PART I – TREATMENT RECOMMENDATIONS
IN CASE OF HEMODYNAMIC INSTABILITY, THE NEED FOR RAPID FLUID RESUSCITATION OVERRIDES THE RISK OF AN OVERLY RAPID INCREASE IN SERUM SODIUM CONCENTRATION.
- An increase by 4-6-mmol/L [Na] is sufficient to reverse most serious manifestations of acute hyponatremia.
- Increase [Na] no more than 10 mEq/L in 24 hour period in pts with LOW RISK Osmotic Demyelination syndrome
- Increase [Na] no more than 8 mEq/L in 24 hour period in pts with HIGH RISK Osmotic Demyelination syndrome (ODS).
- PTS at HIGH RISK of ODS (mnemonic CHAMP):
- Plasma Serum sodium <105
HYPONATREMIA WITH SEVERE SYMPTOMS1:
- For our purposes the only cause of cerebral edema and neurological causes of hyponatremia are the hypotonic (low osmolar) hyponatremia causes.
- IF neurological symptoms are present and hypotonic hyponatremia is presumed or confirmed then 150 ml of 3% (3ml/kg) over 20 min
- Check serum sodium after 20 min while repeating an infusion of 150 ml of 3% over 20 min IF symptoms persist.
- GOAL: Target goal of 5 mmol/L increase in serum Na is achieved
HYPONATREMIA AFTER THE FIRST HOUR1
- As long as the patient is not hypovolemic AND the SEVERE symptoms are treated then
- Use the smallest volume of NS until specific causes are found
- Limit the increase in Serum Na to a total of 10 mEq/L[g]in the first 24hr and an additional 8 mEq/L during every 24hr there after until serum sodium reaches a goal of 130 mmol.
- Check Serum sodium concentration after 6 hour and after 12 hr and then daily until Na has stabilized.
- A sudden increase in urine output to >100ml/h signals increased risk of overly rapid rise in serum sodium concentration
HOW TO CALCULATE THE EXPECTED INCREASE IN PLASMA SODIUM
To calculate the anticipated increase of Serum sodium by infused saline:
- Infused Na = 154 if Normal Saline or 513 if 3% hypertonic saline
- Total Body water (TBW) = Wt x 0.6 if male
- Total Body water (TBW) = Wt x 0.5 if female
- Total Body water (TBW) = Wt x 0.5 if elderly (>65) male
- Total Body water (TBW) = Wt x 0.45 if elderly (>65) female
Example: 70 kg young female with severe cerebral symptoms is given a 3 ml/kg bolus of 3% NaCl (Na= 513 mEq/L) and Serum Na = 108
Infuse Na = 513 mEq/L (hypertonic)
Volume infused = 0.003 L/kg x 70 kg = 0.14 L
Serum Na = 108
TBW = 70×0.5 (young female) = 35L
Final serum Na = 111
TREATMENT GUIDELINES BY CAUSE OF HYPONATREMIA1
- BEER POTOMANIA 15 (BOX 1 from algorithm)
- NPO except medications for 24 h
- No IVFs unless symptomatic
- Prescribe IVFs in finite amounts if needed
- Serum sodium every 2 h
- S Na increase < 10 mEq/L in first 24 h
- S Na increase < 18 mEq/L in first 48 h
- Re-lower serum sodium levels if necessary
- Give all IV medications in D5W
- If caloric intake is needed, use D5W.
- HYPERVOLEMIC causes (BOX 2 from algorithm)
- Recommend against treatment with the sole purpose of aim of increasing the serum sodium concentration in mild or moderate hyponatraemia.
- Fluid restriction (<1.5-1.0L/d or 500ml/d less than the Urine output) to prevent further fluid overload.
- Recommend against vasopressin receptor antagonists.
- Recommend against demeclocycline.
