Cerebral salt wasting syndrome in patients with aneurysmal subarachnoid hemorrhage

Revilla-Pacheco, Francisco; Herrada-Pineda, Tenoch; Loyo-Varela, Mauro; Modiano-Esquenazi, Marcos

doi:10.1179/016164105x17152

Cited by 20 publications

(16 citation statements)

References 27 publications

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“…Treatment with intravenous sodium chloride solution is the specific therapy for cerebral salt wasting [96]. It is often necessary to give large volumes to keep up with urinary losses.…”

Section: Management Of Hyponatremia In the Neurosurgical Patientmentioning

confidence: 99%

Neurosurgical Hyponatremia

Hannon

Thompson

2014

JCM

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Hyponatremia is a frequent electrolyte imbalance in hospital inpatients. Acute onset hyponatremia is particularly common in patients who have undergone any type of brain insult, including traumatic brain injury, subarachnoid hemorrhage and brain tumors, and is a frequent complication of intracranial procedures. Acute hyponatremia is more clinically dangerous than chronic hyponatremia, as it creates an osmotic gradient between the brain and the plasma, which promotes the movement of water from the plasma into brain cells, causing cerebral edema and neurological compromise. Unless acute hyponatremia is corrected promptly and effectively, cerebral edema may manifest through impaired consciousness level, seizures, elevated intracranial pressure, and, potentially, death due to cerebral herniation. The pathophysiology of hyponatremia in neurotrauma is multifactorial, but most cases appear to be due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Classical treatment of SIADH with fluid restriction is frequently ineffective, and in some circumstances, such as following subarachnoid hemorrhage, contraindicated. However, the recently developed vasopressin receptor antagonist class of drugs provides a very useful tool in the management of neurosurgical SIADH. In this review, we summarize the existing literature on the clinical features, causes, and management of hyponatremia in the neurosurgical patient.

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“…Treatment with intravenous sodium chloride solution is the specific therapy for cerebral salt wasting [96]. It is often necessary to give large volumes to keep up with urinary losses.…”

Section: Management Of Hyponatremia In the Neurosurgical Patientmentioning

confidence: 99%

Neurosurgical Hyponatremia

Hannon

Thompson

2014

JCM

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“…A rare differential diagnosis not mentioned in Figure 1 is cerebral salt wasting (CSW), a condition sometimes seen on neurosurgical wards [Brookes and Gould, 2003;Revilla-Pacheco et al 2005;Tageja et al 2009]. Its laboratory constellation resembles SIADH closely, although the spot urinary sodium concentration is usually much greater than 30-40 mmol/liter, sometimes exceeding 150 mmol/liter.…”

Section: Differential Diagnosis Of Siadhmentioning

confidence: 99%

Clinical management of SIADH

Groß¹

2012

Therapeutic Advances in Endocrinology

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Hyponatremia is the most frequent electrolyte disorder and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) accounts for approximately one-third of all cases. In the diagnosis of SIADH it is important to ascertain the euvolemic state of extracellular fluid volume, both clinically and by laboratory measurements. SIADH should be treated to cure symptoms. While this is undisputed in the presence of grave or advanced symptoms, the clinical role and the indications for treatment in the presence of mild to moderate symptoms are currently unclear. Therapeutic modalities include nonspecific measures and means (fluid restriction, hypertonic saline, urea, demeclocycline), with fluid restriction and hypertonic saline commonly used. Recently vasopressin receptor antagonists, called vaptans, have been introduced as specific and direct therapy of SIADH. Although clinical experience with vaptans is limited at this time, they appear advantageous to patients because there is no need for fluid restriction and the correction of hyponatremia can be achieved comfortably and within a short time. Vaptans also appear to be beneficial for physicians and staff because of their efficiency and reliability. The side effects are thirst, polydipsia and frequency of urination. In any therapy of chronic SIADH it is important to limit the daily increase of serum sodium to less than 8-10 mmol/liter because higher correction rates have been associated with osmotic demyelination. In the case of vaptan treatment, the first 24 h are critical for prevention of an overly rapid correction of hyponatremia and the serum sodium should be measured after 0, 6, 24 and 48 h of treatment. Discontinuation of any vaptan therapy for longer than 5 or 6 days should be monitored to prevent hyponatremic relapse. It may be necessary to taper the vaptan dose or restrict fluid intake or both.

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“…La EPS se ha descrito en pacientes con meningitis, traumatismos craneanos, tumores cerebrales, hemorragia sub-aracnoídea, encefalitis, tubercu- losis meníngea, poliomielitis bulbar, adenomas hipofisiarios, hemorragias cerebrales, carcinomatosis meníngea y cirugía intracraneana 1,12,15,16,17,18,19 . También se ha comunicado en patologías extracraneanas como infecciones por HIV, enfermedad de Hodgkin, fractura de cadera y carcinomas metastásicos, razón por lo cual se ha sugerido cambiar el nombre de "cerebral salt wasting syndrome" por "renal salt wasting syndrome" 14,20 .…”

Section: Discussionunclassified