Symptom To Diagnosis - Hyponatremia/Hypernatremia Flashcards
Hyponatremia is defined as serum sodium concentration
<130.
1st step in evaluating the hyponatremic patient is to?
Review the history and evaluate the lab results for a few diagnostic fingerprints that may be present.
Diagnostic fingerprints for hyponatremia:
- History of thiazides ingestion.
- Hyperkalemia –> primary adrenal insufficiency.
- Urine osmolarity = 100 –> Psychogenic polydipsia.
- Marked hyperglycemia –> Hyperglycemia-induced hyponatremia.
For most patients the few diagnostic fingerprints will NOT be diagnostic. What is the key pivotal point in the DDX of hyponatremia?
To determine the patient’s volume status and identify who is clinically hypervolemic, euvolemic, hypovolemic.
DDX of hyponatremia –> Hypervolemia:
- HF.
- Cirrhosis.
- Nephrotic syndrome.
- Renal failure (GFR<5).
DDX of hyponatremia - Euvolemia:
- SIADH.
- Hypothyroidism.
- Psychogenic polydipsia.
- Secondary adrenal insufficiency.
- Exercise-associated hyponatremia.
Etiology of SIADH:
- Cancers (lung, pancreas).
- CNS disease (cerebrovascular accident, trauma, infection, hemorrhage, mass).
- Pulmonary diseases (infections, respiratory failure).
- Drugs.
Drugs that cause SIADH:
- Thiazides.
- ADH analogues.
- Chlorpropamide (6-7%).
- Carbamazepine.
- Antidepressants (TCAs, SSRIs,) + antipsychotics.
- NSAIDs.
- Ecstasy (MDMA).
- Others (cyclophosphamide, vincristine, nicotine, opioids, clofibrate).
DDX of hyponatremia - Hypovolemia:
- Salt and water loss with free water replacement.
- Primary adrenal insufficiency.
- Renal disease.
Conditions in which we have salt and water loss with free water replacement:
- Severe diarrhea with free water ingestion.
- Large burns with free water ingestion.
- 3rd-spacing with free water replacement.
Hyponatremia develops when patients do not excrete their daily ingested excess (or free) water. Free water excretion requires 3 distinct mechanisms:
- Glomerular filtration.
- Separation of water from solute so that free water can be excreted.
- Excretion of free water –> Requires low or absent levels of ADH.
Manifestations of hyponatremia depend on?
Its severity and rapidity of development.
Patients with serum Na levels >130?
Asymptomatic.
Patients with Na 125-130?
- Nausea/vomiting.
2. Abdominal symptoms.
Patients with <125?
- Headache.
- Agitation.
- Confusion.
Patients with <120?
Seizures and coma.
Distinguishing euvolemic from hypovolemic patients is a bit difficult in the evaluation of hyponatremia. The 3 most accurate biochemic parameters are:
- Spot urine sodium.
- Fractional excretion of Na (FENa).
- Fractional excretion of urea (FEUrea)
Spot urine sodium - Hypovolemic patients have increased or decreased urine Na concentration?
Decreased - They avidly reabsorb Na.
18.4mEq/L, compared with 72mEq/L in euvolemic patients.
Spot urine sodium - False(-) results (elevated urine sodium in hypovolemic patients) may be seen in hypovolemia 2o to?
- Primary adrenal insufficiency in which the hypoaldosteronism directly leads to sodium wasting.
- Vomiting with accompanying metabolic alkalosis.
Why vomiting causes urine Na excretion?
The metabolic alkalosis in vomiting causes an obligatory urinary HCO3 loss, which is accompanied by sodium.
Urine Cl may be low in such cases.
Spot urine Na - False(+) results (low urine sodium in euvolemic patients) may be seen in certain euvolemic patients:
- Psychogenic polydipsia –> Euvolemic, but usually have low urine Na concentration due to dilution of the excreted sodium in vast quantities of water.
- Some patients with SIADH ingest little Na causing decreased urinary Na output.
Is FENa sensitive for hypovolemia?
Exceptionally sensitive. (Sens 100%).
FENa>0.5% rules OUT hypovolemia except in patients taking diuretics.
Is FENa specific for hypovolemia?
Spec is imperfect. Certain hypovolemic patients may have low FENa. (SIADH with low Na intake + Psychogenic polydipsia).
Fractional excretion of urea - Is sensitive/specific for hypovolemia?
2 studies suggest a combination of both low FENa (<55%) was HIGHLY sensitive and specific for hypovolemia.
In what hypovolemic patients is FEurea usually low and may be more useful than FENa in such patients?
In patients taking diuretics.
Bottom line about FENa and FEurea?
A high FENa rules OUT hypovolemia (except patients taking diuretics) and a low FENa combined with a low FEurea rules in hypovolemia.
Hyponatremia in cirrhosis?
Hypervolemic hyponatremia.
3% –> Child-Pugh A.
16% –> Child-Pugh B.
31% –> Child-Pugh C.
Hyponatremia and adverse effects in cirrhosis?
Higher freqeuncies of:
- Hepatorenal syndrome.
- Hepatic encephalopathy.
- SBP.
- Death.
Is there a clear precipitant in hyponatremia of cirrhosis?
NO.
Among patients with cirrhosis and ascites, …% have sodium <130mEq/L.
22%.
Pathogenesis of hyponatremia in cirrhosis:
- Hypoalbuminemia + Splanchnic dilatation (possibly due to elevated NO) –> UP ADH + DOWN GFR + Increased proximal reabsorption of solute causing decr. solute delivery to loop of henle.
- Renal arteriolar vasoconstriction –> DOWN GFR + UP Na reabsorption.
- NSAIDs may worsen edema by reducing GFR and worsen hyponatremia. NSAIDs also lower PGE2, which normally antagonizes ADH.
Hyponatremia and hepatic encephalopathy?
Hyponatremia may worsen hepatic encephalopathy.
2 physical exam findings common in cirrhotic patients WITH hyponatremia?
- Ascites present in 100%.
2. Peripheral edema seen in 59%.
Patient with HF and hyponatremia:
Has marked increases in total body sodium retention and content.
Mechanism of impaired free water clearance in patients with HF and hyponatremia?
- Largely due to elevated ADH levels - The fall in CO triggers carotid baroreceptors –> UP ADH.
- Decreased GFR due to renal hypoperfusion –> Increase in proximal Na reabsorption also impair free water excretion.
In which patients with HF is hyponatremia observed?
In patients with severe hyponatremia - Associated with an increased risk of death.