- HYPOVOLEMIC (BOX 3/4 from algorithm)
- It is recommended to restore volume with i.v. 0.9% saline or a balanced crystalloid solution at 0.5–1.0 ml/kg per h
- In case of hemodynamic instability, the need for rapid fluid resuscitation overrides the risk of an overly rapid increase in serum sodium concentration
- In these patients restoring volume will suppress vasopressin secretion causing electrolyte-free water excretion to increase. Therefore, these patients are at high risk of an overly rapid increase in serum sodium concentration. Sudden increases in urine output can act as a warning signal that overly rapid correction of hyponatremia is imminent.
- EUVOLEMIA HYPOTHYROIDISM (BOX 5 from algorithm)
- Unless severe (i.e. myexedma or TSH >50 mIU/mL), other causes of hyponatremia should be sought rather than hypothyroidism.
- Unless the patient has hyponatremic encephalopathy, primary treatment of hyponatremia should consist of thyroid hormone replacement at standard weight-based doses; several days may be needed to normalize the serum Na.
- SIADH (BOX 6 from algorithm)
- In moderate or profound hyponatraemia, restricting fluid intake should be first-line treatment.
- In moderate or profound hyponatraemia, the following are equal be second-line treatments: increasing solute intake with 0.25–0.50 g/kg per day of urea or a combination of low-dose loop diuretics and oral sodium chloride.
- In moderate or profound hyponatraemia, we recommend against lithium or demeclocycline.
- In moderate or severe hyponatraemia, we do not recommend vasopressin receptor antagonists.
- Cerebral Salt Wasting (Box 7 from algorithm)16 17
- CSW is a volume-depleted state
- Depending on the severity isotonic or hypertonic solutions are indicated.
- Additionally, sodium tablets up to 12 g/d may be used can be combined with the IVF
- Once euvolemia is achieved, the goal of therapy is to prevent volume depletion by matching the urinary output.
- Fludrocortisone has also been used for the treatment of CSW at doses of 0.1 to 1 mg/d (stimulating reabsorption of sodium and water)
- The most common adverse effect associated with fludrocortisone was hypokalemia in up to 73% of patients.
TREATMENT OF CHRONIC HYPONATREMIA AND NO SEVERE SYMPTOMS1
HOW TO TREAT OVERCORRECTED HYPONATREMIA1:
- Prompt intervention for re-lowering the serum sodium concentration if it increases >10 mmol/l during the first 24 h or >8 mmol/l in any 24 h thereafter
- We recommend discontinuing the ongoing active treatment.
- Consulting an expert to discuss if it is appropriate to start an infusion of 10 ml/kg body weight of electrolyte-free water (e.g. glucose solutions) over 1 h under strict monitoring of urine output and fluid balance.
- We recommend consulting an expert to discuss if it is appropriate to add i.v. desmopressin 2 mg, with the understanding that this should not be repeated more frequently than every 8 h.
PART II – DIAGNOSIS
Chances are if you are reading this you have probably seen a case or two of hyponatremia. Well, defining hyponatremia isn’t really hard. In fact treating acute symptomatic hyponatremia isn’t that hard either. So what makes this electrolyte disturbance so painful? It’s the over abundance of math, renal physiology and lack of organization that exists within the literature; enough to make doctors have flashbacks of their USMLE days. Fear not friends, we are going to make this simple and painless. Unless simple and painless are not your thing, then I have for you the sadist’s ball gag equivalent of math in the optional section to appease even the most vicious of IM attendings. No more google-ing 40 different articles to treat that hyponatremic patient, everything in one neat package! So lets get to it!
First off some definitions:
TAKE HOME POINT:
|Severe/Profound||<125||Profound in UK|
|Acute vs Chronic||Time of development (48 hr cutoff)
|Tonicity||Dealing with osmolarity||There can be unaccounted osmoles (EtOH)|
|Hypotonic||Hypo-osmolar||Type of hyponatremia|
|Volemia||Dealing with the pt volume status||Difficult to asses clinically.|
Table 1. Classification of Hyponatremia (US units: mEq/L) 1, 2
So far, not horrible; Right?
