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Year : 2009  |  Volume : 4  |  Issue : 1  |  Page : 50-51

Hyponatremia in a patient with meningitis and Crohn disease: Cerebral salt wasting or SIADH?

1 Department of Pediatrics, Faculty of Medicine, Gaziosmanpasa University Tokat, Turkey
2 Clinics of Pediatrics, Ministry of Health Ankara Training and Research Hospital Ankara, Turkey

Correspondence Address:
Resul Yilmaz
Department of Pediatrics, Faculty of Medicine Gaziosmanpasa University 600 30, Tokat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1817-1745.49113

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How to cite this article:
Yilmaz R, Tasar MA, Dallar Y. Hyponatremia in a patient with meningitis and Crohn disease: Cerebral salt wasting or SIADH?. J Pediatr Neurosci 2009;4:50-1

How to cite this URL:
Yilmaz R, Tasar MA, Dallar Y. Hyponatremia in a patient with meningitis and Crohn disease: Cerebral salt wasting or SIADH?. J Pediatr Neurosci [serial online] 2009 [cited 2022 May 25];4:50-1. Available from: https://www.pediatricneurosciences.com/text.asp?2009/4/1/50/49113


Electrolyte disorders, especially hyponatremia, are common problems in patients with CNS disease. Although hyponatremia due to CNS disease is often attributed to SIADH, CSW and SIADH have similar laboratory findings and they overlap in their association with intracranial diseases. [1],[2] In SIADH, there is a relatively volume-expanded state with hyponatremia, decreased serum osmolality, and inappropriately high ADH. [3] On the other hand, CSW is characterized by natriuresis with concomitant diuresis, decreased intravascular volume, and extracellular fluid depletion. [2],[3] Thus, SIADH and CSW treatment require different approaches. SIADH treatment requires fluid restriction, whereas CSW treatment consists of fluid replacement with saline and mineralocorticoid. [4],[5] Improper therapy can worsen the underlying condition and it is important that clinicians distinguish properly between CSW and SIADH. [6],[7]

A 16 year-old male was admitted to the hospital with nausea and vomiting. One week before admission, his oral intake had become poor and he had been vomiting 5-6 times a day for two weeks. Three to four days before the hospital admission, his stools were bloody. He was treated as Crohn disease patient for three months with sulfasalazin, ferrous sulphate, folic acid, and omega 3.

Physical examination revealed that the patient was dehydrated and lethargic. His temperature was 38.2 0 C, the pulse rate was 100 beats per minute, and the blood pressure 90/60 mm Hg. His weight was 31 kg (< 3 P) and his height was 153 cm (< 3 P). His eyes were sunken and there was tenting of the skin. Bowel movements were positive and increased bowel sounds were heard by auscultation. He had nuchal rigidity and positive Kernig and Brudzinski signs. The other results of the physical examination were normal.

Laboratory tests performed after admission showed: the complete blood count WBC 6600/mm 3 , hemoglobin 9.7 g/dL, platelets 119000/mm 3 . A peripheric blood smear showed 87% neutrophils, 17% leukocytes, hypochromia, and anisocytosis. The serum contained 127 mmol/L sodium, 3.95 mmol/L potassium, 96.6 mmol/L chloride, 5 mg/dL urea, 0.4 mg/dL creatinine, and 0.7 mg/dL uric acid.

Monteux test was negative and a computed tomographic (CT) scan of the head was normal. Cerebrospinal fluid examination revealed a lymphocytic picture (130 cells/mm 3 ) with 65 mg/dL (0-45 normal) protein and 20 mg/dL glucose levels. Simultaneously performed laboratory tests revealed that levels of serum glucose and chloride were 90 mg/dL and 108 mmol/L respectively.

Based on these findings indicating meningitis, intravenous ceftriaksone was started and 20 mL/kg normal saline was given in one hour for volume depletion. This was followed by hypertonic NaCl (3% NaCl) with an IV fluid dose of 2500 mL/m 2 /day. On day two, hemiplegia developed in the right side of the body and a CT scan of the head was repeated and found to be normal. Biochemical tests were repeated and severe hyponatremia was detected (Na: 118 mmol/L) despite saline resuscitation. Hypovolemia persisted without any source of GIS fluid loss; a normal serum urea level (4.8 mg/dL) and increased urine output (4.5 L/day) were also noted. Serum osmolality was 225 mOsm/kg and urine Na 294 mmol/L. However, SIADH was ruled out because of the increased fractional Na (3.1%) and uric acid (3.2%) excretion seen with the observed polyuria.

The patient had the clinical and laboratory findings of CSW and was managed with IV fluids: hypertonic sodium solutions and IV corticosteroids (prednisolone 2 mg/kg/day). Serum sodium levels increased gradually to the level of 136 mmol/L [Figure 1]. On day 10, the patient became confused, developed respiratory distress, and died on day 11.

Electrolyte disorders are common problems in patients with central nervous system insult such as trauma, infection, or hemorrhage. The management of electrolyte and fluid balance in these patients can be difficult. The serum sodium levels, rapid alterations of sodium levels, and the duration of hyponatremia are factors that worsen the underlying CNS conditions.

