it has been reported that over 50% of patients admitted for sah develop hyponatremia ( 1 - 3 ) .
sah - associated hyponatremia can be caused by excessive intravenous fluid therapy , diuretic therapy , cerebral salt - wasting syndrome ( csws ) , and syndrome of inappropriate antidiuretic hormone ( siadh ) ( 4 ) .
both csws and siadh cause hyponatremia by increasing renal excretion of sodium , and both are associated with serum hypo - osmolality and high urine osmolality ( 5 - 8 ) .
( 3 ) reported that siadh is more likely to occur than csws ( 35.4% vs. 22.9% , 71.4% vs. 0% ) in this patient population , yet csws has similar mortality rates and duration of hospital stay to siadh .
the high urine sodium level observed in patients with csws is secondary to urine sodium wasting rather than volume expansion ( 11 ) .
although the precise mechanism of salt wasting is poorly understood , several studies have begun to shed light on the pathophysiology of this disease .
first , impaired sympathetic neural input to the juxtaglomerular apparatus may reduce proximal tubule sodium , urate , and water reabsorption and decrease renin and aldosterone release ( 12 ) .
second , brain injury might increase the secretion of human atrial natriuretic peptide ( hanp ) and brain natriuretic peptide ( bnp ) , leading to an increase in sodium excretion and urine volume ( 1,10,13 ) .
in contrast , hyponatremia secondary to siadh is a result of an excess of water rather than a deficiency of sodium .
excessive secretion of antidiuretic hormone ( adh ) is caused by stimulation of the hypothalamus after trauma or ischemia .
high levels of adh increase water reabsorption in the distal convoluted renal tubule , causing fluid retention and dilutional hyponatremia ( 14,15 ) .
first , csws is characterized by volume depletion , while siadh is not ( 5,16 ) . however , the evaluation of extracellular fluid volume is notoriously difficult .
second , changes in uric acid homeostasis may provide clues to the cause of hyponatremia . in siadh
in contrast , in csws , hypouricemia and increased renal uric acid excretion persist after correction of serum sodium .
furthermore , the fractional excretion of uric acid ( feua ) is greater than 10% after correction of hyponatremia in csws but is less than 10% after correction of hyponatremia in siadh ( 17 ) .
it is important to distinguish between csws and siadh in patients with hyponatremia because treatment of these two syndromes is very different .
he had been in good health until 4 days prior to presentation , at which point he fell and developed sah .
two days following discharge , he developed a headache , nausea , thirst , and impaired consciousness , prompting readmission . on admission ,
his blood pressure was 127/72 mmhg , pulse rate was 61 beats per minute , and oxygen saturation was 98% while breathing ambient air .
the laboratory findings included marked hyponatremia ( 106 mmol / l ) , plasma hypo - osmolality ( 220 mosm / l ) , urine hyper - osmolality ( 468 mosm / l ) , and elevated urine sodium ( 115
his serum arginine vasopressin peptide ( avp ) level was 2.2 pg / ml , and his serum creatinine , thyroid hormone , and adrenal cortical hormone levels were within normal limits .
although his physical examination findings were normal , he reported increased urination and excessive thirst . furthermore , his inferior vena cava diameter was 8 mm on ultrasound , indicating volume depletion .
together , the data suggested a diagnosis of csws , and he was treated with sodium repletion ( 300 to 600 meq daily ) .
however , the serum sodium level did not improve ( 119 mmol / l ) , and he continued to excrete high levels of sodium .
starting on hospital day 10 , he was treated with fludrocortisone ( 0.05 to 0.1 mg daily ) .
shortly thereafter , the serum sodium level gradually improved ( 135 mmol / l ) , and the urine sodium level decreased ( figure ) .
the fractional excretion of uric acid was 11.9% after correction of hyponatremia , which is consistent with a diagnosis of csws .
his blood pressure was 148/78 mmhg , and his pulse rate was 64 beats per minute .
he was again noted to be hyponatremic ( 118 mmol / l ) and was thus readmitted to our hospital .
similar to his prior hospitalization , laboratory tests revealed hypo - osmolality ( 245 mosm / l ) , urine hyper osmolality ( 545 mosm / l ) , and increased renal excretion of sodium ( 82 mmol / l ) .
his physical examination findings were unremarkable , but unlike at his previous hospitalization , the diameter of his inferior vena cava was normal ( 14 mm ) on ultrasound .
