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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 18  |  Issue : 1  |  Page : 95-99
Cerebral Salt Wasting in a Patient with Head Trauma: Management with Saline Hydration and Fludrocortisone


Department of Medicine, Division of Nephrology, King Khalid University Hospital, Riyadh, Saudi Arabia

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   Abstract 

Hyponatremia secondary to the syndrome of inappropriate anti-diuretic hormone secretion is commonly observed in patients with various neurological disorders. Cerebral salt wasting (CSW), although uncommon, has also been reported to frequently result in hyponatremia. Here, we report a case of CSW in a patient with head trauma without evidence of cerebrovascular injury or brain edema. He was diagnosed on the basis of high fractional excretion of urinary sodium and uric acid along with extremely low serum uric acid. Improvements in serum sodium levels after saline hydration and fludrocortisone administration further supported the diagnosis, even in the presence of normal brain and atrial natriuretic peptide levels.

Keywords: Hyponatremia, Cerebral salt wasting, SIADH

How to cite this article:
Askar A, Tarif N. Cerebral Salt Wasting in a Patient with Head Trauma: Management with Saline Hydration and Fludrocortisone. Saudi J Kidney Dis Transpl 2007;18:95-9

How to cite this URL:
Askar A, Tarif N. Cerebral Salt Wasting in a Patient with Head Trauma: Management with Saline Hydration and Fludrocortisone. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2019 Dec 9];18:95-9. Available from: http://www.sjkdt.org/text.asp?2007/18/1/95/31854

   Introduction Top


Hyponatremia is a common disorder that occurs with a number of intracranial afflictions including head injuries, tumors, infections, stroke etc. It occurs in up to 30% of patients with subarachnoid hemorrhage (SAH). [1] The syndrome of inappropriate anti-diuretic hormone (SIADH) secretion is the cause of hyponatremia in the majority of such cases. [2] Hyponatremia secondary to cerebral salt wasting (CSW) has also been reported as a result of various neurosurgical disorders, although infrequently. [3],[4],[5],[6],[7],[8],[9],[10],[11],[12] Confusion in differentiating SIADH from CSW arises since both results in similar electrolyte disturbances. [2], [13], [14] Herein, we report a case of a young patient with head trauma, who was sub­sequently diagnosed with CSW.


   Case Report Top


A 17-year-old male was admitted to the King Khalid University Hospital, Riyadh, Saudi Arabia following a road traffic accident. He suffered multiple injuries to the face, chest, and pelvis and experience closed-head trauma. He was unconscious with a Glasgow coma scale of 7/15, had a blood pressure of 100/60 mm Hg and pulse of 90 / min. He was resuscitated, intubated and a computerized tomography (CT) scan revealed an intact brain with no evidence of subdural hematoma, SAH, intra-cerebral bleeding or cerebral edema. Multiple facial bone fractures, subcutaneous emphysema in the right chest along with right lung contusion and multiple pelvic bone fractures were noted. His baseline investigations were normal with a serum sodium (Na) level of 138 mmol/L. On day six of admission, his serum sodium decreased to 120 mmol/L. Clinical evaluation at that time revealed a central venous pressure (CVP) of 5 cm water; there was no evidence of edema and oxygenation was maintained on 35% FiO2. His urine output was around three liters per day with a net negative fluid balance. Pseudo-hyponatremia was excluded since he had normal serum glucose, protein and lipid levels and low serum osmolality. His urinary Na was 229 mmol and urine osmolality was 630 mOsm/Kg. A diagnosis of hypovolemic hyponatremia was made and saline infusion was started. His serum Na rose to 136 mmol/L by day nine and subsequently dropped to 123 mmol/L by day 15. Re­evaluation of the patient showed that he was normotensive with no peripheral edema and his CVP line was removed. He still had a urine output of 3-4 L/day. Urinary Na and fractional excretion of Na [FE Na ] were high at 245 mmol/L and 2.2% respectively, along with a high urine osmolality: of 783 mOsmol/Kg. A careful evaluation of his Na intake revealed that he received >700 mmol/L of Na from parenteral nutrition and other intravenous fluids. His urinary excretion of Na at the same time was also of the same magnitude. A renal salt losing state was therefore evident. Acute tubular necrosis was excluded due to the absence of any cause such as hypotension, medications or sepsis. Thyroid function tests and serum cortisol levels were also normal. A diagnosis of CSW versus SIADH was therefore entertained. The patient's serum uric acid level was found to be extremely low at 56 mmol/L with a high fractional excretion of urate [FE urate ] of 55%. A trial of fluid restriction from day 15 resulted in an additional drop in serum Na to 116 mmol/L with low serum uric Acid and high FE urate of 20%. Cerebral salt wasting was confirmed and saline hydration was initiated on day 20. Oral fludrocortisone 0.3 mg daily was added on day 24 and this resulted in gradual improvement of serum Na to 139 mmol/L by day 37. Under the influence of fludrocortisone, the FE Na decreased while the FE urate remained high and serum uric acid continued to be low [Table - 1]. The brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) levels, tested at this stage, were normal at 10 pg/ml (normal <17) and 22 pg/ml (normal 5-43) respectively. The patient was seen one month later in the nephrology clinic with normal electrolytes and serum uric acid. Fludrocortisone was tapered and discontinued three weeks later. Repeat investigations three weeks after discontinuation of fludrocortisone were normal.


