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hyponatremia

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Alexander Divin

on 20 October 2013

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Transcript of hyponatremia

Divin, MD / PGY-2
HYPONATREMIA
Capital Health System / Jan, 2013
Hyponatremia is defined as a serum sodium concentration less than 135 meq/L
Clinical Presentation:
ACUTE < 24 hrs
CHRONIC > 72 hrs
primary polydipsia
overhydration 2 to extreme exercise
use of thiazide diuretics, illicit drugs(ecstasy)
postoperative administration hypotonic fluids
Increased neuronal cell volume --> neurogenic symptoms --> cerebral edema (Na decreases by more than 10meq/L) --> high mortality
Nausea, fatigue, headache --> obtundation,
seizures, coma, hypoxia, respiratory arrest
less likely to develop symptomatic cerebral edema
Extrusion of intracellular solutes --> restoring normal cell voulume
May develop superimposed acute symptomatic hyponatremia
Unclear benefits of sodium correction
1st step: Measured Plasma osmolarity (Posm)
Decreased
Increased
Normal
>295 mosm/kg H20
Glu (effective osmole) --> Translocation of water from the intracellular to ECF compartment -->reducing extracellular Na
Decrease in the sodium level by
1.6 meq/L for every 100mg/dL
increase of plasma glucose above 100mg/dl
Hyperglycemia
Mannitol

when IVIG is given in a maltose or sucrose solution

to patients with renal failure
Administration of Maltose or sucrose
275-295 mosm/kg H2O
Nonconductive irrigation solutions (glycin, sorbitol)
addition of an isosmotic but non sodium-containing fluid to the extracellular space
absorption of irrigation solutions during TURP/TURB or hysteroscopy or laparoscopic surgery
Pseudohyponatremia
Laboratory artifact, less common now with the use of ion-specific electrodes
in patients with hyperproteinemia or severe hyperlipidemia
<275 mosm/kg H2O
2nd Step: Urine osmolality (U osm)
3rd step:

urine sodium concentration(Una)
+
volume status
U osm < 100
Primary polydipsia
Low dietary solute intake
Sarcoidosis
U osm >100
Beer protomania
Hypervolemia
Euvolemia
Hypovolemic

excretion of each liter of urine requires
50 mOsm of solute --> diminished ability to excrete excess of water in settings of low solutes intake
U
NA
< 20
vomiting
diarrhea
burns
U
NA
< 20
chronic heart failure
cirrhosis
nephrotic syndrome
U
NA
> 40
adrenal insufficiency
hypothyroidism
SIADH
EXTRARENAL
>10
U
NA
RENAL

diuretic -induced
IMPAIRED RENAL WATER EXCRETION IN THE PRESENCE OF CONTINUED WATER INTAKE
Case #1
HPI: A 42 yo woman brought to ER from TPH, presents with altered mental status for a few days.

PMH: Schizophrenia, Depression, Anxiety, HBV, Chronic back pain.

Medications: Risperidone, Zoloft, Ibuprofen
On physical exam the patient awake, confused, responds to verbal and painful stimuli, moaning
BP 130/80, HR 80, RR 20, O2 sat 100%
Neck: no JVD
CVS: RRR, normal S1, S2, no m/r/g
Lungs: CTA B/L
Abd: NT/ND, no organomegaly
Ext: no edema
Sosm:
250
Uosm:
45
Urine Na:
10
121
3.5
89
21
5
0.6
104
11.7
33.7
170
3.4
Central defect in thirst regulation ?
Excessive secretion or renal action of ADH ?
Antipsychotic drugs that by its anticholinergic action cause dry mouth thus enhancing thirst ?
Understanding of pathophysiology

Kidney ability to excrete urine ranging from 50mOsm/L H2O to a maximum of 1200mOsm/L H2O.




~ 700mOsm in western diet




100mOsm solute diet would be excreted in a urine output of 100/50 = 2 liter at maximal dilution
Understanding of pathophysiology
Case # 2
HPI: A 47 year old man c/o 10 days of progressive dyspnea. Right sided pleuritic chest pain started a few days prior to admission . He complains of a chronic cough. He has had problems with weakness and difficulty walking.

PMH: unremarkable
Medications: none
PE: VS: T 98 P 96 BP 160/70 RR 20
General: No acute distress
Neck: supple, no thyromegaly
Heart: S1, S2 normal, no murmurs rubs or gallops
Lungs: decreased breath sounds right thorax,left sided crackles at the base
Abdomen: + BS, no masses or organomegaly
Extremities: no edema
Neuro: 3/5 proximal muscle strength, sensation intact,
deep tendon reflexes sluggish
Sosm:
235
Uosm:
332
Urine Na:
50
116
4.1
86
21
5
0.6
90
12.7
36.7
539
18
Chest x- ray revealed pneumonia with pleural effusion.
Thoracentesis showed an empyema which required a chest tube.
TSH =
26.8
Free T4
< 0.023
Free T3
= 1.16
Understanding of pathophysiology
Understanding of pathophysiology
Hypotonic Hyponatremia with Appropriately low Urine Osmolality

