Apr 3, 2020
In this podcast, Dr. Kimberlee Thielen, an internal medicine physician and nephrologist with Kidney Specialists of Minnesota, discusses hyponatremia, more specifically a water balance issue.
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When we are talking about hyponatremia we are not talking about Na+ problems but rather a water balance issue.
The normal amount of Na+ in the plasma water is usually 136-142 meq/L.
The body's Na+ balance is important for volume regulation which is controlled by renin angiotensin/Aldosterone system. This is different than the body's water balance which is maintained by antidiuretic hormone (ADH).
Normal physiology of water balance requires ADH which involves the hypothalamus-post pituitary and the kidneys.
To understand hyponatremia you need to first understand the physiology of water balance and where ADH is produced. ADH is produced in post pituitary and released by 2 physiologic stimulators: (1) elevated serum osmolality, (2) decrease circulating volume.
The majority of serum osms are made up of sodium. When your Na+ is high there are osmoreceptors in your hypothalamus that sense increased extracellular serum Na+ which synthesizes ADH which is released once again from the post-pituitary.
The posterior pituitary can also synthesize ADH 2nd low volume status regardless of serum osmolality.
Parasympathetic response from left atrium, aortic arch & carotids sense the low volume status or volume contraction with decrease arterial blood flow thereby stimulating a vagus nerve response which leads to the posterior pituitary releasing ADH.
ADH once released acts at the renal collecting tubule via cyclic AMP which inserts water channels called aquaporins in the collecting tubules flowing via the medullary interstitial osmotic gradient. Next water moves from the intratubular space to the medullary interstitial space thereby concentrating the osmolality. So the further you travel through the kidney more water is removed from intratubular space to medullary interstitium concentrating the urine.
A normal healthy person can concentrate their urine upwards of 1200 milli osms and dilute it to around 60 milli osms, which narrows as we age, likely to nephron drop.
We all tend to lose some GFR as we age.
Nephron Drop Out attrition of nephron units that scar up generally due to athrescleortic disease.
ADH- insert aquaporins into collecting tubules - based on osmolality of urine and interstitial water will flow down the osmotic gradient through the aquaporins. Collecting tubules as they go deeper into the kidney the medullary interstitial osmotic gradient increases. The water that is reclaimed is through a complex peritubular capillary network returning to the venous system.
Hyponatremia in most patients is going to be hypo-osmolar hyponatremia.
When talking about hyponatremia we are generally talking about a serum Na+ less than 135 mew which once again is a water balance issue.
Most cases of hyperosmolar hyponatremia are clinical relevant and usually caused by hyperglycemia, prostate or uterine surgery, glycine, sorbitol, mannitol, IVIG. You get an increased osmolar state in the blood which pulls water from intracellular space leads to hyponatremia.
Pseudohyponatremia are iso-osmolar and generally a laboratory artifact. Can have your lab run serum Na+ via direct ion selective electrode measurement to obtain true Na+ level.
What is hypo-osmolar hyponatremia? Causes are divided into 3 categories: (1) water intoxication, (2) SIADH, (3) volume stimulated ADH.
You can differentiate by 2 urine tests: Test #1- Urine Osmolality which we would expect to be low or max dilute. Test #2 is Urine Sodium.
Water Intox - The urine Osms are maximally dilute.
SIADH and Volume stimulate ADH urine osms not max dilute. Urine sodium is low in volume stimulated ADH and generally >40 meq per/L in SIADH. Which is due to the kidney seeing itself as euvolemic. So this will cause the release of sodium into the urine.
In volume stimulated ADH the kidney perceives itself ischemic or underperfused. So the urine Na+ <25 meq/L. Etiologies tend to favor heart failure, AS, dec L&R ventricular function, GI illnesses, diarrhea, diuretics, nephrotic syndrome, cirrhosis and decreased circulating volume. Urine osms are not max dilute and urine sodium is low. To summarize...again the baroreceptors such as aortic arch, left atrium and carotid sense low volume stimulates ADH from the posterior pituitary which takes precedence and independent of hypo-osmolar state.
Medications that cause SAIDH include: antidepressants, TCAs, MOAs, anticonvulsant/antiseizure, antipsychotics, cancer drugs. In addition, you need to make sure the adrenal, thyroid axises are intact.
Other causes of SIADH include TB, viral syndrome, small cell lung CA tumors that cause ectopic production of ADH. Malignancy associated SIADH tumors with head and neck cancer/neuroblastoma, pulm injury, pneumonia, post surgical pt., opiates, nausea.
Beer Potomania is hyponatremia that is due to low solute intake. Generally, these patients have low protein and salt input with high fluid or water intake. The patients have difficult times excreting free water directly related to poor diet, low solute delivery with suppression of ADH.
Inability to effectively excrete free water load b/c not enough solute load to get rid of your water intake.
Reset osmostat phenomenon is a normal physiologic adaption where the osmostat has lower reset response. ADH tends to be released at a lower threshold. Seems to occur more as we age. These pts. are often chronically hyponatremia.
Treatment of pt symptoms is a guide of acuity. With sudden changes of decreased serum sodium. Cells via the osmotic gradient will tend to swell resulting in an increased intracranial pressure. These patients may present with slight confusion, nausea, malaise, headache. Severe cases when patients present with obtunded, seizing, lethargic.
Often fluid restriction is a good first option for treatment of these patients.
Next would be normal saline and then 3% hypertonic saline on rare occasions depending on the severity.
You do not want to change serum sodium quickly specifically if it's not acute.
Once again looking at the urine osms will paint the picture for the patients presentation and predict or guide what's going to happen with treatment.
Acute symptomatic hyponatremia we want to correct the serum sodium by about 4-6 meq/L over a few hours to prevent herniation. You do not correct more than 8 meq in a 24 hr period.
The 4 goals for hospitalized patients with hyponatremia would be to implement conservative measures, ID harmful drugs as well as the cause, limit further fluid intake to prevent further decline of the serum sodium. relieve symptoms such as ICP. Avoid excess correction as we do not want to cause osmotic demyelination. Be aware of acute vs chronic hyponatremia and watch for patient who have undergone osmotic adaptation.
Once again a recurring theme Urine Osms are going to best predict the clinical course of the therapy for the patient.
As soon as the patient is volume expanded ADH will be turned off and the patient will begin dumping urine. Need to pay attention to urine output. If there is a change in urine output, you need to recheck Urine Osms.
Desmopressin is used for patient that are overcorrecting too quickly. Essentially Desmopressin promotes ADH to take up more water.
Osmotic demyelination syndrome can occur days or sometimes weeks later before onset.
In summary, here are some take home points:
Symptoms once again should dictate who rapidly you wish to correct the serum sodium.
If you truly have acute CNS findings of hyponatremia such elevated ICP confusion, seizures etc. you want to use 3% Hypertonic saline for those patients. Change the serum Na+ by 4-6 meq/L over a few hours, making sure to not correct more than 8 meq/L over a 24 hr time period.