   Discussion Top


Hyponatremia secondary to head trauma or other central nervous system pathologies is well known and mostly presents as SIADH. [2], [13], [14] In 1950, Peters et al described hyponatremia due to salt wasting in three patients with cerebral disease, seven years prior to the description of SAIDH by Schwartz. [3], [15] CSW was regarded as a rare entity, although several case reports and case series in both adult and pediatric patients have been reported. [3],[4],[5],[6],[7],[8],[9],[10],[11],[12]

Common to SIADH and CSW is hypo­natremia, increased urinary Na excretion and high urinary osmolality, as seen in our patient. SIADH however, is a relatively volume expanded state with inappropriately high ADH levels. [2] In contrast, patients with CSW have appropriately high ADH levels secondary to the volume depletion that results from Na loss. [2], [13], [15] Evaluation of volume status may be difficult in general as discussed by Chung et al in their review of the subject. [16] Patients in the intensive care unit setting could be assessed by the measurement of their CVP. A high urine output will further support salt losing nephropathy rather than SIADH. This point was stressed in the previous publications as a clue to the diagnosis. In our patient, urine output continued to be more than 3-4 liters per [13], [15] day.

Definitive diagnosis can be made by documenting elevated levels of the natriuretic peptides; ANP and BNP, although this may not be a universal finding in all patients. [13],[17],[18] In our patient, the levels were within the normal range as observed by other authors as well.[13],[18]

Proximal tubular function defects in patients with SIADH and CSW may also help in differentiating the two conditions. Blood urea nitrogen (BUN) increases in patients with volume contraction as is seen in CSW, whereas in patients with SIADH with volume expanded state, the BUN is usually on the lower side. This, however, is not always observed and not very helpful. [2] This was evident in our patient [Table - 1], in whom the BUN levels remained in the normal range and occasionally decreased despite the presence of volume depletion.

Increased excretion of uric acid in patients with SIADH is also the result of a defect in net uric acid reabsorption in the proximal tubule. [19],[20] The cause of this defect is unlikely to be volume expansion and remains elusive. Patients with AIDS and other neurological disorders have also been found to have higher fractional excretion of uric acid [FE urate ] even in the absence of, or even after correction of, hyponatremia as reviewed in detail by Maesaka. [2] The differentiation between SIADH and CSW can therefore be made by the observation that FEurate continues to be high even after correction of hyponatremia in the latter condition. [21],[22] In our patient, the FEurate was 55% initially and 18% even when serum Na had been corrected to139 mmol/L [Table - 1].

Management of SIADH and CSW are quite different. Although both conditions require high salt intake, volume restriction is required in SIADH while volume expansion is required in CSW. Wijdicks et al did a retrospective analysis of 134 patients with subarachnoid hemorrhage, of whom 17 patients were diagnosed with SIADH. Fifteen of these patients deteriorated after fluid restriction and thus might have had CSW. [4] Appropriate management of CSW is fluid replacement with saline and addition of fludrocortisones, similar to the treatment course undertaken for our patient. [2],[13],[14],[23] Interestingly, in our patient, the FE Na decreased significantly to <1%, likely under the influence of fludrocortisone, while the patient maintained high FE urate and increased serum Na levels.

Another interesting aspect in our patient was the absence of any obvious cerebrovascular injury or edema contributing to CSW development. Following a detailed literature search, we found one case report similar to our patient who presented with CSW without evidence of cerebrovascular injury or brain edema.[11]

In conclusion, hyponatremia secondary to CSW in patients with various neurosurgical disorders, even in the absence of obvious injury, is not a rare occurrence. Diagnosis can be established by the presence of volume depletion and high fractional excretion of Na and urate along with high urine osmolality. The BNP levels, if available, may support the diagnosis. Management requires salt and water repletion along with fludrocortisone. It is therefore important to monitor patients with head trauma even in the absence of obvious injury for prompt diagnosis and management of potentially dangerous electrolyte abnormalities.