We need to talk about epidemiology not because every chapter on any disease starts out this way but because it will help us down the road. So lets push on. Hyponatremia is probably the most common electrolyte abnormality3. Based on studies from the first half of the 2000’s the incidence[a]of hyponatremia is about 30-40% of admitted patients worldwide. The largest amount were found in the ICU with hyponatremia <125 mEq being an independent predictor of mortality. Values <126 mEq/L and < 116 mEq/L were found in about 6% and 1% of the patients, respectively4. In ED populations it is obviously lower than in admitted patients. ED based studies outside the US found a prevalence of 3-5% for all adults but 10-17% in those patients age 65 and older. These studies also found an increase in hyponatremia for both groups during the summer months 1-2% greater than the above numbers 5, 6. In the geriatric population 78% of episodes of hyponatremia were precipitated by increased fluid intake, administered orally or as intravenous hypotonic fluid. Finally, up to 17% of chronic alcoholic patients had hyponatremia secondary to Beer Potomania[b]
OPTIONAL: OsmolaLity or OsmolaRity?
To jump back a bit we should define osmolaLity and osmolaRity. Osmolality (with an “L”) is a measure of the osmoles per kilogram (Osm/Kg), osmolarity (with an “R”) is defined as the number of osmoles per liter (L) (Osm/L). Don’t worry we don’t have to know how many kg our patients are to calculate their osmolality. If the L and the R were flipped it would probably be easier to remember but lets just remember that the L is for weight and the R is for volume. This is important because we calculate osmolaRity but measure osmolaLity so we should keep track of the units. If you want to not be accurate then you don’t have to worry because we are dealing with water in the body, so we can approximate osmolaLity to equal the osmolaRity[c].
DETERMINING A DIFFERENTIAL DIAGNOSIS
Figuring out the differential our patients have for their hyponatremia is probably the most difficult part of this diagnosis. However, here is where I am going to try (or at least try to try) to simplify it.
Click Here for the Hyponatremia Algorithm: Hyponatremia 2.0-3
In order to decide the reason for the hyponatremia in our patients we need to have a starting point. We used to talk about volume status as the starting point but this makes things too difficult furthermore the reliability of volume status by clinical exam is less than accurate. Instead we are going to start with the osmolality.
TAKE HOME POINT: NO ALGORITHM EXISTS IN ISOLATION! THE HISTORY AND PHYSICAL ARE STILL GOING TO BE KEY IN ELUCIDATING THE CAUSES!
STEP 1: DETERMINE OUR PATIENT’S SERUM OSMOLALITY
The first branch point into our differential diagnosis is figuring out what is the serum osmolality (tonicity). We can do this two ways: order an extra lab value of serum osmoles (not usually part of “first round of orders”) or we can estimate (oh thank god!) a serum olsmolarity. To do this we us the formula:
Serum Osm [mmol/L]= 2[Na+] + Glucose + Bun (Equation 1)
This probably looks a bit strange to US doctors since it’s missing some numbers. That’s because we don’t use [mmol/L] in the US, instead we use the crazy units of [mEq/L]. So to go from mmol to mEq (or mg same thing for our purposes) we have to divide the molecules by their molecular weight. In fact, any good British child will tell you to convert their glucose to US values by dividing by 18![d]So now our formula becomes the familiar:
Serum Osm [mEq/L]= 2[Na+] + Glucose/18 + Bun/2.8 (Equation 2)
TAKE HOME POINT:
To estimate the serum osmolarity [mEq/L] use the formula:
2[Na+] + Glucose/18 + Bun/2.8
OPTIONAL: HOW GOOD IS EQUATION 2 AT ESTIMATING OSMOLALITY
How good is this formula for estimating serum osmoles? When equation 1 (also referred to as the Smithline-Gardner formula) is compared to the mean measured osmolality in healthy patients it gives an osmolal gap (OG, i.e the difference between calculated and measured Osm) close to zero and an SD of 4 mmol/L. When applied to patients in which an osmolality was clinically indicated (i.e where it would theoretically matter) the variability in the OG is approximately +/- 7 mmol/L. This held true as long as ethanol was not adulterating the sample7. Remember that ethanol will contribute to serum osmolarity and will need to be divided by 3.78. Thus equation 2 (in the US) is proposed to be adopted by all clinicians and laboratories along with a “fudge” factor of +/- 10 mmol/L for the gap7. To really get the most accurate answer here you would likely have to order a serum osmoles but it would appear that this estimation holds up pretty well to start treatment.
