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Admitting

Conference
Jan Andre Montemayor, M.D.
March 16, 2015

Objectives
Cite the clinical coarse of a patient with
hyponatremia

Discuss the approach to diagnosis


Discuss management

M.M. 63F
Hypertensive (2014)
Non smoker
Non alcoholic beverage drinker
Previously admitted due to weakness, d/c stable

Chief Complaint
Body weakness

History Present illness


3 weeks PTA

Vomiting x2 PIF
Took unrecalled medications
No relief

DOA

Persistence of vomiting
Associated with weakness described as loss of
balance

At the E.R.
Wheelchair borne, conversant weak looking
Stable vital signs BP 140/80 PR 72 RR 20 36.3.
Dry lips, -NVE, CBS, NRRR, no edema, pulses good
CBC, Baseline CBG 97, Na 120, K 4.30, and Crea 74
Initial IMP: Acute gastroenteritis with signs of
dehydration with a consideration of electrolyte
imbalance probably secondary to poor oral intake

Started on hydration of PNSS

Course in the Wards


1st hospital day

Still complains vomiting


Slight dizziness
Given Betahistine which provided minimal relief.

Second hospital day

Complained of slight difficulty of breathing


Hooked to ECG which showed normal sinus
rhythm with non specific wave changes

Hooked to nasal cannula for O2 support

4th hospital day

Repeat Na 108
No clinical signs improvement
Referred to Internal medicine for comanagement
Further Review of history, patient was noted
fluid intake at home (3L?)

PHYSICAL EXAMINATION AT TIME WHEN PX SEEN:

General: Lethargic arousable to name calling, however


uncooperative.

Vital Signs BP 130/80 PR 75 RR 20 afebrile.


SKIN: warm to touch, good skin turgor
HEENT: anicteric sclerae, pink palpebral conjunctivae, moist
buccal mucosa, no neck vein engorgement

CHEST & LUNGS: symmetric chest expansion, clear breath


sounds

HEART: adynamic precordium, normal rate regular rhythm,


no murmur

ABDOMEN: non-tender, non globular normoactive bowel


sounds

EXTREMITIES: grossly normal extremities, full pulses

IMP: Symptomatic hyponatremia acute probably


secondary to 1.) Water intoxication 2.) r/o SIAD

Monitor NVS q2 I/O qshift


Dx
BUN, RBS, Non fasting lipid profile, FT4, TSH, Urine
osmolarity

Tx
Given furosemide 20mg IV
Suggest to incorporate 30%NaCl 20mL in current
IVF

Fluid restriction 1L

5th hospital day


No dizziness, still bedbound, no headaches, 1
episode of vomiting
VS 130/80 95 20 afebrile
(-)NVE, CBS, no edema

Na 115
referred to a nephrologist
given tolvaptan tablet

6th hospital day

Awake, conversant, good appetite, complains of


left arm weakness

(-) NVE, CBS, pulses good


Na 129
Deferral of next tolvaptan dose

7th hospital day

Signs of clinical improvement was marked


More awake, responsive and conversant
VS BP 130/90 PR 75 RR 20 Temp 36.4

On the 10th hospital day patient was discharged

, per

Discussion

Sodium is the main ECF


determinant

Hyponatremia
Serum sodium < 135 mmol/L

ski G. et al. Clinical practice guideline on diagnosis and treatment of hyponatrem


an Journal of Endocrinology (2014) 170, G1G47

Hyponatremia means there is an


excess of water over sodium
Hypernatremia reflects deficit of
water over sodium

To detect excess Sodium in the body:


Do a thorough PHYSICAL EXAMINATION
Plasma/Intravascular volume
Look at the vital signs: increased BP
Signs of volume overload: Jugular venous pressure

Interstitial Fluid volume


Edema

Clinical approach to hyponatremia.

Tzamaloukas A H et al. J Am Heart Assoc 2013;2:e005199

2013 Tzamaloukas A H et al.

Pseudohyponatremia: Correction
factors
Hyperglycemia:
Corrected serum Na+ =
Measured Na +[2.4 ((RBS (mg/dl) 100)/100)]

cal practice guideline on diagnosis and treatment of hyponatremia . Journal of Endocrinology 2014;170

Patients baseline
characteristics:
There is no pseudohyponatremia:
CBG = 99mg%
Physical examination: No volume depletion
(BP = 140/90; HR = 72/min), good skin turgor

Clinical approach to hyponatremia.

Tzamaloukas A H et al. J Am Heart Assoc 2013;2:e005199

2013 Tzamaloukas A H et al.

Establishment of
chronicity
3 days prior to consult, patient already
presented with vomiting along with generalized
weakness described as loss of balance.

However, during patients admission: Na


monitoring showed abrupt fall in serum sodium
concentration

There is acute hyponatremia with chronic


hyponatremia (Baseline Na = 120, sudden
fall to 108 in 3 days, then to 104 1 day
later), a fall of 4 meq/L/day

Definition based on time of


development
Acute hyponatremia:
documented to exist <48 h

Chronic hyponatremia:
documented to exist for at least 48 h.

If hyponatremia cannot be classified:


consider it being chronic, unless there is clinical or
anamnestic evidence of the contrary

Clinical approach to hyponatremia.