 
   References Top

1.Fox JL, Falik JL, Shalhoub RJ. Neurosurgical hyponatremia: the role of inappropriate antidiuresis. J Neurosurg 1971;34:506-14.  Back to cited text no. 1  [PUBMED]  
2.Maesaka JK, Gupta S, Fishbane S. Cerebral salt wasting syndrome: does it exist? Nephron 1999;82: 100-9.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Peters JP, Welt LG, Sims EA, Orloff J, Needham J. A salt wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians 1950; 63: 57-64.  Back to cited text no. 3  [PUBMED]  
4.Wijdicks EF, Vermeulen M, tenHaaf JA, Hijdra A, Bakker WH, van Gijn J. Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol 1985;18: 211-6.  Back to cited text no. 4    
5.Ishikawa SE, Saito T, Kaneko K, Okada K, Kuzuya T. Hyponatremia responsive to fludro-cortisone acetate in elderly patients after head injury. Ann Intern Med 1987;106:187-91.  Back to cited text no. 5  [PUBMED]  
6.Cranong CA, Kappy MS. Cerebral salt wasting in children, the need for recognition and treatment. Am J Dis Child 1993;147(2):167-9.  Back to cited text no. 6    
7.Atkin L, Coady AM, White MC, Mathew B. Hyponatremia secondary to cerebral salt wasting syndrome following routine pituitary surgery. Eur J Endocrinol 1996; 135:245-7.  Back to cited text no. 7    
8.Ti Lk, Kang SC, Cheong KF. Acute hyponatremia secondary to cerbral salt wating syndrome in a patient with tuber­culous meningitis. Anaesth Intensive Care 1998;26:420-3.  Back to cited text no. 8  [PUBMED]  
9.Donati-Genet PC, Dubuis JM, Girardin E, Rimensberger PC. Acute symptomatic hypo-natremia and cerebral salt wasting after head injury an important clinical entity. J Pediatr Surg 2001;36:1094-7.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Brookes MJ, Gould TH. Cerebral salt wasting syndrome in meningoencephalitis: a case report. J Neurol Neurosurg Psychiatry 2003;74: 277.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Steelman R, Corbitt B, Pate MF. Early onset of cerebral salt wasting in a patient with head and facial injuries. J Oral Maxillofac Surg 2006; 64 (4): 746-7.  Back to cited text no. 11    
12.Sherlock M,O'Sullivan E, Agha A, et al. The incidence and pathophysiology of hyponatraemia after subarachnoid hemo­rrhage. Clin Endocrinol 2006; 64:250.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Singh S, Bohn D, Carlotti AP, et al. Cerebral salt wasting: truths, fallacies, theories, and challenges. Crit Care Med 2002;30:2575-9.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Harrigan MR. Cerebral salt wasting syn­drome. Crit Care Clin 2001;17 (1): 125-38.  Back to cited text no. 14    
15.Schwartz WB, Bennett W, Curelop S, Bartter FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med 1975;23:529-42.  Back to cited text no. 15    
16.Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med 1987;83:905-8.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Berendes E, Walter M, Cullen P et al. Secretion of brain natriuretic peptide in patients with aneurismal subarachnoid hemorrhage. Lancet 1997;349:245-9.  Back to cited text no. 17    
18.Bismark PV, Ankermann T, Eggert P, Claviez A, et al. Diagnosis and Manage­ment of Cerebral Salt Wasting (CSW) in Children: the role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Child's Nervous System, Springer-Verlag 2006. Published online; 11 April 2006, WWW.Springerlink.com   Back to cited text no. 18    
19.Beck LH. Hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone. N Engl J Med 1979;301:528-30.  Back to cited text no. 19    
20.Decaux G, Dumont I, Waterlot Y, Hanson B. Mechanisms of hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone. Nephron 1985; 39:164-8.  Back to cited text no. 20    
21.Maesaka JK, Cusano AJ, Thies HL, Siegal FP, Dreisbach AW. Hypouricemia in acquired immunodeficiency syndrome. Am J Kidney Dis 1990;15:525-7.  Back to cited text no. 21    
22.Cusano AJ, Thies HL, Siegal FP, Dreisbach AW, Maesaka JK. Hypona­tremia in patients with acquired immune deficiency syndrome. J Acquir Immune Defic Syndr 1990;3:949-53.  Back to cited text no. 22    
23.Hasan D, Lindsay KW, Wijdicks EF et al. Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage. Stroke 1989;20:1156-61.  Back to cited text no. 23    

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Correspondence Address:
Nauman Tarif
Consultant Nephrologist, Department of Medicine King Khalid University Hospital, P.O. Box 2925 [38], Riyadh 11461
Saudi Arabia
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PMID: 17237900

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