STEP 2: NARROWING THE DIFFERENTIAL DIAGNOSIS
Only true (hypotonic) hyponatremia matters so exclude other causes.
The normal human plasma osmolality is 275-300 mOsm/Kg9. Therefore, we need to see if we have hypertonic or isotonic hyponatremia. Hypertonic (also called Translocational or redistributive hyponatremia) causes include: hyperglycemia[e], mannitol, and sometimes a contrast load. Isotonic (also called Pseudo or normo-osmolal hyponatremia) causes include: hyperlipidemia and hyperproteinemia. Once we have excluded these causes by a value of <275 mOsm/kg then we can say that we have a true hypotonic or hypo-osmolar hyponatremia.
TAKE HOME POINT:
Calculate the serum osmolarity. If it is <275 mOsm/Kg then the causes are “true” or hypotonic causes1which can truly cause symptomatic hyponatremia.
OPTIONAL: URINE OSMOLALITY
The normal response to hyponatremia is marked suppression of ADH secretion, resulting in the excretion of maximally dilute urine with an osmolality below 100 mOsm/kg and a specific gravity ≤1.003. Vasopressin (ADH) levels are what really differentiates the type of hyponatremia at this point. The first type will have high vasopressin levels and high urine Osm with low Na. Here high vasopressin causes inability to excrete water and consists of the classic 3 groups of hyponatremia: hypovolemic, euvolemic and hypervolemic. The second type will have low serum vasopressin levels and typically low urine osmolality. Thus, mechanisms other than vasopressin are responsible. These types includes: chronic renal failure, psychiatric disorders, potomania, and low solute load excreted in the urine. However we can’t measure Vasopressin (ADH) so we use low osm and low sodium to represent this group. Values above 100 mOsm/kg indicate an inability to normally excrete free water, most commonly because of persistent secretion of ADH. Therefor the urine osmolality can help us. Once again we have 2 options to determine osmolality: order it or to estimate it.
OPTIONAL: ADH – A PHYSIOLOGIC ASIDE
To jump back a bit to med school physiology lets understand what ADH does. ADH (Vasopressin) is released from the posterior pituitary. It does this in response to 2 motivating factors: 1. Low Blood pressure via Angiotensin II released from the kidney and activating the V2 receptor; 2. High plasma osmolality (Hypertonicity) either by too little water or too many solutes. Once ADH is release it works on the principal cells in the collecting duct to stimulate aqauporin-2 channels to be inserted on the collecting duct to reabsorb more water back into the blood. So ADH “ADDs H20″ to the plasma. Thus in the algorithm when there is low URINE osmolality this must mean that ADH is not working and is “ADH independent”
STEP 3: CALCULATE URINE OSMOLALITY
The normal response to hyponatremia causes a urine osmolality below 100 mOsm/kg. To estimate the urine Osm from the urine we can use the Urine specific gravity (USG) and the following equation:
UOsm = (USG -1) x 25,000 Equation 311.