P osm= 2 [Na+] + [Glucose]/18 + [ BUN ]/2.8
decreased ability of the
kidney to excrete water
Cortisol deficiency :
increasing CRH, which stimulates ADH release, low CO, BP

Aldosterone deficiency:
renal sodium loss, hypovolemia, and baroreceptor-mediated ADH release

Severe hypothyroidism:
The reduction in cardiac output and GFR (decrease ECF)may be nonosmotic stimuli to ADH release

Diuretic use
Euvolemic patient + Hypotonic Hyponatremia with an Inappropriately High Uosm
SIADH -diagnosis of exclusion
Case # 3
VS: T 98 P 60 BP 95/55 RR 20 , no orthostasis
General: No acute distress, MMM
Neck: supple, no thyromegaly
Heart: S1, S2 normal
Lungs: CTA B/L
Abdomen: + BS, no masses or organomegaly
Extremities: no edema
Neuro: normal
Sosm:
245
Uosm:
342
Urine Na:
60
119
6.1
84
21
26
1.0
75
11.4
33.7
102
4.4
Bilateral adrenal metastases on CT scan
TSH
normal
Cortisol
level 3.7
Cosyntropin test
no response
70-year-old female, with h/o non small cell lung cancer, chronic back pain, c/o fatigue, dizziness for 1 month. As per family she became more forgetfull recently. Weight loss
10 lbs x 2 months, poor appetite.
Meds: percocet 10/325 PRN
The most common causes of SIADH ?
CNS disorders :
Mass lesions, Hemorrhage
Drugs:
Ecstasy, COX-2 inhibitors, Desmopressin, NSAIDs, Opiates, SSRi, Vasopressin
Postoperative settings:
Anesthesia, Nausea, Pain
Pulmonary disorders:
Infections, Positive pressure mechanical ventilation
Tumors:
Respiratory tract tumors, Small cell carcinoma
Something goes wrong and ADH is made

Reabsorbtion water at collecting tubule
(plasma osm drops <--> urine osm increases)

volume increases

ANP released by muscle cells in atrial myocytes

dilation of renal arteries --> increase GFR & inhibition of aldosterone.
Pathophysiology simple
Pathophysiology simple
Once kidneys see low concentration of sodium, they say
"wow, i need to pass out this dilute urine"
but the SIADH says
"HOLD ON TO WATER"
louder than the kidney can say
"get rid of water."
P osm<275 U osm> 100 Urine na>40

• Sodium 115 - 132
• Careful testing shows
– Decreased attention
– Unstable gait
• Odds ratio for falls – 67!
• Changes > mild alcohol intake
The myth of asymptomatic hyponatremia
Case # 4
VS: T 98 P 60 BP 155/85 RR 20
General: Not in acute distress, obese,
Neck: supple, no thyromegaly, +JVD
Heart: S1, S2 normal
Lungs: +mild rales at bases b/l
Abdomen: + BS, NT/ND, mild hepatomegaly
Extremities: +1 pitting edema LE B/L
Neuro: normal
Sosm:
267
Uosm:
112
Urine Na:
15
120
6.1
84
21
31
1.6
75
13.3
40.1
233
5.5
68-year-old male with h/o non- ischemic CHF, HTN, DM2 c/o cough w clear sputum, worsening SOB, lower extremities swelling x1 week. The patient is non compliant with medications and diet.
Meds: lisinopril, coreg, aldactone, pravastatin
ROS: + weight gain
Pathophysiology pearls
Reducing of cardiac output and systemic blood pressure
Body perceives volume depletion, in spite of increased plasma and ECF volumes
decrease the pressure on
baroreceptors in the carotid sinus
decrease the pressure on
renal afferent arteriole
ADH secretion
Aldosterone secretion
Urine sodium <20
P osm < 275, Low sodium
Patients whose serum sodium levels fall below 125meq/L solely as a result of heart failure usually have near end-stage disease
aggressive treatment
How to manage ''asymptomatic" hyponatremia?


Hyponatremia treatment


– Active seizures
– Respiratory failure
Very aggressive treatment
Bolus 100 cc of 3% NaCl over 10 minutes

Can repeat 1 or 2 times until clinical
improvement or Na increased 2-4 mEq/l

Then start aggressive treatment

– Seizures (not active)
– Decreased mental status
– Headache, nausea and vomiting
3% NaCl at rate 1cc/kg/hr
• Stop infusion when symptoms relieved
• Check serum sodium every 2 hours

Avoid sodium increase of greater than 15-20 mEq/l over 48 hours
(osmotic demyelination syndrome)
• Slow down at Na = 125-130 mEq/l
• Immediate rate is not important – rate over 48
hours represents risk for demyelination
True hypovolemia
Correct etiology of hypovolemia
Isotonic saline
Hypervolemic hyponatremia
Treat underlying cause
Fluid and water restriction
Furosemide
Vasopressine receptor antagonists(vaptans)
Euvolemic hyponatremia / SIADH
Treat underlying cause
Discontinue offending drugs
Fluid restriction
Furosemide
Ensure udequate solute and protein intake
Demeclocycline
– creates nephrogenic DI
– ~ $10 / day
– Takes about 3-4 days to work
Tolvaptan
– Blocks ADH
– ~$177 / day
– Works immediately
THANK YOU !
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