Demyelinative diseases after liver transplantation:the etiology

Luo, Yiqian; Guo, Weijian; Fu, Zhi-ren

doi:10.3724/sp.j.1008.2010.00104

Cited by 1 publication

(1 citation statement)

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“…Besides, as a result of the donor liver's normal ability to degrade antidiuretic hormone and aldosterone, a lot of water and relatively small amount of sodium excreted and as a result the concentration of serum sodium increased further. The great fluctuation of serum sodium levels in a short time can cause excessive fluctuations of plasma osmolality, endothelial injury, intercellular tight junctions open up, cross-vascular transshipment increases and large amounts of myelin toxic substances release, all contributing to the occurrence risk of CPM [20]. Abbasoglu et al [21] regarded preoperative hepatic encephalopathy as another risk factor of CPM, and other scholars believed that the lack of brain inositol in patients with chronic liver disease may increase their sensitivity of serum sodium levels fluctuations [22].…”

Section: Rapid Correction Of Hyponatremia and Preoperative Hepatic Enmentioning

confidence: 99%

Clinical Analysis of Central Pontine Myelinolysis after Liver Transplantation

Wang¹,

Zhang²,

Qu³

et al. 2014

OALib

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Objective: To discuss the etiology, diagnosis and treatment of central pontine myelinolysis (CPM) by analyzing 4 cases of our center and 26 cases reported by others in our country. Methods: We analyzed the clinical feature, diagnosis and treatment of 4 CPM cases and then compared them with 26 CPM cases reported between 2000 and 2010. Results: The average age of our 4 cases (3 men and 1 woman) was 47.5 years old. All cases were diagnosed by MRI scan. The patients all had been diagnosed as liver cirrhosis and most of the CPM related symptoms were observed within 2 weeks after surgery, including neural and psychic symptoms and physical impairment. Rapid correction of hyponatremia during perioperative period and high blood concentration of FK506 may be the main causes. All cases received etiological and symptomatic combination treatment and were continued with neural function training after hospital discharge. A long-term follow-up (29.5 ± 15.0 months) showed an improvement of neural function to different degrees. Conclusion: CPM after liver transplantation is a severe complication, of which the etiology and pathogenesis were not clear. MRI scan is the main method for confirmative diagnosis. Etiological prevention and timely treatment may improve the prognosis.

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Section: Rapid Correction Of Hyponatremia and Preoperative Hepatic Enmentioning

confidence: 99%