STEP 3a: URINE OSMOLALITY <100 mOSm
So if the urine Osm are calculated and less than 100 mOsm/kg then it is likely that a relative excess water intake is the umbrella cause of the hypotonic hyponatremia1. Thus the differential includes: Primary polydipsia, beer potomania, water dilution in formulas of infants, tap water enemas in infants, or very low sodium intake. Again this is because the normal response to hyponatremia is suppression of ADH, resulting in the excretion of a very dilute urine If that’s the case you are done and all you need to do is fluid restrict! We will speak more about beer potomania later on since it deserves special attention.
TAKE HOME POINT: UOsm <100 implies water excess
STEP 3b: URINE OSMOLALITY >100 mOSm
If urine osmolality > 100 mOsm/kg then likely there is impairment of the renal concentrating ability. Now, it gets a little more complicated. *At this point more lab testing will likely be needed. My feeling is if you are going to order a urine sodium, you might as well order everything at once[f]. At this point I recommend ordering:
Serum: cortisol, Osmoles, TSH, Uric acid
Urine: creatinine, potassium, sodium, Uric acid,
OPTIONAL: HOW GOOD IS THE URINE SPECIFIC GRAVITY FOR ESTIMATING URINE OSMOLARITY?
In a study by Imran, 504 urine specimens from patients on whom a simultaneously drawn USG and an osmolality were available were examined. They found good linear correlation between USG and Urine Osm when measured either by reagent strip or refractometry. Urine samples were divided into ‘‘clean’’ and ‘‘pathological’’ urines. Pathologic urines on reagent strip included: glucose, ketones, urobilinogen, bilirubin, and protein and ketones, bilirubin, and urobilinogen, for samples measured using refractometry. The study found that pathological urines did not correlate as well to urine Osm as the non-pathological12. In another study of only hyponatremic patients it was found that USG has a linear relationship with measured urine osmolality in patients with hyponatremia. A multiplying factor of 20-33 is better than 30-40 in predicting urine osmolality of most patients with hyponatremia11. The commonly used formula to predict UOsm from USG uses a multiply of 30 but from the above two studies it would appear that multiplying by 25 gives a closer approximation and less likely to overestimate. Hence equation 3.
STEP 4: URINE Na <30 mEq/L
If urine sodium concentration ≤ 30 mmol/L, then most likely low effective arterial volume (see below optional section on What the hell does “low effective arterial volume” mean) is the cause of the hypotonic hyponatraemia. Really what we have to focus on here is whether the patient has HYPERvolumic or HYPOvolemic causes. The cutoff of urine sodium of 30 is randomly picked based on studies and is used by guidelines2. Using a cutoff of <30 suggests the above diagnoses and diuretics wont affect this diagnosis1.
OPTIONAL: What the hell does “low effective arterial volume” mean
Early observations in patients with cardiac failure demonstrated renal sodium and water retention that resulted in an increase in extracellular fluid (ECF) volume and edema. This degree of sodium and water retention in normal individuals would lead to an increase in renal sodium and water excretion, yet the reverse occurs in patients with heart failure. A similar sequence of events occurs in patients with cirrhosis and pregnancy. Renal sodium and water retention in edematous disorders continued to be perplexing. A term for sodium and water retention in edematous disorders was proposed to be due to a decrease in “effective blood volume” rather than “total blood volume”. For many years, however, this enigmatic term, which was used to explain sodium and water retention in patients with heart failure or cirrhosis, was never defined. Use of the term “decreased effective blood volume” can be considered outdated and be replaced by “arterial under-filling.” However, use of the term persists in clinical medicine, as “decreased effective arterial blood volume”13.
STEP 5: DETERMINE THE VOLUME STATUSHYPERVOLEMIA OR HYPOVOLEMIC
Although I said before that determining clinical volume status is more difficult at this stage the causes of hyponatremia from hypovolemic and hypervolemic reasons should be more obvious. Hypervolemic causes would include: CHF, Cirrhosis, and Nephrotic syndrome. Hypovolemic causes would include: Diarrhea and vomiting, third spacing, diuretics. It should be noted that a third cause of low urine sodium is very low sodium intake but this is rare in western diets. Also know there are insufficient data to suggest that increasing serum sodium concentration improves patient-important outcomes in moderate hyponatraemia with expanded extracellular fluid volume, in cirrhosis or heart failure.
