
Oxytocin
Vasopressin
Hereditary
(gain-of-
function
mutations in
the
vasopressin
V2 receptor)
Idiopathic
Transient
Endurance
exercise
General
anesthesia
Nausea
Pain
Stress

44. • SIAD may be difficult to distinguish from
cerebral salt wasting, a syndrome of
hyponatremia and ex- tracellular-fluid volume
depletion in patients with insults to the
central nervous system.43,44 The pri- mary
feature that differentiates cerebral salt wast-
ing from SIAD is extracellular-fluid volume
deple- tion, but clinical assessment of volume
status is imprecise

48. Cerebral Salt Wasting
 Hyponatremia caused by impaired renal tubular
function -> inability of kidneys to conserve salt
 Salt wasting leads to volume depletion
 Two theories:
 Impaired sympathetic neural input -> failure of
aldosterone release -> no sodium resorption
 BNP release decreases sodium resorption, inhibits
renin/aldosterone release, decreases autonomic
outflow at level of brainstem

49. Cerebral Salt Wasting
Commonly occurs in subarachnoid
hemorrhage population (7%)
Carcinomatous, infectious meningitis
Encephalitis
Poliomyelitis
CNS tumors
CNS surgery – usually within the first 10 days

50. CSW

52. Cerebral Salt Wasting
• Treat with volume repletion
– 0.9% NaCl
– 3% NaCl is sometimes warranted
– Fludrocortisone

53. MANAGEMENT OF HYPONATREMIA
Water deficit
1. Estimate total-body water (TBW): 50% of body weight in women and 60% in men
2. Calculate free-water deficit: {([Na+]-140)/140} x TBW
3. Administer deficit over 48–72 h, without increasing the plasma Na+ concentration by
>10 mM/24 h
Ongoing water losses
4. Calculate electrolyte-free water clearance, CeH2O:
where V is urinary volume, UNa is urinary [Na+], UK is urinary [K+], and PNa is plasma [Na+]
Insensible losses
5. 10 mL/kg per day: less if ventilated, more if febrile
Total
6. Add components to determine water deficit and ongoing water loss; correct the
water deficit over 48–72 h and replace daily water loss. Avoid correction of plasma
[Na+] by >10 mM/d

54. Remember....
• Elevated BUN and creatinine in routine chemistries also can indicate renal
dysfunction as a potential cause of hyponatremia,
• whereas hyperkalemia may suggest adrenal insufficiency or hypoaldosteronism.
• Serum glucose also should be measured; plasma Na+ concentration falls by 1.6 to
2.4 mM for every 100-mg/dL increase in glucose due to glucose-induced water
efflux from cells; this "true" hyponatremia resolves after correction of
hyperglycemia.
• Measurement of serum uric acid also should be performed; whereas patients with
SIAD-type physiology typically will be hypouricemic (serum uric acid <4 mg/dL),
• volume-depleted patients often will be hyperuricemic.
• In the appropriate clinical setting, thyroid, adrenal, and pituitary function should
also be tested;
• hypothyroidism and secondary adrenal failure due to pituitary insufficiency are
important causes of euvolemic hyponatremia,
• whereas primary adrenal failure causes hypovolemic hyponatremia
• A cosyntropin stimulation test is necessary to assess for primary adrenal
insufficiency.