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Journal articles on the topic 'Encephalopaty'

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Published: 9 March 2023

Last updated: 10 March 2023

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1

Tonello, S., S. Montagnese, S. Schiff, P. Amodio, P. Bizzotto, P. Pesce, A. Gatta, M. Bolognesi, D. Sacerdoti, and G. Bombonato. "245 SPLENO-SYSTEMIC SHUNTS AND COVERT HEPATIC ENCEPHALOPATY." Journal of Hepatology 58 (April 2013): S105. http://dx.doi.org/10.1016/s0168-8278(13)60247-0.

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2

Sturniolo, L., F. Balzola, A. Ottobrelli, M. Torrani, S. Martini, E. Morello, A. Smedile, et al. "229 GLUTEN/CASEIN-FREE DIET AND LIVER ENCEPHALOPATY." Journal of Hepatology 50 (April 2009): S93. http://dx.doi.org/10.1016/s0168-8278(09)60231-2.

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3

Rakhimbaeva, G. S. "242 Methabolic encephalopaty: basis factors in apoptotic cells." International Journal of Developmental Neuroscience 14 (July 1996): 109. http://dx.doi.org/10.1016/0736-5748(96)80431-x.

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4

Sorodoc, Laurentiu, Catalina Lionte, Victorita Sorodoc, Ovidiu Petris, and Irina Jaba. "Is MARS system enough for A.phalloides-induced liver failure treatment?" Human & Experimental Toxicology 29, no. 10 (February 23, 2010): 823–32. http://dx.doi.org/10.1177/0960327110363327.

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Patients with Amanita phalloides-induced liver failure (LF) have a high mortality, despite significant advances in intensive care managemet. Our study evaluated the effect of Molecular Absorbents Recirculating System (MARS) comparative with optimal intensive care (OIC) in adults with this condition, in the absence of liver transplantation (LT). Six consecutive patients (women, range 16—61 years) affected by A.phalloides-induced LF were treated with OIC (3 patients) and MARS (3 patients). Laboratory parameters and hepeatic encephalopaty were evaluated 15 min before and 24 hours following each MARS treatment. Three 6-hour sessions per patient were performed in MARS group, with a statistically significant decrease in ammonia (p value 0.011), alaninaminotransferase (ALT) and prothrombin time (PT) (p value 0.004). Two patients had a significant rebound in bilirubin (+116%; p value 0. 04) 24 hours following MARS. Mortality in MARS group was 66.7%. Survival rate in OIC was 0%. Negative prognostic markers: lack of PT and hepatic encephalopaty improvement, rebound in bilirubin, and delay of MARS therapy initiation. No significant adverse reactions occurred during MARS. MARS is an effective depurative therapy in adults with A.phalloides-induced LF, but alone is not enough. Survival is predicted by the results of the initial MARS, amount of mushroom consumed, and time from toxin exposure.

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5

Puryatni, Anik, and Tom J. de Koning. "ENCEPHALOPATY AKUT PADA ANAK DENGAN KELAINAN METABOLISME BAWAAN (PENDEKATAN PRAKTIS)." Jurnal Kedokteran Brawijaya 24, no. 3 (March 19, 2008): 3–2008. http://dx.doi.org/10.21776/ub.jkb.2008.024.03.7.

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6

Soto, S., E. Castro, J. L. Ulla, S. Vazquez, R. Baltar, V. Alvarez, J. Vazquez-Sanluis, L. Ledo, and E. Vazquez-Astray. "313 HYDROXIZYNE IMPROVED INSOMNIA IN CIRRHOTIC INPATIENTS WITH GRADE I ENCEPHALOPATY." Journal of Hepatology 48 (January 2008): S124. http://dx.doi.org/10.1016/s0168-8278(08)60315-3.

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7

ARMENDARIZBORUNDA, J., J. GALVEZGASTELUM, A. SEGURAFLORES, C. BEASZARATE, and A. MIRANDA. "366 Combined hupa plus MMP-8 gene therapy reverts cirrhosis and improves hepatic encephalopaty." Hepatology 38 (2003): 336–37. http://dx.doi.org/10.1016/s0270-9139(03)80409-3.

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8

Pironti, Erica, Francesca Cucinotta, Francesca Granata, Maria Spanò, Maria Bonsignore, Henry Houlden, Vincenzo D. Salpietro, Antonella Gagliano, and Gabriella Di Rosa. "Preliminary Results of Whole Exome Sequencing in a Cohort of Sicilian Children with Early-Onset Epileptic Encephalopaty." European Journal of Paediatric Neurology 21 (June 2017): e169. http://dx.doi.org/10.1016/j.ejpn.2017.04.718.

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9

Bombushkar, Igor, Anatoliy Gozhenko, Mykhaylo Korda, Xawery Żukow, and Igor Popovych. "Peculiarities of relationships between plasma levels of nitrogenous metabolites and EEG & HRV parameters in patients with postradiation encephalopaty." Journal of Education, Health and Sport 12, no. 10 (October 31, 2022): 335–55. http://dx.doi.org/10.12775/jehs.2022.12.10.040.