TAKE HOME POINT: AFTER THIS POINT THERE IS NO SHAME IN CALLING A CONSULT OR PHONING A FRIEND TO GET HELP. FROM HERE ON OUT IT GETS WAY MORE COMPLICATED AND CONSULTATION IS A GOOD IDEA
STEP 6: URINE SODIUM >30 mEq/L
If the urine sodium is >30 mEq/L then one needs to consider if the patient is on diuretics. When I say diuretics I’m mostly refering to Thiazide and Thiazide-like diuretics. Potassium sparing diuretics can contribute to hyponatremia but less so. Loop diuretics are much less likely to cause hyponatremia. In fact diuretics can cause a urine sodium of <30 mEq/L also but we will touch on how to differentiate this as well. If the patient is NOT on diuretics then again we must decide if the patient has hypovolemia or Euvolemia
STEP 7: HYPOVOLEMIA OR EUVOLUMIA
Determining volume status in this category may be more subtlebut hypovolemia should be more obvious than euvolemia in this group. Thus, if by clinical exam, the patient is hypovolemic then the causes include: vomiting, primary adrenal insufficiency and renal/cerebral salt wasting.Determining euvolemia is much more subtle, however, if the ECF is normal by clinical exam then the causes include: SIADH, secondary adrenal insufficiency, and hypothyroidism (realistically unless hypothyroidism is severe such as myxedema or TSH >50 mIU/mL, then other causes of hyponatremia should be considered10).
STEP 8: USING FRACTION OF EXCRETED URIC ACID (FEurate)
As I said above the big problem at this branch point is that determining whether a patient is euvolemic or not can be very difficult. Additionally the treatments of SIADH and salt wasting are differentbecause of fluid restricting patients with SIADH as opposed to administering salt and water in salt wasting14. One way to differentiate this is by the fractional excretion of uric acid (urate). FEurate is normally 4%–11%and will stay normal in the excess water states with low urine osmoles because the concentrating ability is preserved (BOX 1 conditions). If the FEurate is <4%, it is consistent with pre-renal (BOX 2,3,4 conditions) including volume depleted states or edematous states such as CHF, cirrhosis, nephrotic syndrome,and pre-eclampsia.
STEP 9: DIFFERENTIATING SIADH AND SALT WASTING BY FEurate
Distinguishing these two can be very different because the only real difference is that in salt wasting there is a decrease in volume. However, the treatments are very different. The FEurate is especially helpful in distinguishing these two entities. In SIADH and Salt wasting (either cerebral or renal) FEurate is increased to >11% while the sodium is low. However, they can be differentiated after correction of the sodiumto >130. In SIADH, correction of hyponatremia will normalize FEurate to <11%, however in salt wasting the FEurate will still be inceased to>11%. One important caviat is that for the FEurate to be valid the patients serum creatinine must be <1.5 mg/dL14.
OPTIONAL: SIADH DIAGNOSTIC CRITERIA1:
- Effective serum osmolality < 275 mOsm/kg
- Urine osmolality > 100 mOsm/kg at some level of decreased effective osmolality
- Clinical euvolaemia
- Urine sodium concentration > 30 mmol/L with normal salt and water intake
- Absence of adrenal, thyroid, pituitary or renal insufficiency
- No recent use of diuretic agents
- 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 > 0.5%
- Fractional urea excretion > 55%
- Fractional uric acid excretion > 12%
- Correction of hyponatremia through fluid restriction
ALTERNATE LABS TO AID IN DETERMINING VOLUME STATUS
Fractional Excretion Of Sodium FENa
It is calculated by
In patients with normal renal function and hyponatremia cut off for FENa is <0.1%.
<0.1%- hypovolemic hyponatremia
>0.1%- hypervolemic and normovolemic hyponatremia.
In hyponatremia due to SIADH, the blood urea nitrogen (BUN) is usually less than 5 mg/dL. However, as urea excretion decreases with aging the absence of a low BUN cannot be used to exclude SIADH in older patients10.
Fractional Excretion of Uric Acid14
This is calculated as:
FEUrate <4% implies: Volume Depletion Addison’s Disease Edematous states, CHF
Cirrhosis, Nephrotic syndrome
FEUrate 4-11% implies: psychogenic polydipsia
FEUrate >11% implies: HCTZ, Salt Wasting
After normalization of Na to >130 FEurate will be <11% in SIADH and >11% in Salt wasting
OPTIONAL – BEER POTOMANIA
Cases of a hypoosmolal (Hypotonic) syndrome in beer drinkers were first described in 1972. Up to 17% of chronic alcoholic patients had hyponatremia. Although not consistently reported in patients with beer potomania, low urine osmolality on admission laboratory test results was not a consistent finding. In addition to the history of excess beer drinking, often a recent history of binge drinking or illness was present. This may potentially precipitate a rapid decrease in serum sodium levels. The maximum urinary dilution capability is 50 mOsm/L, a large amount of water (>20 L) must be ingested under normal situations to overwhelm the capacity for urinary dilution. For example, if the patient excretes only 100 mOsm/d, greater than 2 L of fluid intake with a urinary dilution capability of 50 mOsm/L will result in net water retention and subsequently hyponatremia. Patients with beer potomania have a history of significant beer drinking, often long term, in conjunction with a poor diet. The net result is very low osmole intake because beer has very little sodium and no protein, but has some calories that prevent endogenous protein breakdown (urea generation). Because the obligatory solute loss in a day is approximately 250 mOsm in these patients, with a urinary dilution capability of 50 mOsm/L, water intake greater than 5 L (or 14 cans of beer) results in hyponatremia. The net effect is an excess of free water without the solute for diuresis. ADH levels are expected to be suppressed in patients with beer potomania. The low ADH levels limit free-water reuptake in the collecting tubules of the kidney and explain why these patients have brisk diuresis when solute is presented. Sodium chloride in IV fluids is a common source of the solute load while hospitalized. Urine osmolality on recheck after the solute is introduced is low in these patients because of the low ADH levels. Based on a solute concentration of 308 mEq/L (154×2) in 0.9NaCl solution and the kidney’s diluting ability of 50 mOsm/L, significant diuresis can occur with 1 L of NS solution in the setting of a low-ADH state. This water diuresis can produce large increases in serum sodium levels in a short period. Attempting to replace this with electrolyte-free water to prevent a rapid increase in sodium levels can be difficult. Beer potomania is unusual because the cause of hyponatremia is multifactorial, including low osmole intake. Furthermore, as these patients convert to a low ADH state, the rate of correction may be dramatic. One study found that 18% of patients presenting with beer potomania developed ODS. Three large retrospective reviews of patients who presented with symptomatic severe hyponatremia found no benefit to aggressive correction of chronic hyponatremia. If the patient is asymptomatic, fluid restriction and monitoring the patient despite the degree of hyponatremia is the recommended approach. If the serum sodium level increase occurs at a rate that will exceed the desired goal, D5W infusion should be started to match urine output. The D5W rate can be adjusted every 2 hours based on serum sodium level change. If serum sodium levels increase to greater than either the 24- or 48-hour goals, D5W rate should be increased to decrease the serum sodium level to the recommended goal. Desmopressin may be considered if diuresis occurs at an excessive rate that the infused D5W is unable to match; based upon the current rate of serum sodium level change, the goal will be exceeded despite D5W; the goal has been already been exceeded; or last, symptoms of ODS develop15. A large rise in serum Na after infusion of a test volume of isotonic saline suggests the presence of hypovolemia.
MEDICATIONS COMMONLY ASSOCIATED WITH DECREASED SERUM SODIUM18:
- Spasovski G, Vanholder R, Allolio B et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Nephrol Dial Transplant 2014; 29 Suppl 2, i1-i39.
- Hoorn EJ, Zietse R. Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines. J Am Soc Nephrol 2017; 28, 1340-1349.
- Anderson RJ, Chung HM, Kluge R, Schrier RW. Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Ann Intern Med 1985; 102, 164-168.
- Upadhyay A, Jaber BL, Madias NE. Incidence and prevalence of hyponatremia. Am J Med 2006; 119, S30-5.
- Giordano M, Ciarambino T, Castellino P et al. Seasonal variations of hyponatremia in the emergency department: Age-related changes. Am J Emerg Med 2017; 35, 749-752.
- Imai N, Osako K, Kaneshiro N, Shibagaki Y. Seasonal prevalence of hyponatremia in the emergency department: impact of age. BMC Emerg Med 2018; 18, 41.
- Choy KW, Wijeratne N, Lu ZX, Doery JC. Harmonisation of Osmolal Gap – Can We Use a Common Formula. Clin Biochem Rev 2016; 37, 113-119.
- Purssell RA, Pudek M, Brubacher J, Abu-Laban RB. Derivation and validation of a formula to calculate the contribution of ethanol to the osmolal gap. Ann Emerg Med 2001; 38, 653-659.
- Plasma osmolality. Wikipedia
- Sahay M, Sahay R. Hyponatremia: A practical approach. Indian J Endocrinol Metab 2014; 18, 760-771.
- Sumethkula V, Choojitaromb K, Ingsathitc A, Radinahamed P. The Correlation between Urine Specific Gravity and Urine Osmolality in Patients with Hyponatremia. nternational Journal of Sciences: Basic and Applied Research (IJSBAR) 2017; 31, 181-189.
- Imran S, Eva G, Christopher S, Flynn E, Henner D. Is specific gravity a good estimate of urine osmolality. J Clin Lab Anal 2010; 24, 426-430.
- Schrier RW. Decreased effective blood volume in edematous disorders: what does this mean. J Am Soc Nephrol 2007; 18, 2028-2031.
- Maesaka JK, Imbriano L, Mattana J, Gallagher D, Bade N, Sharif S. Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia. J Clin Med 2014; 3, 1373-1385.
- Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis 2007; 50, 673-680.
- Momi J, Tang CM, Abcar AC, Kujubu DA, Sim JJ. Hyponatremia-what is cerebral salt wasting. Perm J 2010; 14, 62-65.
- Yee AH, Burns JD, Wijdicks EF. Cerebral salt wasting: pathophysiology, diagnosis, and treatment. Neurosurg Clin N Am 2010; 21, 339-352.
- Filippatos TD, Liamis G, Christopoulou F, Elisaf MS. Ten common pitfalls in the evaluation of patients with hyponatremia. Eur J Intern Med 2016; 29, 22-25.
[e]Remember: each mg increase in blood glucose above 100 mg/dl decreases the serum sodium by 1.6 meq/l. This is negligible when blood sugar is less than 300 mg/dl. When serum triglycerides are above 100 mg/dl, for every 500 mg/dl rise in serum triglycerides, fall in serum sodium will be about 1.0 mEq/L. When serum protein is above 8 gm/dl, for every 1 gm/dl rise in serum protein, fall in serum sodium will be about 4.0 mEq/L10.
[h]As a means of increasing solute intake, daily intake of 0.25–0.50 g/kg urea can be used. The bitter taste can be reduced by the following recipe in Sachets: 10 g urea + 2 g NaHCO3 + 1.5g citric acid + 200 mg sucrose to be dissolved in 50–100 ml water. Alternately using a commercially available urea powder drink mix (Ure-Na by Nephcentric)2