A New Algorithm to Differentiate Salt-wasting Syndrome from SIADH

In cerebral salt-wasting (CSW), natriuretic factor is produced in response to a central insult.  Natriuretic factor decreases sodium transport in proximal renal tubule which leads to urinary loss of sodium (and water) and depletion of extracellular volume.  Hypovolemia then triggers secretion of ADH, renin and aldosterone, which provides a negative feedback to decrease secretion of natriuretic factor.


Differentiating CSW from syndrome of inappropriate antidiuretic hormone (SIADH) is problematic, laboratory work-up (urine and plasma sodium levels and urine and plasma osmolarity) is similar in both conditions.  CSW patients are usually volume depleted while SIADH patients are euvolemic.  The traditional approach of examining patient clinically to to determine volume status is inaccurate.

An interesting paper published in 2014 suggested a new algorithm to differentiate SIADH from CSW based on the effect of sodium correction on the fractional excretion of urate (FEUa).  FEurate is calculate using the folllowing formula:






Another formula:



Normal FEUa = 4-11%, SIADH & CSW FEUa = >11%.  FEUa determines the percent excertion of the filtered load of urate at the glomerulus.

In SIADH, FEUa normalizes after correction of hyponatremia (see graph below):


whereas in CSW, FEUa remains elevated >11% after correction of hyponatremia.  The reason is probably because natriuretic factor also decreases urate transport in the proximal tubule.



Based on this finding, the paper suggests a new algorithm for determining the etiology of hyponatremia that omits reliance of UNa (and also plasma renin, aldosterone, atrial or brain antriuretic peptide, BUN/creatinine ratio).


Based on this algorithm, a patient with hyponatremia should undergo correction of sodium by any means (water restriction or isotonic / hypertonic saline). Observing whether FEUa normalizes or remains increased would differentiate SIADH from CSW syndrome.






Maesaka, J., Imbriano, L., Mattana, J., Gallagher, D., Bade, N. and Sharif, S. (2014). Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia. Journal of Clinical Medicine, 3(4), pp.1373-1385.



Venous Blood Gas – VBG-ABG correlation

Venous blood gas can be used toestimate systemic CO2 and pH levels.

Possible sites of VBG:

  1. peripheral venous sample (from venipuncture)
  2. central venous sample (from central venous catheter)
  3. mixed venous sample (from distal port of PAC)

Values from VBG:

  1. PvO2 – venous oxygen tension
  2. PvCO2 – venous carbon dioxide tension
  3. pH
  4. SvO2 – oxyhemoglobin saturation
  5. HCO3 – serum bicarbonate

PvCO2, pH, HCO3 – assess ventilation and/or acid-base status

SvO@ – guides resuscitation

PvO2 – no value



  1. Central venous sample
    1. pH – 0.03 to 0.05 pH units lower than arterial pH
    2. PvCO2 – 4-5 mm Hg higher than PaCO2
    3. HCO3 – little or no increase
  2. Mixed venous sample – similar tocentral venous sample
  3. peripheral venous sample
    1. pH – 0.02 to 0.04 pH units lower than arterial pH
    2. HCO3 –  1-2 mEq/L higher
    3. PvCO2 – 3-8 mm Hg higher than PaCO2

*varies with hemodynamic stability



Uptodate.com. (2018). UpToDate. [online] Available at: https://www.uptodate.com/contents/venous-blood-gases-and-other-alternatives-to-arterial-blood-gases?search=venous%20blood%20gas&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 [Accessed 22 Oct. 2018].

Equations for Phenytoin Dosing and Monitoring

#1.  loading dose for subtherapeutic phenytoin concentration:



#2. adjust for renal disease



#3. adjust for hypoalbuminemia



#4. adjust in elderly and critically ill with hypoalbuminemia




**Vd = volume of distribution (0.5-1 L/kg)



Tesoro, E. P. and G. M. Brophy. “Pharmacological Management Of Seizures And Status Epilepticus In Critically Ill Patients”. Journal of Pharmacy Practice 23.5 (2010): 441-454.

**Thanks to Benjamin Wee (Clinical Pharmacist @ Lenox Hill Hospital) for giving me this resource.

Bicaudate Index

Diagram showing the method for measuring the bicaudate index (A / B). A = the width of the frontal horns at the level of the caudate nuclei; B = the diameter of the brain at the same level.





The bicaudate index is a commonly used linear measure of the lateral ventricles. To account for the natural changes in the size of ventricles with aging, BCI is then divided by the upper limits of ‘normal’ for age to calculate the relative bicaudate index.

Diagnosis of hydrocephalus is established when RBCI is >1. Normative values determined from subjects without neurological disease, in the mid to late 1970s.


Divide the width of the frontal horns, at the level of the caudate nuclei, by the corresponding diameter of the brain. Perform measurement on the cut which included the Foramen of Monro.  If the foramen of Monroe is in between two cute, use mean value for of the two cuts.


Bicaudate index plotted against age. The density ellipsoid includes 95% of the data points.



Normal BCI values, stratified by age group, in a cohort of SAH patients without co-existing hydrocephalus.




Gijn, Jan van et al. “Acute Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage”. Journal of Neurosurgery 63.3 (1985): 355-362.

Dupont, Stefan and Alejandro A Rabinstein. “CT Evaluation Of Lateral Ventricular Dilatation After Subarachnoid Hemorrhage: Baseline Bicaudate Index Balues”. Neurological Research 35.2 (2013): 103-106.


CSF WBC Correction for Traumatic Tap

If peripheral WBC is normal, then use ratio of 1:500 or 1:750.

If peripheral WBC abnormal, then use the following formula:

  • WBCcsf = WBCblood x RBCcsf / RBCblood
  • or  WBCc * RBCb = WBCb*RBCc
  • or WBCc/RBCc = WBCb/RBCb

The result is the number of artificially introduced WBCs.

True WBCcsf is then calculated by subtracting the artificially introduced WBCs from the actual WBCcsf


“WBC Correction For Traumatic Tap – Labce.Com, Laboratory Continuing Education”. Labce.com. N.p., 2016. Web. 17 Aug. 2016.