How common CSW is uncertain. Previous studies show that it is as common as SIADH whereas some studies say that it is overstated. [8] CSW is regarded as a rare entity [5] in childhood and its prevalence is insufficient, there being mostly isolated case reports and the report of one small series in literature.

Central nervous system infections, including tuberculosis meningitis, bacterial meningitis, and viral meningoencephalitis can cause cerebral salt wasting. However, there are a few case reports in literature that describe the association of CSW with infection. [9] The mechanism by which cerebral disease leads to renal salt wasting is not well known. Decisions regarding treatment can be taken by investigating the levels of natriuretic peptides (ADH, ANP, BNP, renin-aldosterone axis elements). AVP and BNP were shown to be elevated eight days after cerebral injury when compared to the controls. [4] However, this may not be an universal finding in all patients. [5] Controversy exists around the cause of hyponatremia in tuberculosis meningitis as some studies report the cause to be inappropriate secretion of ADH whereas others cite increased ANP levels as the cause. [10],[11]

Due to the distinction between CSW and SIADH, CWS responds to sodium and water replacement, whereas SIADH is treated by fluid restriction. Our case had symptomatic hyponatremia with polyuria and natriuresis. Urinary Na and fractional excretion of Na were also high. This salt-losing condition ruled out SIADH wherein urine output is usually high. This feature plays an important role in the diagnosis, as discussed in previous reports. [8] In our patient, a high urine output (> 4-5 litres per day) lasted for five days. A diagnosis of CSW was made on the basis of the following findings: 1. marked natriuresis with negative sodium and water balance, 2. the patient's hyponatremic and relatively salt-depleted state despite infusions of hypertonic saline solutions, and 3. persistent high fractional uric acid excretion rates throughout the course of the disease.

There is no evidence in literature that Crohn disease and/or salazopryrine cause salt wasting.

The key feature of CSW is the hyponatremia which is the initial marker that leads to the diagnosis. The next most important event is treating and protecting the patient from its negative effects by matching the Na and water input to their output. Mineralocorticoid therapy was found to be effective in most patients. Doses of 0.1-0.4 mg/day fludrocortisone with saline and water replacement increased Na concentrations to normal serum levels. [4],[9] We could not obtain fludrocortisone and other steroids which have higher mineralocorticiod activity than prednisolone, therefore, 2 mg/kg/day prednisolone doses were used. Sodium levels increased to 136 mmol/L with this additional therapy.

In conclusion, one reason for hyponatremia in patients with meningitis can be cerebral salt wasting and management must take this situation into consideration. [12] Glucocorticosteroids can be used as alternatives for the mineralocorticoid, fludrocortisone, when it can not be obtained.

   References Top

1.Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatremia in cranial disease: Perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). J Neurosurg 1981;55:938-41.  Back to cited text no. 1    
2.Palmer FB. Hyponatremia in neurosurgical patient: Syndrome of inappropriate antidiuretic hormone secretion versus cerebral salt wasting. Nephrol Dial transplant 2000;15:262-8.  Back to cited text no. 2    
3.Kinik ST, Kandemir N, Baykan A, Akalan N, and Yordam N. Fludrocortisone treatment in a child with severe cerebral salt wasting. Pediatr Neurosurg 2001;35:216-9.  Back to cited text no. 3    
4.Sherlock M, O'Sullivan E, Agha A, Behan LA, Rawluk D, Brennan P, et al . The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf) 2006;64:250-4.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Taplin CE, Cowell CT, Silink M, Ambler GR. Fludrocortisone therapy in cerebral salt wasting. Pediatrics 2006;118:e1904-8.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.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.  Back to cited text no. 6  [PUBMED]  Medknow Journal
7.Kurtoglu S, Atabek ME, Keskin M, Patiroglu T, Kumandas S, Topaloglu N. Rhabdomyosarcoma with coexistent diabetes insipidus and cerebral salt wasting as postoperative complication. Pediatr Int 2006;48:79-81.  Back to cited text no. 7    
8.von Bismarck P, Ankermann T, Eggert P, Claviez A, Fritsch MJ, Krause MF. Diagnosis and management of cerebral salt wasting (CSW) in children: The role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Childs Nerv Syst 2006;22:1275-81.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Inatomi J, Yokoyama Y, Sekine T, Igarashi T. A case of cerebral salt-wasting syndrome associated with aseptic meningitis in an 8-year-old boy. Pediatr Nephrol 2008;23:659-62.   Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Singh S, Bohn D, Carlotti AP, Cusimano M, Rutka JT, Halperin ML. Cerebral salt wasting: Truths, fallacies, theories, and challenges. Crit Care Med 2002;30:2575-9.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Narotem PK, Kemp M, Buck R, Crows E, van Delen JR, Bholla KD. Hyponatremic natriuretic syndrome in tuberculous meningitis: The probable role of atrial natriuretic peptide. Neurosurgery 1994;34:982-8.  Back to cited text no. 11    
12.Brookes M J and Gould T H. Cerebral salt wasting syndrome in meningoencephalitis: A case report. J Neurol Neurosurg Psychiatry 2003;74:277.  Back to cited text no. 12    


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