The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage

Sherlock, Mark; O’Sullivan, Eoin; Agha, Amar; Behan, Lucy Ann; Rawluk, D; Brennan, Paul M.; Tormey, William; Thompson, Christopher J.

doi:10.1111/j.1365-2265.2006.02432.x

Cited by 253 publications

(186 citation statements)

References 31 publications

Supporting

Mentioning

164

Contrasting

Unclassified

Order By: Relevance

“…This is usually attributed to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion [77,78]. SIADH results in impaired systemic water excretion.…”

Section: Vasopressin Receptor Antagonistmentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

View full text Add to dashboard Cite

Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NC Ca-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A-and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.Keywords Cerebral edema . Hyponatraemia . Osmotherapy . NKCC1 . SUR1/TRPM4 . Vaptan . Glyburide Overview of Perturbations in Brain Fluid HomeostasisCerebral edema in the neurointensive care setting can occur with a heterogenous group of neurological diseases, which typically fall under the categories of metabolic [1, 2], infectious [3], neoplastic [4], cerebrovascular [5][6][7], and traumatic [8,9] brain injury. Irrespective of the inciting process, cerebral edema results in the pathological accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between 4 distinct fluid compartments within the cranium; fluid is present within: 1) the blood in the cerebral blood vessels, 2) the cerebrospinal fluid in the ventricular system and subarachnoid space, 3) the interstitial fluid of the brain parenchyma, and 4) the intracellular fluid of the neurons and glia. These fluid compartments are not isolated, and specific movements of solutes and water from one compartment to another occur under normal conditions. When dysregulation of this normally tightly controlled fluid balance...

show abstract

“…This is usually attributed to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion [77,78]. SIADH results in impaired systemic water excretion.…”

Section: Vasopressin Receptor Antagonistmentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

View full text Add to dashboard Cite

show abstract

“…According to some data available, the incidence of CSWS can equal or even exceed that of SIADH in patients undergoing neurosurgery (11)(12)(13). However, in a recently published article on patients with subarachnoid haemorrhage (SAH), SIADH was the commonest cause of hyponatraemia after SAH (14).…”

Section: Cswsmentioning

confidence: 99%

“…It is important to take into account that in some cases hyponatraemia may be supported by a mixed condition of SIADH and CSWS (14).…”

Section: Differential Diagnosis Of Siadh and Cswsmentioning

confidence: 99%

Early hyponatraemia after pituitary surgery: cerebral salt-wasting syndrome

Guerrero¹,

Pumar²,

Soto³

et al. 2007

eur j endocrinol

View full text Add to dashboard Cite

Hyponatraemia is a common complication in patients undergoing neurosurgery. It can be caused either by the syndrome of inappropriate secretion of antidiuretic hormone or by the cerebral saltwasting syndrome (CSWS). CSWS frequently occurs in patients suffering from subarachnoid haemorrhage and brain injury, but it is rare after pituitary tumour surgery. However, this diagnostic possibility should be considered as these disorders require specific treatment and have different prognoses.In this article, we present a case of acute and early hyponatraemia caused by CSWS after pituitary tumour surgery. We also revise the aetiology, mechanisms, differential diagnosis and treatment of hyponatraemia after pituitary surgery. European Journal of Endocrinology 156 611-616 Case reportA 35-year-old woman presented with headaches and decreased visual acuity, which she had been experiencing for several months. She did not have any clinical manifestations of endocrine dysfunction and her baseline hormonal parameters were normal. The campimetry revealed minimum central vision in the superior nasal quadrant of the right eye and temporary hemianopsia in the left eye.Nuclear magnetic resonance revealed a tumour of 4 cm in the pituitary with a central cyst which compressed the optic chiasm and invaded the cavernous sinuses. The patient underwent transsphenoidal surgery and the tumour was partially resected. No postoperative complications occurred and postoperative hormonal parameters were normal (i.e. thyroid hormones, 24-h urinary free cortisol and basal plasma cortisol, gonadotrophins, oestradiol, prolactin, growth hormone (GH) and insulin-like growth factor I). The anatomopathological examination confirmed pituitary adenoma with focal follicle-stimulating hormone positivity.Ten months later, the patient underwent a new intervention due to the significant growth of tumoural rests. Hypotonic solution (i.e. infusate of 0.2% sodium chloride in 5% dextrose in water (1500 ml/day)) was administered in the first 48 h after surgery. Early baseline hormonal assessment did not show any deficit. The only postoperative complication was acute hyponatraemia with excessive natriuresis. At 48 h postsurgery, asymptomatic hyponatraemia (126 mEq/l, the normal range being 135-145 mEq/l) with serum osmolality of 264 mOsm/kg (normal range 275-300 mOsm/kg) and elevated natriuresis (urine sodium 215 mEq/l, diuresis 3250 ml/24 h and urinary osmolality 706 mOsm/kg) were detected. Twenty-four hours later, the patient presented with nausea and vomiting; natraemia had decreased to 116 mEq/l, and natriuresis levels remained elevated (118 mEq/l, diuresis 2100 ml/24 h). The examination showed dry mucous membranes and slightly decreased skin turgidity; arterial systolic pressure was between 110 and 100 and diastolic pressure between 60 and 70 mmHg. No other symptoms of volume depletion were found. The patient was administered 3% hypertonic saline solution (31 ml/h for 2 days and then 15 ml/h). Natraemia levels rose to 124 mEq/l in 24 h; at this point, the s...

show abstract

“…This syndrome was first described by Bartter & Schwartz (9), who described the characteristic pattern of abnormalities including hyponatraemia, clinical euvolaemia, evidence of inappropriate concentration of urine and natriuresis. It commonly causes hyponatraemia in general medical inpatients (10,11), and is the commonest cause of hyponatraemia in neurosurgical patients (3,12). There are a number of clinical algorithms available to aid the clinician to distinguish SIADH from other forms of hyponatraemia, and the accurate identification of the cause of hyponatraemia is the key to successful treatment.…”

Section: Epidemiology Of Hyponatraemiamentioning

confidence: 99%

Hyponatraemia: new associations and new treatments

Thompson

2010

European Journal of Endocrinology

View full text Add to dashboard Cite

The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage

Cited by 253 publications

References 31 publications

Novel Treatment Targets for Cerebral Edema

Novel Treatment Targets for Cerebral Edema

Early hyponatraemia after pituitary surgery: cerebral salt-wasting syndrome

Hyponatraemia: new associations and new treatments

Contact Info

Product

Resources

About