Cerebral Salt Wasting Syndrome


Article Author:
Steven Tenny


Article Editor:
William Thorell


Editors In Chief:
David Wood
Andrew Wilt
Hajira Basit


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
9/13/2019 2:25:16 PM

Introduction

Cerebral salt wasting (CSW) is a potential cause of hyponatremia in the setting of disease of the central nervous system (CNS). Cerebral salt wasting is characterized by hyponatremia with elevated urine sodium and hypovolemia. In the current literature, professionals debate if cerebral salt wasting is a distinct condition or a special form of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). It is important to distinguish between cerebral salt wasting and SIADH as the 2 are treated with opposite treatment strategies. For cerebral salt wasting the patient is given fluids and sodium supplementation. For SIADH the patient is fluid restricted. Cerebral salt wasting tends to resolve within weeks to months after onset but can remain a chronic issue. Leading theories for the pathophysiology of cerebral salt wasting include the release of brain natriuretic peptide (BNP) or damage to the hypothalamus with subsequent disorder sympathetic system.[1]

Etiology

The etiology of cerebral salt wasting (CSW) is not completely understood. Cerebral salt wasting is most commonly seen after a central nervous system insult. The most commonly described precipitating insult is aneurysmal subarachnoid hemorrhage. Why cerebral salt wasting occurs more frequently after aneurysmal subarachnoid hemorrhage versus traumatic subarachnoid hemorrhage or other CNS insult is not well defined. Why cerebral salt wasting is uncommon after other injuries or diseases is also not well defined.

Epidemiology

Since cerebral salt wasting (CSW) is still a debated condition, its exact incidence and prevalence may be hard to pin down. Cerebral salt wasting is most commonly seen after aneurysmal subarachnoid hemorrhage but can be seen after other insults to the central nervous system. Other conditions in which cerebral salt wasting has been reported include: after surgery for a pituitary tumor or acoustic neuroma or calvarial remodeling, glioma, infections including tuberculous meningitis and viral meningitis, metastatic carcinoma, and cranial trauma.

Some have calculated that cerebral salt wasting accounts for up to one-quarter of severe hyponatremia after aneurysmal subarachnoid hemorrhage. The incidence of cerebral salt wasting for other CNS insults is mostly reported as case reports. The incidence and prevalence of cerebral salt wasting outside of patients with CNS insult is not reliably reported.

Pathophysiology

The true etiology of cerebral salt wasting (CSW) remains an area of debate and research. As noted, some argue cerebral salt wasting does not exist and is a form of SIADH.

There are two current theories for the etiology of cerebral salt wasting: effect of a circulating factor or sympathetic nervous system dysfunction.

Some research points to the brain releasing brain natriuretic peptide (BNP) after injury, which then enters systemic circulation through a disrupted blood-brain barrier. The BNP acts on the collecting ducts of the renal tubules to inhibit sodium reabsorption as well as decrease the release of renin.

The second theory suggests that an injured sympathetic nervous system can no longer promote sodium reabsorption and stimulate renin release due to injury to the hypothalamus. The exact mechanism of cerebral salt wasting remains open to debate.

History and Physical

The most common presenting story for cerebral salt wasting is hyponatremia after aneurysmal subarachnoid hemorrhage.[2] A few days after the hemorrhage the patient’s serum sodium begins to drop while the urine sodium increases. The patient’s fluid status also decreases, and the patient becomes hyponatremia and hypovolemic.  With treatment, the cerebral salt wasting resolves within a few weeks to months, and long-term treatment is not commonly required.

Cerebral salt wasting has also been reported after surgery of the central nervous system including pituitary surgery, vestibular schwannoma resection, and calvarial remodeling. Additionally, cerebral salt wasting has been seen after a head injury, intracranial malignancy, and central nervous system (CNS) infections.

Evaluation

It is critically important to distinguish cerebral salt wasting (CSW) from the syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) as the treatments are opposite. Evaluation for cerebral salt wasting begins with a basic metabolic panel (BMP) to identify the hyponatremia (serum sodium less than 135 meq/L). Urine studies are commonly checked for urine sodium and osmolality. Urine sodium is typically elevated above 40 meq/L. Urine osmolality is elevated above 100 mosmol/kg. The patient must also have signs or symptoms of hypovolemia such as hypotension, decreased central venous pressure, lack of skin turgor, or elevated hematocrit.

Syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) will have a similar laboratory picture as cerebral salt wasting with hyponatremia and increased urine sodium. However, with SIADH, the patient is euvolemic to hypervolemic from the retained free water as compared to the hypovolemic picture of cerebral salt wasting.[3][4]

Other potential causes of hyponatremia should also be sought including polydipsia, renal disease, use of diuretics, heart failure, hypothyroidism, heart failure, malignancies, hormone deficiency, and pseudohyponatremia. Many times cerebral salt wasting becomes a diagnosis of exclusion after labs reveal serum hyponatremia with increased urine sodium level.

Treatment / Management

The treatment of cerebral salt wasting (CSW) and syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) are very different, so it is critical to have the correct diagnosis prior to initiating treatment.

As cerebral salt wasting typically occurs after aneurysmal subarachnoid hemorrhage, the first treatment strategies are targeted at treating the underlying subarachnoid hemorrhage and aneurysm or another CNS insult. Secondly, the patient must be volume repleted while treating the hyponatremia. Typically, the patient is started on isotonic saline for mild to moderate cases of hyponatremia of cerebral salt wasting. The isotonic fluid provides the fluid for the hypovolemic patient as well as helps to restore the body sodium stores. For moderate to severe cases of hyponatremia, more aggressive sodium replenishment may be required with either hypertonic saline such as 3% hypertonic saline and/or salt tabs (1 to 2 grams up to three times daily) as well as limiting free water intake. Some have advocated for the use of fludrocortisone as well for treatment of cerebral salt wasting.[4]

When correcting the hyponatremia, the serum sodium should be monitored frequently. Overcorrection of the serum sodium can lead to hypernatremia which can cause muscle twitching, lethargy, seizure, and death. Additionally, the hyponatremia should not be corrected too quickly. There is the risk of central pontine myelinolysis if the hyponatremia is corrected too quickly, especially for long standing hyponatremia. Most experts recommend correcting no more than 10 meq/L/24 hours or 1 meq/L every 2 hours. 

The most important issue is to distinguish between cerebral salt wasting and syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) as they are treated with opposite approaches.  In cases of SIADH, the treatment is typically fluid restriction, hypertonic saline, demeclocycline and/or furosemide.  If the patient truly has cerebral salt wasting, they are hypovolemic, and the SIADH treatment modalities would be detrimental by exacerbating the hypovolemia.[5][6][7]

Differential Diagnosis

It is critical to distinguish between cerebral salt wasting and syndrome of inappropriate secretion of antidiuretic of hormone (SIADH). Both conditions are characterized by hyponatremia with elevated urine sodium, concentrated urine, and no edema. The key distinguishing factor is that in cerebral salt wasting the patient is hypovolemic versus in SIADH the patient is euvolemic to hypervolemic.[3] The differential of the etiology of CSW is:

  • Head injury
  • Brain tumor
  • Stroke
  • Intracranial surgery
  • Intracerebral hemorrhage
  • Craniosynostosis repair
  • Tuberculous meningitis

Enhancing Healthcare Team Outcomes

Cerebral salt wasting often occurs after significant CNS pathology such as aneurysmal subarachnoid hemorrhage. Care for such patients must be coordinated between multiple specialties as the treatment of cerebral salt wasting may include additional fluid volume which can exacerbate issues including cerebral edema, pulmonary edema, heart failure, and renal dysfunction. Additional attention should be paid to the carrier fluids for the other medications and to avoid too much free water to the patient. Patients can require continued management of their hyponatremia for weeks to months or more after the original insult. During treatment, the patient's GCS and neurological exam must be continually assessed. The outcomes for most patients with cerebral salt wasting not due to a subarachnoid hemorrhage are good. However, some patients may continue to have mild neurological deficits despite optimal treatment.[8][9]

Outcomes can be improved with the participation of an interprofessional team. Primary care providers, emergency department physicians, neurologists, neurosurgeons, specialty care nurses, and pharmacists can all be involved. Critical care and neuroscience nurses care out treatments, monitor patients, provide education to patients and their families, and provide updates on the patient's condition to the team. Pharmacists review medications prescribed and drug-drug interactions. [Level 5]


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Cerebral Salt Wasting Syndrome - Questions

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A 56-year-old female is in the hospital 3 days after an aneurysmal subarachnoid hemorrhage. She has hyponatremia with decreased skin turgor and elevated hematocrit. Her urine sodium is elevated. Her vital signs are unremarkable and chloride is within the reference range. What is the most likely diagnosis?



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What differentiates cerebral salt wasting syndrome from syndrome of inappropriate secretion of antidiuretic of hormone (SIADH)?



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Which of the following is not an appropriate treatment for cerebral salt wasting syndrome?



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Which of the following is a theorized pathophysiology for cerebral salt wasting syndrome?



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Which of the following is found in patients with cerebral salt wasting syndrome?



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A 65-year-old female becomes suddenly unresponsive and is taken to the emergency room where workup reveals subarachnoid hemorrhage. A posterior communicating artery aneurysm is identified and treated. One day after presentation, she is alert and interactive but having severe headaches. Five days after admission, she is witnessed to have a seizure. Her workup identifies serum sodium of 122 meq/L, urine sodium of 55 meq/L, urine osmolality of 111 mosmol/kg, and hypovolemia. What is the most appropriate treatment?



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A 16-year-old female suffers significant head injury after falling off a trampoline. Her past medical history is significant for diabetes mellitus type I and asthma. She initially has post-concussive symptoms in the hospital. After three days into her hospital stay, she starts feeling very lethargic and begins to look dehydrated. On examination, her blood pressure is 110/60 mmHg, the pulse is 89/min regular, and she has signs of dehydration. Her labs suggest serum sodium of 127 mEq/L and urinary sodium of 54 mEq/L. What should be the treatment plan for her underlying disorder?



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A 64-year-old male has rupture of his anterior communicating artery aneurysm and is admitted to the hospital. His aneurysm is treated, and he is initially doing well. Still, four days into his hospital course, he is found to be hyponatremic, and a workup suggests cerebral salt wasting as the etiology of his hyponatremia. What is the best initial therapy for this patient?



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Cerebral Salt Wasting Syndrome - References

References

Leonard J,Garrett RE,Salottolo K,Slone DS,Mains CW,Carrick MM,Bar-Or D, Cerebral salt wasting after traumatic brain injury: a review of the literature. Scandinavian journal of trauma, resuscitation and emergency medicine. 2015 Nov 11     [PubMed]
Oh JY,Shin JI, Syndrome of inappropriate antidiuretic hormone secretion and cerebral/renal salt wasting syndrome: similarities and differences. Frontiers in pediatrics. 2014     [PubMed]
Yee AH,Burns JD,Wijdicks EF, Cerebral salt wasting: pathophysiology, diagnosis, and treatment. Neurosurgery clinics of North America. 2010 Apr     [PubMed]
Cerdà-Esteve M,Cuadrado-Godia E,Chillaron JJ,Pont-Sunyer C,Cucurella G,Fernández M,Goday A,Cano-Pérez JF,Rodríguez-Campello A,Roquer J, Cerebral salt wasting syndrome: review. European journal of internal medicine. 2008 Jun     [PubMed]
Jin S,Long Z,Wang W,Jiang B, Hyponatremia in neuromyelitis optica spectrum disorders: Literature review. Acta neurologica Scandinavica. 2018 Jul     [PubMed]
Moritz ML, Syndrome of Inappropriate Antidiuresis. Pediatric clinics of North America. 2019 Feb     [PubMed]
Maesaka JK,Imbriano LJ,Miyawaki N, High Prevalence of Renal Salt Wasting Without Cerebral Disease as Cause of Hyponatremia in General Medical Wards. The American journal of the medical sciences. 2018 Jul     [PubMed]
John CA,Day MW, Central neurogenic diabetes insipidus, syndrome of inappropriate secretion of antidiuretic hormone, and cerebral salt-wasting syndrome in traumatic brain injury. Critical care nurse. 2012 Apr     [PubMed]
Rahman M,Friedman WA, Hyponatremia in neurosurgical patients: clinical guidelines development. Neurosurgery. 2009 Nov     [PubMed]

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