Lenox Hill Hospital CAUTI Team.
Lenox Hill Hospital CAUTI Team.
In cerebral salt-wasting (CSW), natriuretic factor is produced in response to a central insult. Natriuretic factor decreases sodium transport in proximal renal tubule which leads to urinary loss of sodium (and water) and depletion of extracellular volume. Hypovolemia then triggers secretion of ADH, renin and aldosterone, which provides a negative feedback to decrease secretion of natriuretic factor.
Differentiating CSW from syndrome of inappropriate antidiuretic hormone (SIADH) is problematic, laboratory work-up (urine and plasma sodium levels and urine and plasma osmolarity) is similar in both conditions. CSW patients are usually volume depleted while SIADH patients are euvolemic. The traditional approach of examining patient clinically to to determine volume status is inaccurate.
An interesting paper published in 2014 suggested a new algorithm to differentiate SIADH from CSW based on the effect of sodium correction on the fractional excretion of urate (FEUa). FEurate is calculate using the folllowing formula:
Normal FEUa = 4-11%, SIADH & CSW FEUa = >11%. FEUa determines the percent excertion of the filtered load of urate at the glomerulus.
In SIADH, FEUa normalizes after correction of hyponatremia (see graph below):
whereas in CSW, FEUa remains elevated >11% after correction of hyponatremia. The reason is probably because natriuretic factor also decreases urate transport in the proximal tubule.
Based on this finding, the paper suggests a new algorithm for determining the etiology of hyponatremia that omits reliance of UNa (and also plasma renin, aldosterone, atrial or brain antriuretic peptide, BUN/creatinine ratio).
Based on this algorithm, a patient with hyponatremia should undergo correction of sodium by any means (water restriction or isotonic / hypertonic saline). Observing whether FEUa normalizes or remains increased would differentiate SIADH from CSW syndrome.
Maesaka, J., Imbriano, L., Mattana, J., Gallagher, D., Bade, N. and Sharif, S. (2014). Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia. Journal of Clinical Medicine, 3(4), pp.1373-1385.
Single Brain Metastases:
Multiple Brain Metastases:
SRS vs surgery:
Hatiboglu, M., Akdur, K. and Sawaya, R. (2018). Neurosurgical management of patients with brain metastasis. Neurosurgical Review.
An algorithm for the diagnosis and management of CVT:
CTV, CT venography; CVT, cerebral venous thrombosis; ICH, intracerebral
hemorrhage; LMWH, low molecular weight heparin; MRV, magnetic resonance venography; PRES, posterior reversible encephalopathy syndrome; UHF,
Table 1 Major risk factors and conditions associated with CVT
Table 3 Clinical presentations of CVT:
Society of Neurointerventional Surgery (SNIS) Recommendations:
► A combination of MRI/MRV or CT/CTV studies should be performed in patients with suspected CVT (class I; level of evidence C).
► DSA as a diagnostic modality is indicated in cases of suspected CVT when the diagnosis of CVT cannot be reliabl established with non-invasive imaging alone (class IIa; level of evidence C).
Medical and surgical treatment
► Anticoagulation with unfractionated heparin or low molecular weight heparin is reasonable in patients with CVT (class IIa; level of evidence C).
► Decompressive craniectomy may be considered in patients with large parenchymal lesions causing herniation or intractable intracranial hypertension (class IIb; level of evidence C).
► Endovascular therapy may be considered in patients with clinical deterioration despite anticoagulation, or with severe neurological deficits or coma (class IIb; level of evidence C). The duration of anticoagulation therapy before declaring it to be a ‘failure’ and proceeding with endovascular therapy is unknown.
► There is insufficient evidence to determine which endovascular approach and device provides the optimal restoration of venous outflow in CVT. In many cases, a variety of treatment approaches is required to establish sinus patency.
Radiologic Findings in CVT:
Lee, S., Mokin, M., Hetts, S., Fifi, J., Bousser, M. and Fraser, J. (2018). Current endovascular strategies for cerebral venous thrombosis: report of the SNIS Standards and Guidelines Committee. Journal of NeuroInterventional Surgery, 10(8), pp.803-810.
NASCET (North American Symptomatic CEA Trial) – CEA vs medical reduced risk of stroke (17%) and death (7%) at 2 years for stenosis >70%.
ACAS (Asymptomatic Carotid Artery Stenosis Trial) – CEA vs medical reduced risk of stroke or death (6%) at 5 years for stenosis >60%.
CREST (Carotid Revascularization Endarterectomy vs Stenting Trial) – CEA vs CAS in both symptomatic and asymptomatic – comparable rates of primary outcome measures (death, stroke, MI, stroke at 4 years). Periop stroke more in stenting, periop MI more in CEA. **NB Periopr stroke more disabling (based on 1 year in QOL assessment).
Experiences with carotid endarterectomy at Sree Chitra Tirunal Institute. Unnikrishnan M, Siddappa S, Anto R, Babu V, Paul B, Kapilamoorthy TR, Sivasankaran S, Sandhyamani S, Sreedhar R, Radhakrishnan K – Ann Indian Acad Neurol (2008)
Lee, Kiwon. The Neuroicu Book. 1st ed. Print.
“Initial Treatment Of Malignant Glioma In Older Adults”. Uptodate.com. 2017. Accessed 8 Mar. 2017.
Management of DCI is presented here as a three-stage algorithm. Tier One therapy should be initiated for new DCI which can manifest as neurological deterioration, characteristic imaging findings or MMM abnormalities indicating ischemia. Tier Two therapy hsould be started in cases of refractory DCI(inadequate reversal of ischemia after first-line therapy.)
Francoeur, Charles L. and Stephan A. Mayer. “Management Of Delayed Cerebral Ischemia After Subarachnoid Hemorrhage”. Critical Care 20.1 (2016).