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HYPO & HYPER NATREMIA - Fen Lecture Series - PPSX

The document discusses sodium homeostasis and disorders of sodium balance including hyponatremia and hypernatremia. Key hormones that regulate sodium balance are arginine vasopressin and aldosterone. Causes, clinical features, evaluation, and treatment approaches for hypo- and hypernatremia are covered in detail.

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Vivian Chow
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90 views55 pages

HYPO & HYPER NATREMIA - Fen Lecture Series - PPSX

The document discusses sodium homeostasis and disorders of sodium balance including hyponatremia and hypernatremia. Key hormones that regulate sodium balance are arginine vasopressin and aldosterone. Causes, clinical features, evaluation, and treatment approaches for hypo- and hypernatremia are covered in detail.

Uploaded by

Vivian Chow
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPSX, PDF, TXT or read online on Scribd
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HYPO & HYPER NATREMIA

Fendra Wician, MD
SODIUM HEMOSTASIS
Sodium
• Major extracellular cation
• Na+ is the predominant solute contributing to
osmolality
• Na+ is actively pumped from the intracellular
to the extracellular space
• Na+ leaves the body primarily through urinary
excretion  tightly regulated
SODIUM HEMOSTASIS
Key hormones
• ADH = AVP = vasopressin
• Aldosterone
SODIUM HEMOSTASIS
ADH
• primary hormone that regulate Na consentration

Stimuli for secretion:


• Hyperosmolality (as small as ↑ 1%)
• ↓ effective arterial volume (EAV) (≥10%)
• angiotensin II
• Pain, nausea, multiple medications

Action:
• insertion of aquaporin-2 channels in collecting ducts  passive water
reabsorption
SODIUM HEMOSTASIS
Plasma osmolality is maintained by strict regulation :
• ADH = arginine vasopressin system
• thirst

If plasma osmolality increases:


• ADH ↑  water is retained by the kidneys  ↓ serum
osmolality

If plasma osmolality decreases,


• ADH ↓  diuresis of free water  return to
homeostasis
SODIUM HEMOSTASIS
Aldosterone :
• primary hormone that regulates total body sodium (and volume)

Stimuli for secretion:


• hypovolemia (via renin and angiotensin II)
• hyperkalemia

Action:
• stimulate Na+ reabsorption and potassium (K+) secretion in the renal
collecting tubule.
• ↑ secretion Hydrogen (H+)  electronegative lumen generated by Na+
reabsorption

• The renin-angiotensin-aldosterone axis modulates Na+ retention and


excretion to regulate total body volume
TOTAL BODY WATER
HYPONATREMIA
HYPONATREMIA
Na : 135-145 meq/L
Hyponatremia  Na < 135meq/L

• most common electrolyte balance disorder in


clinical practice

• Related to ↑ mortality, morbidity & length of


hospital stay
HYPONATREMIA
Related to worse prognosis in :
• liver cirrhosis,
• pulmonary hypertension,
• myocardial infarction,
• chronic kidney disease,
• hip fractures
• pulmonary embolism

Unclear if Hypo Na :
• marker for poor prognostic outcomes or
• reflection of disease severity
HYPONATREMIA
PATHOPHYSIOLOGY
• EXCESS of WATER relative to SODIUM
• Almost always due to ↑ ADH
– Appropiate (ex: hypovolemia or ↓ effective arterial
volume)
– Inappropiate  SIADH

• Rarely due to ↓ ADH appropiately


 primary polydipsia (ingestion >12L/d free water)
HYPONATREMIA - HISTORY
• Acute vs chronic (>48h)
• Severity of symptoms
• Risk for neuro complication :
– alcoholism,
– malnourished,
– cirrhosis,
– older females
– on thiazides,
– hypoxia,
– hypoK
HYPONATREMIA – SIGN & SYMPTOMS
DIAGNOSTIC ALGORITHM

Treat immediately
OSMOLALITY
• Number of particles (osmoles, Osm) dissolved in solution

• Water moves between body compartments lower osmolality to


higher osmolality

• Only effective osmoles (substances that do not freely cross cell


membranes) induce a water shift

• Predominant effective osmole: sodium


• Ineffective osmole (does not induce fluid shift): urea

• The body regulate osmolality  primarily via :


– retention or excretion of water
– not osmoles (i.e., sodium, Na+)
Serum osmolality
2 x Na (meq/L) + {BUN (mg/dL) /2.8} + {glucose (mg/dL) / 18}

Corrected serum Na
Measured Na + 2.4 (glucose (mg/dL) – 100
100 mg/dL
Hypotonic Hypo Na
Evaluation of volume status
Hypo Na & GI losess
• Gastric contents and stool are hypotonic

• Protracted vomiting or diarrhea w/o replacement


of fluid  lead to vol depletion & hyper Na

• However, if patients ingest fluid & food low in


sodium content in conjunction with a
baroreceptor-mediated stimulus to ADH
secretion
Hypo Na will result instead
Hypo Na & exercise
• Exercise induced hypo Na (EAH)
• Hyponatremia after vigorous endurance exercise such
as marathons, ultramarathons, and triathlons is well
described

• originally was considered to be a form of volume-


depletion-related hyponatremia  resulting from loss
of Na & Cl in sweat during exercise

• However, current evidence indicates that excessive


water retention in the face of ↑ ADH secretion is
responsible for most cases of EAH
EAH therapy
• Guidelines for appropriate fluid ingestion during
marathons are available

• In general, runners should drink primarily when


thirsty, with an input 400-800 mL/h;

• ↑ amount  for heavier, faster runners during


high-temperature conditions,
• ↓ amount  for lighter, slower runners during
low-temperature conditions.
Hypo Na & diuretic use
Most common cause : Thiazide

On literature review  diuretic induced hyponatremia


• 73% caused by thiazides alone
• 20% caused by thiazides in combination with antikaliuretic agents
• 8% were caused by furosemide

Thiazides produce hyponatremia by at least 3 separate mechanisms:


• interfere with function of the distal tubule diluting site
• produce volume depletion that stimulates nonosmotic AVP release
• deplete potassium leading to cellular uptake of sodium
Hypo Na & duretic use
• Diuretic-induced hyponatremia is always a
chronic hyponatremia
 so limits for rate of correction of chronic
hyponatremias should be observed

• Numerous ODS (osmotic demyelinating


syndrome reported) following correction of
Hypo Na
Hypotonic Hypo Na
Evaluation of volume status
Hypotonic Hypo Na
Evaluation of volume status
THERAPY
THERAPY
Acute sx:
• initial rapid correction of Na (2 mEq/L/h for the first 2–3 h)
until sx resolve
• Frequent lab check

Rate of ↑ Na should not exceed :


• 6 (chronic)
• 8 (acute) mEq/L/d
• to avoid central pontine myelinolysis/osmotic
demyelination syndrome

• CPM/ODS: paraplegia, dysarthria, dysphagia


THERAPY
HYPERNATREMIA
HYPERNATREMIA
• Na >145 meq/L
• associated with ↑ morbidity & mortality in
the inpatient setting

Caused by:
• net water loss (increased loss or decreased
intake)
• sodium gain (rarely)
HYPERNATREMIA
Risk factors:
• Impaired thirst mechanism
• restricted access to water (e.g., those with
altered mental status, intubated patients,
infants, older adults)
SIGN & SYMPTOMS
In adults, symptoms tend to be mild and may include :
• anorexia
• muscle weakness
• restlessness
• nausea, and vomiting

Severe symptoms are likely to occur with acute increases in


plasma sodium levels or at concentrations > 160 mEq per L.

Hypernatremia can cause brain shrinkage, resulting in vascular


rupture and intracranial bleeding.
ETIOPATHOGENESIS
Water loss can be :
• pure water loss (e.g., in diabetes insipidus)
• hypotonic fluid loss (e.g., renal, GI, or
cutaneous losses)

• Sodium gain is usually iatrogenic from the


infusion of hypertonic solutions
THERAPY
THERAPY
THANK YOU
THERAPY
Rapid correction
• Most reports use a total of 500 ml of fluid
• repeated 150 ml infusions, given every 20 min,
may be a reasonable and safer approach

• If the symptoms improve after Na ↑ 5 mmol/l


 recommend stopping the infusion and starting
cause-specific treatment to maintain achieved
serum sodium concentration.
Hypo Na & Primary Adrenal Insuff
Therapy
• Awal: Volume replacement with isotonic saline
• Fludrocortisone to replace chronic
mineralokortikoid insuff  to prevent
hypovolemia induced hiponatremia

• Acquired mineralocorticoid deff only cause


volume depletion & Hypo Na if:
– Bilateral adrenal failure dari adrenal destruction atau
adrenalectomy
Hypo Na & Primary Adrenal Insuff
• Patient with mineralokortikoid deff should always
suspect to have glukokortikoid deff condition
 immediate th/ with glucocorticoid “stress
dose” (50-100mg hydrocortisone q8)

• Stress dose Hydrokortisone also activate


mineralocorticoid receptor maka fludrokortison
blm dibutuhkan sampai nantinya mentitrasi
steroid ke dosis maintenance
Hypo Na ec SIADH
• Acute symptomatic hyponatremia is best
corrected with hypertonic (3%) saline given
either via bolus or continuous intravenous
infusion

• Patients with euvolemic hypo-osmolality due


to SIADH will not respond to isotonic saline,
which in some cases will cause the
hyponatremia to worsen.

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