Tzamaloukas A H et al. J Am Heart Assoc 2013;2:e005199

2013 Tzamaloukas A H et al.

Definition based on biochemical


severity
"Mild" hyponatremia:
Serum sodium concentration between 130 and
135 mmol/L

Moderate" hyponatremia:
Serum concentration between 125 and 129
mmol/L

Profound" hyponatremia:
Serum concentration less than 125 mmol/L

Definition based on
symptoms
Moderately symptomatic hyponatremia
biochemical degree of hyponatremia in the presence of
moderately severe symptoms of hyponatremia
Nausea without vomiting
Confusion
Headache

Severely symptomatic hyponatremia


as any biochemical degree of hyponatremia in the
presence of severe symptoms of hyponatremia
Vomiting
Cardiorespiratory distress
Abnormal and deep somnolence
Seizures
Coma (Glasgow Coma Scale 8)

Our patient has:


Acute hyponatremia (rapid fall in serum Na+ to
104 mmol/L in 4 days)

Chronic hyponatremia
(Admitting serum

Na = 120mmol/L)

Profound hyponatremia (Na+ < 125 mmol/L)


Severely symptomatic hyponatremia (vomiting,
somnolence)

Clinical approach to hyponatremia.

Tzamaloukas A H et al. J Am Heart Assoc 2013;2:e005199

2013 Tzamaloukas A H et al.

The recommendation:

cal practice guideline on diagnosis and treatment of hyponatremia . Journal of Endocrinology 2014;170

Grade system for grading


recommendations

cal practice guideline on diagnosis and treatment of hyponatremia . Journal of Endocrinology 2014;170

Management:
Our patient was initially given plain NSS and
Furosemide

hange in Na+ = [Na(infusate) Na+ (patient


(Total body water + 1)

Patients body weight: approx.


Change in Na+ =
50kg
(154-104)/ ( 25 +
Total body water: 50 kg x .50 =
1)
25.0
= 1.9
Na+ in Normal saline 154
mmol/L
Patients Na+ = 104 mmol/L
Thus, 1 L of NSS is expected to increase the
serum [Na+] by 1.9

Management:

rogue-Madias formula:
hange in Na+ = [Na(infusate) Na+ (patient
(Total body water + 1)
Change in Na+ =
(154-104)/ ( 27.5 + 1)
= 1.9
1 L of NSS is expected to increase the serum [Na+] by
1.9
To increase the serum [Na+] by 10-12 mmol in 24 hours,
we need to give
5.2L - 6.3L of NSS

urosemide is a loop diuretic which causes excretion


f more water than Na+

Algorithm for the diagnosis of


Hyponatraemia

Hyponatremia

Exclude hyperglycemia and other causes


of non hypotonic hyponatremia
Hypotonic hyponatremia
Acute or severe
symptoms

Yes

No
Urine
osmolality
> 100 mosm/kg

100
mosm/kg

Urine Na
concentration
30 mmol/L

> 30 mmol/L

Low effective arterial


blood volume

Diuretics or
kidney disease
Yes
No

2014 European Society of Endocrinology, European Society of Intensive Care Medicine,

Robert Schrier. Body Water Homeostasis: Clinical Disorders of Urinary Dilution and Concentration. J
Am Soc Nephrol 2006;17: 18201832

In overtly symptomatic
hyponatremia:

There is no place in the initial treatment for


aquaretics .

Note that normal saline can exacerbate


hyponatremia in patients with SIAD, who may
excrete the sodium and retain the water. (Pts with
SIAD have normal capacity to excrete the solutes)

A liter of normal saline contains 154 mEq sodium


chloride (NaCl) and 3% saline has 513 mEq NaCl.
Management decisions should also factor in
ongoing renal free water and solute losses.

Alternately, the combination of intravenous


normal saline and diuresis with a loop diuretic
(eg, furosemide) also elevates the serum sodium
concentration. This latter approach is often
useful for patients with high urine osmolality,
because the loop diuretic acts to reduce urine
osmolality. Concomitant use of loop diuretics
increases free water excretion and decreases
the risk of fluid overload.

Why was Tolvaptan given?


A diagnosis of SIAD was made
Euvolemia
Urine Na = 104mmol/L
Calculated serum osmolarity = 264 mmol/L
Urine osmolarity: 323 mmol/L

Criteria for diagnosing


SIAD
Decreased effective osmolality of the extracellular
fluid (Posm <275 mOsmol/kg H2O).

Inappropriate urinary concentration (Uosm >100


mOsmol/kg H2O with normal renal function) at some
level of plasma hypo-osmolality.

Clinical euvolemia, as defined by the absence of signs


of hypovolemia (orthostasis, tachycardia, decreased
skin turgor, dry mucous membranes) or hypervolemia
(subcutaneous edema, ascites).

Elevated urinary sodium excretion (>20-30 mmol/L)


while on normal salt and water intake.

Absence of other potential causes of euvolemic hypoosmolality: severe hypothyroidism, hypocortisolism


(glucocorticoid insufficiency).
Verbalis J, et al. Diagnosis, Evaluation, and Treatment of Hyponatremia: Expert Panel
Recommendations. The American Journal of Medicine (2013) 126, S1-S42

Supplemental criteria for


SIAD dx:
Serum uric acid <0.24 mmol/l (<4 mg/dl)
Serum urea <3.6 mmol/l (<21.6 mg/dl)
Failure to correct hyponatraemia after 0.9% saline
infusion

Fractional sodium excretion (FENA) >0.5%


FENA = [(UNa/PNa)/(Ucrea/Pcrea)] x 100

Fractional urea excretion >55%


Fractional uric acid excretion 12%
Correction of hyponatraemia through fluid restriction

cal practice guideline on diagnosis and treatment of hyponatremia . Journal of Endocrinology 2014;170

AVP induced mechanism of renal water


reabsorption

Verbalis J, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel