Hyponatremia is corrected after the disease is aggravated? The culprit is...

Case 1, 48 years old, rectal cancer surgery and post-radiation chronic diarrhea, diagnosis of Wernicke encephalopathy(A, B) axis T2WI indicates the high signal of the inner two-sided thalamus around the brain-guided pipepatients develop edgy hyponatremia for 3 weeks and quickly correct it after a full recovery from Wernicke's encephalopathy(C) Axis T2WI indicates a high signal of symmetry in the brain bridge, which surrounds the normal brain bridge tissue and retains the cortical spinal cord beam(D, E) DWI indicates the same area dispersion restriction and ADC reduction(F, H) right-hand hippocampus T2Flair high signal, mild dispersion restrictionCase 2patient woman, 22 years old, was found in a friend's home with consciousness disorder, irritation unresponsive, admitted to the hospital with a full-scale straight-syllm attackBlood biochemical sage tip severe hyponatremia (113 mmol/L), rapid sodium correction 6 hours after the blood sodium rose to 136 mmol/LAfter 5 days, the patient can open his eyes spontaneously, but he or she cannot perform the action as directed2 weeks after the cranial brain MRI showed a two-sided base section, the hypothalamus and the central symmetry of the brain bridge T2Flair high signal (A, B)DWI shows limited circular dispersion around the central lesions of the brain bridge, and the ADC high signal area has no signal reduction (C, D)The shaft level T2Flair shows a two-sided symmetry of the central front trench and the gray high signal (E) near the central trenchCase 3patient male, 41 years old, due to quadriplegic tremor, strong straight hospital, a few days later progresstotind silence Patients have acute gastroenteritis, blood sodium 117 mmol/L, after 24 hours blood sodium rose to 128 mmol/L admitted to the 7th day of the cranial brain MRI axis T2WI brain bridge Trident-like high signal (A), while the called high-signal lesions also tired of the double-sided shell nucleus, tail nucleus and thalamus (B) After 6 months of review of the brain MRI showed persistent trigeminal lesions, while the base and thalamus lesions subsided (C, D) These patients were clinically diagnosed as osmotic demyelinization syndrome (osmotic demyelinization syndrome, ODS) ODS is a rare acquired non-inflammatory central nervous system demyelinating disease According to the demyelination site is divided into the central myelin soy (central pontine myelinolysis, CPM) and the outer myelin solubility (extrapontine myelinolysis, EPM) Adams first proposed CPM in 1959 HistopathologicalODS is a non-inflammatory demyelinator, while neurons and associated axons remain relatively reserved, with fewer protrusions of glial cells and macrophages leaching The brain bridge is largely sliced to show a two-sided symmetrical brown lesions (arrows), indicating that the central myelin of the bridge dissolves Sumuin-Ired staining shows the central myelin of the bridge brain dissolved, showing a large number of foam tissue cells (arrows) and neurons (arrows), but without associated inflammation Luxol? Fast? Blue staining shows significant demyelination boundaries: the purple area on the left is demyelinated tissue, and the blue area on the right is the normal brain bridge tissue the of the 's causeof Table 1 The etiology of ODS hyponatremia and the pathophysiological mechanism of correcting hyponatremia
the most common cause of ODS is hyponatremia, but OSD occurs in every patient with hyponatremia The risk factors are persistent hyponatremia (e.g duration of 48 hours, blood sodium reduction rate of 0.5 mmol/h) and hyponatremia correction a Initial state b Edema occurs in cells during acute hyponatremia c The compensation mechanism after the extension of hyponatremia is the transfer of inorganic ions such as potassium and chlorine from the cell to the extracellular gap, while organic osmosis such as alanine, glutamate, taurine, glycine and inositol are released from within the cell to the outside of the cell Then the cell volume returns to normal, and the penetration gradient inside and outside the cell is balanced d Chronic hyponatremia e Chronic hyponatremia cells are in a relatively high permeable environment and the permeation gradient cannot be recovered quickly, while the loss of organic osmosis is much greater than re-inggability Wrinkles occur due to osmosis pressure cells and trigger apoptosis clinical performance
The clinical performance of ODS imaging performance more than half of OSD patients had only CPM, 12.8% of patients had EPM, and CPM and EPM co-exists 31.1% DWI dispersion restriction and enhanced post-scan enhancement were 45.5% and 20.6%, respectively (1) CPM patients with MRI characteristics are bridge brain base minister T1, long T2 signal, T2Flair high signal The lesions show the "bat wing" sign, the "trident" sign or the "pig nose" sign bat wing the trigeminal ization the pig nose (2) EPM patients with MRI lesions can be symmetrical to the tail nucleus, shell nucleus, thalamus, mido-brain, cortex gray matter, seahorse, cerebellum, ementomyandum and hypothalamus The incidence of the base and thalamus is highest diagnosis and differential diagnosis there is no clear diagnostic criteria for OSD, clinical diagnosis is mainly based on the presence of possible triggers, etiology, clinical manifestations and characteristic imaging signs CPM needs to be identified with brain bridge tumors, infarction, encephalitis, etc When the patient only manifests as EPM, there are certain difficulties in diagnosis, which need to be identified with Wernicke encephalopathy, hepatic encephalopathy, NMOSD, MOG-related encephalomyelitis, etc prognosis and prevention recent studies have shown that about 33%-50% of OSD patients have a good prognosis, and another 16%-34% of patients can live independently However, 33 to 55 per cent of patients still need care and serious deaths The predictors of poor prognosis were severe hyponatremia (114mmol/L), hyponatremia with hypokalemia and decreased alertness A good prognosis for patients needs to be detected early through MRI tests for OSD, improved intensive care technology, and early rehabilitation nonspecific treatment of OSD, mainly to support the treatment of the disease, active treatment of the original disease is the key Patients with chronic hyponatremia must be careful enough to correct hyponatremia, and should be slow to replenish sodium at a rate not exceeding 0.5 mmol/L/h, and not more than 12 mmol/L per day Author: Shen Yaoyao Source: , Medical Neurology Channel, : jyzxjiangqin on 2020-4-19 comment: treatment of patients with hyponatremia from the MedSci Medical App