he was initially treated with sodium repletion ( 300 to 400 meq daily ) and fludrocortisone ( 0.1 mg daily ) but his serum sodium level did not improve .
he was subsequently treated with fluid restriction ( 800 ml / day ) , and his serum sodium level improved ( 140 mmol / l , figure ) .
the fractional excretion of uric acid was 4.9% after correction of hyponatremia , which is consistent with a diagnosis of siadh .
he continued to do well over the next four months , requiring no additional hospitalizations or medications .
it has been reported that hyponatremia in patients with central nervous system ( cns ) diseases can be attributed to excessive fluid therapy , diuretic use , csws , or siadh ( 8) . although csws and siadh have similar laboratory findings , including hyponatremia , serum hypo - osmolality , and increased renal excretion of sodium , the pathophysiology and treatment of these syndromes are very different .
hyponatremia due to csws improves with fluid repletion and fludrocortisone , while hyponatremia due to siadh improves with fluid restriction and vasopressin-2 receptor antagonists .
thus , the correct etiology of hyponatremia must be identified before starting the appropriate therapy .
csws is characterized by extracellular volume depletion , which stimulates adh release ( 1,10 ) .
this is accompanied by increased production of hanp and bnp and impaired release of renin , despite fluid depletion .
siadh , which is characterized by excessive extracellular volume , causes similar changes in renin , hanp and bnp .
hence , changes in these serum markers can not be used to differentiate csws from siadh .
other factors may be more useful in differentiating these two syndromes , including extracellular volume status , changes in uric acid homeostasis , and response to fluid restriction .
table 2 shows the laboratory and physical findings during the patient 's first and second hospitalizations , leading to the diagnoses of csws and siadh .
for example , the fractional excretion of uric acid was greater than 10% after the correction of hyponatremia during the first hospitalization , but it was less than 10% during the second hospitalization ( table 1 , 2 ) .
furthermore , the response to fluid restriction differed between the first and second hospitalizations . the sensitivity and specificity of these findings for the diagnosis of csws and siadh are unknown
. therefore , these differences may simply be diagnostic tools , rather than strict definitions of disease .
nonetheless , the data suggest that his initial presentation was consistent with csws and his second presentation was consistent with siadh .
there are no previous reports suggesting that csws may transform into siadh , and no reports of a temporal association between the two syndromes .
siadh can occur hours to months after brain injury ; our patient may therefore have suffered from late - onset siadh , leading to the observed time difference between csws and siadh ( 18 ) . in our case ,
natriuretic factors such as anp and bnp were initially increased by direct damage to the brain .
natriuretic factors would lead to a diminished activity of the renin - angiotensine - aldosterone system and increased natriuresis in the distal renal tubule ( 19 ) .
inappropriate secretion of adh increases water reabsorption in the distal renal tubule , which is consistent with late - onset siadh , resulting in increased natriuresis .
it is also possible that the patient developed both syndromes simultaneously but that the laboratory findings during his first admission were most consistent with csws .
after fluid therapy and fludrocortisone treatment , the csws resolved , revealing the residual siadh .
we might also need to consider how much the patient drank , particularly after the first hospital discharge , as excessive drinking can result in an excess of water , which would exacerbate siadh .
however , the patient did not consume a large amount of water at his home .
he reported that he consumed 1 to 1.5 liters of water per day , which would not cause an excess of water . without precise data on the amount he drank after the first hospital discharge , though , conclusions are difficult to make .
we herein report a rare case of csws and siadh following sah . distinguishing between csws and siadh may help prevent complications resulting from inappropriate treatment .
 hyponatremia is a common finding after subarachnoid hemorrhaging ( sah ) and can be caused by either cerebral salt - wasting syndrome ( csws ) or syndrome of inappropriate antidiuretic hormone ( siadh ) . 
 distinguishing between these two entities can be difficult because they have similar manifestations , including hyponatremia , serum hypo - osmolality , and high urine osmolality . 
 we herein report the case of a 60-year - old man who suffered from sah complicated by hyponatremia . during his initial hospitalization , 
 he was diagnosed with csws . 
 he was readmitted one week later with hyponatremia and was diagnosed with siadh . 
 this is the first report of sah causing csws followed by siadh . 
 these two different sources of hyponatremia require different treatments . 
Introduction
Case Report
Discussion
The authors state that they have no Conflict of Interest (COI).