BMJ Case Reports 2009; doi:10.1136/bcr.09.2008.0966
  • Novel treatment (new drug/intervention; established drug/procedure in new situation)

Cerebral salt wasting syndrome in a patient affected of spontaneous frontoparietal subdural haematoma

  1. Mariaina Cerdá-Esteve1,
  2. Mariona Badia2,
  3. Javier Trujillano2,
  4. Cecília Vilanova2,
  5. Javier Maravall3,
  6. Dídac Mauricio3
  1. 1
    Hospital Universitario Arnau de Vilanova. IRBLLEIDA, 1. Endocrinology and Nutrition Service, Rovira Roure 80, Lleida, 25198, Spain
  2. 2
    Hospital Universitario Arnau de Vilanova, Intensive Care, Rovira Roure 80, Lleida, 25198, Spain
  3. 3
    Hospital Universitario Arnau de Vilanova, Endocrinology and Nutrition Service, Rovira Roure 80, Lleida, 25198, Spain
  1. Mariaina Cerdá-Esteve, MCerda{at}
  • Published 13 October 2009


Ever since cerebral salt wasting syndrome (CSW) was first described in 1950, there have been debates over its existence and whether it has an important place in the differential diagnosis of hyponatraemia. We report the case of a neurosurgical patient with sustained hyponatraemia and abnormally high sodium loss in the urine, with signs of fluid volume depletion. Hyponatraemia was not corrected after an intravenous infusion of saline solution. Stable concentrations of blood sodium above 130 mmol/l were achieved with the administration of 100 mg of hydrocortisone daily, with an ensuing reduction in sodium elimination through the urine.


Cerebral salt wasting syndrome (CSW) is defined as renal loss of sodium during intracranial disease leading to hyponatraemia and a decrease in extracellular fluid volume. Since CSW was first described in 1950 by Pers et al, its existence has been debated1,2 but finally agreed upon.36 The main difficulty in defining this disorder is differentiating it from inadequate secretion of antidiuretic hormone (SIADH). However, we believe it is important to discuss its treatment. As we prepared to treat the patient presented in this case report, a systematic search of the literature in PubMed, using the terms “CSW and corticoids”, found treatment for this pathology only for paediatric cases using corticoids. No cases of this disorder in patients with spontaneous frontoparietal subdural haemorrhage were found.

Case presentation

The patient was a 53-year-old white man. He worked as a construction worker, and had a history of moderate alcoholism, took no medications, and had not undergone previous surgery.

The patient presented to the emergency room after an episode of disorientation, instability, an alteration of his ability to walk, and a clouding of consciousness. Later, he had convulsions with a generalised tonic-clonic seizure. A head computed tomography (CT) scan was performed, which showed a spontaneous acute left frontoparietal subdural haematoma with a midline shift >5mm. An emergency craniotomy was performed to evacuate the subdural haematoma. The patient went into the intensive care unit for postoperative monitoring. Intracranial pressure was monitored and remained stable without hyperosmolar therapy. During the first 72 h after surgery, isotonic saline solution was infused with central venous pressure (CVP) monitoring, achieving a positive water balance. From the third day after surgery, the patient showed sustained hyponatraemia with abnormally high sodium loss in the urine with negative salt and water balance. It was also noted that the central venous pressure (CVP) fell <5 mm Hg despite adequate fluid replacement, urine output increased between 90–400 ml/h, blood pressure dropped to between 90–100 mm Hg systolic and 45–60 mm Hg diastolic, and heart rate increased above 110 beats/min. The examination showed dry mucous membranes, slightly decreased skin turgidity, and a weight loss of 1.5 kg. Sugar concentrations were <150 mg/dl at every time point.


To rule out a hormonal problem, the following values were determined without treatment with hydrocortisone. The blood cortisol concentration at 8 h was 423 nmol/l. The short corticotropin test (250 μg adrenocorticotropic hormone (Synancthen) injected intravenously) showed a normal cortisol response with a value of 786 nmol/l at 30 min and 911 nmol/l at 60 min. The patient had 6.15 pmol/l 8 h corticotrophin, 1.7 mU/l thyrotropin, 14.6 pmol/l free thyrotoxin, and 58 ng/l brain natriuretic peptide. All values measured were within normal range.

Blood sodium values decreased progressively from the third day until a maximum of 120 mmol/l, with abnormally high sodium loss in the urine (with a maximum detected loss of 714 mmol/24 h), despite the administration of increasing doses of saline solution and normalisation after treatment with corticoids (fig 1). Blood potassium and urinary potassium concentrations were normal.

Figure 1

Variations in sodium concentrations in the different phases of intensive treatment. Phase 1, immediate postoperative period after subdural haematoma evacuation. Phase 2, manifestation of hyponatraemia. Patient with haemodynamic stability, central venous pressure 6–11 mm Hg. Phase 3, treatment with supplementary parenteral sodium. Minimum level of serum sodium of 120 mmol/l with excessive sodium excretion (maximum of 714 mmol/24 h). Phase 4, response to corticoid treatment (intravenous hydrocortisone 100 mg/day) with fluctuations due to variations in the level of sodium supplementation. Phase 5, corticoid treatment progressively discontinued with sodium values of around 130 mmol/l. Phase 6, new decrease in serum sodium values causing re-establishment of corticoid treatment.

CVP was monitored during fluid infusion with hypertonic saline solution, and fluid balance was computed daily during the 75 days the patient stayed in the ICU. Body weight change was measured weekly.

Differential diagnosis

Alterations in sodium are frequently found in critically ill neurologic and neurosurgical patients.7 The first step after finding pseudohyponatraemia is to check glycaemia.

After confirming that the patient was suffering from real hyponatraemia, we performed a differential diagnosis, taking into account the data we had obtained with SIADH.8 SIADH has normal or high plasma volume, while CSW is characterised by low plasma volume. Decreased extracellular volume with negative salt and water balance are the key diagnostic factors for CSW which distinguish it from SIADH. It was felt that our patient had CSW based on the clinical features which include hypotension, increased skin turgidity, dry mucous membranes, hyponatraemia associated with hypovolaemia (low CVP), elevated urine rate flow with high urinary sodium excretion, and negative salt and water balance. Clinical examination and biochemical investigations suggest extracellular volume depletion.


Fluid replacement therapy was started, initially with isotonic saline solution and later with hypertonic saline solution guided by CVP monitoring, which remained between 6–11 mm Hg. The patient had a negative response to the hyponatraemia, so treatment was initiated with 100 mg of hydrocortisone parenterally (with a maximum dose of 200 mg/day), and the treatment was maintained over 26 days (fig 1) leading to a normalisation of the blood sodium value and a decrease of sodium loss in urine. After progressive withdrawal of the hydrocortisone, the patient experienced a recurrence of hyponatraemia and excessive natriuresis, forcing re-initiation of cortisone treatment 10 days after withdrawal which was maintained for 3 weeks in a downward trend.

Outcome and follow-up

The patient was in the ICU for an extended period due to severe neurological damage from prolonged mechanical ventilation. He achieved progressive neurological recovery, and was discharged from the ICU with a score of 3 for functional recovery in the Glasgow Outcome Scale (conscious but disabled).


It is important to distinguish between SIADH and CSW in neurological patients (head injury,9 infectious,10 spontaneous cerebral haemorrhage,11 etc). Both are characterised by a decreased sodium serum concentration and increased urine sodium concentration. However, they differ with respect to volaemic states since SIADH is associated with normovolaemia or hypervolaemia, whereas CSW is associated with fluid depletion.12,13 The management of CSW begins with treatment of the underlying neurological process. CSW is characterised by the requirement of salt replacement in order to compensate for renal salt wasting using either isotonic or hypertonic saline serum.6 Replacement should be done slowly in order to avoid complications such as pontine myelinolysis.4,14

The mechanisms by which intracranial disease leads to renal salt wasting remain unclear, though some hypotheses involve the release of natriuretic factors (atrial natriuretic peptide, brain natriuretic peptide, C-type natriuretic peptide, and oubain-like peptide) together with decreases of sympathetic input to the kidney. These factors increase urinary sodium excretion and diminish effective arterial blood volume.15,16

Fludrocortisone has been reported to be effective in isolated case reports and in paediatric patients in doses of 0.05–0.1 mg twice daily. It acts directly on the renal tubule to enhance sodium reabsorption.1721 Fludrocortisone is the best treatment for CSW but it has to be delivered orally. Hydrocortisone, although less effective, also has mineralocorticoid activity and can be delivered by the parenteral route. In a low digestive tolerance scenario, as in the case reported here, hydrocortisone is an effective alternative to fludrocortisone.22,23

Learning points

  • Disorders of sodium and water balance are common in critically ill adult neurologic patients.

  • Decreased extracellular volume with negative salt and water balance are the key diagnostic factors of cerebral salt wasting syndrome (CSW).

  • Mineralocorticoids, in addition to salt replacement, are a useful treatment in CSW.

  • Mineralocorticoids are a useful treatment both in children and in adults with this syndrome.


  • Competing interests: none.

  • Patient consent: Patient/guardian consent was obtained for publication


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