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Background. Recently we shown that nitrogenous plasma metabolites (uric acid, bilirubin, urea and creatinine), even in the absence of uremia, are able to influence the state of the anxiety, autonomic and central nervous and endocrine systems, apparently through aryl hydrocarbon and adenosine receptors of neurons and endocrine cells and/or directly. Sexual dimorphism in the neurotropic effects of uric acid in neurologically healthy patients was also revealed. The purpose of this study is to compare nitrogenous-neural relationships in neurologically healthy men and those with post-radiation encephalopathy (PREP). Materials and Methods. The object of observation were neurologically healthy 31 men (24÷69 y) and 19 patients (26÷61 y) with PREP. The relationships between plasma levels of nitrogenous metabolites, on the one hand, and EEG and HRV parameters, on the other, were analyzed. Results. By constructing regression models with stepwise elimination it was found that the multiple correlation coefficient (R±µ) of creatinine with neural parameters in patients with PREP significantly exceeded that of control patients (0,762±0,069 vs 0,409±0,107; t=2,62; p=0,011). With regard to urea, the differences are insignificant (0,801±0,059 vs 0,694±0,066; t=1,17; p>0,2), and with regard to bilirubin (0,548±0,115 vs 0,402±0,107; t=0,94) and uric acid (0,496±0,124 vs 0,549±0,089; t=0,32), there are practically no differences. Conclusion. Post-radiation encephalopathy is accompanied not only by deviations from the norm of a number of EEG and HRV parameters, but also by their increased sensitivity to creatinine and, to a lesser extent, urea, but not to bilirubin and uric acid.

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10

Yulianti Bisri, Dewi, and Tatang Bisri. "Pertimbangan Anestesi Perioperatif untuk Pasien Bedah Saraf dengan Covid-19." Jurnal Neuroanestesi Indonesia 10, no. 1 (February 19, 2021): 55–62. http://dx.doi.org/10.24244/jni.v10i1.324.

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The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, Hubei province China, in December 2019, and spread fast to all the world more than 190 countries. Patients should be screened for covid-19 using a combination of history, computed tomography (CT) chest, and real time quantitative polymerase chain reaction (RT-qPCR) testing depending on institutional policies. Neurological symptom as dizziness, headache, hypogeusia and hyposmia, common (36%) at covid-19 patient. Encephalopaty and changed mental status exist in patient infected by SARS-CoV-2 virus. Cerebrovascular diseases more in severe covid-19; acute ischemic stroke had reported in 5.7% and altered level of consciousnes in 15% patient. Surgical measuremet cranial and spinal rutine is safe, endoscopic endonasal surgery not safe and must be avoided. Extubation after general anesthesia if possible do air negative pressure room, and personil still use personal protection equipment (PPE) level 3. Must be avoid patient cough during extubation. After extubation, give oxygen nasal canule, surgical mask, and high flow oxygen (give <6 L/min) avoided given the risk of aerosolization

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11

Ramos, J. Curto, H. Dolengevich, M. A. Morillas Romerosa, and E. Mateos Pascual. "“New” drugs associated with chemsex? 2C-B in sexual context. A case report and review." European Psychiatry 64, S1 (April 2021): S577. http://dx.doi.org/10.1192/j.eurpsy.2021.1539.

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IntroductionThe intentional use of drugs before or during sexual intercourse (chemsex), due to its impact on mental health, is a phenomenon of high importance in men who have sex with men.ObjectivesWe report the case of a patient with polysubstance acute intoxication, including 2C-B, in order to review the evidence about the mechanisms of action of 2C-B, its efects on sexual pleasure, toxicity, patterns of abuse and somatic and mental health related consequences it may present.MethodsCase report and narrative review.ResultsWe present the case of a patient using 2C-B as a substance in chemsex practice. As the patient presented in our emergency with psychotic symptoms, he was diagnosed with “stimulant acute intoxication” and “acute psychotic symptoms induced by stimulants”. 2C-B increases dopamine (DA) serotonin (5-HT) and norepinephrine (NE) and cause stimulating and hallucinogenic effects.ConclusionsMSM is a group vulnerable to the problematic use of drugs in a sexual context. Several mental health problems have been associated with chemsex users such as psychotic sypmptoms, suicidal ideation, encephalopaty, delirium. Polysubstance use is common in chemsex practice and it can be difficult to identify the drugs used in states of acute intoxication but psychiatrists must explore the use of differents drugs from the “classic chemsex drugs” (mephedrone, GHB and metanphetamine) including 2C-B and other substances such as cocaine, MDMA, ketamine, and other cathinones different from mephedrone.

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12

Agut, T., M. Leon, A. Alarcón, J. Arnaez, G. Arca, M. Camprubí, V. Tenorio, and A. García-Alix. "How Good is the Correlation Between Early Magnetic Resonance Imaging (MRI) and Late MRI in Infants with Hypoxic Ischemic Encephalopaty (HIE) Treated with Hypothermia?" Pediatric Research 70 (November 2011): 143. http://dx.doi.org/10.1038/pr.2011.368.

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13

Bouchet, Antoine, Carolina Ossandón, Paola Haeger, and Gustavo Bresky. "Treatment with Melatonin Improves Cognitive Behavior and Motor Skills in a Rat Model of Liver Fibrosis." Annals of Hepatology 17, no. 5 (July 31, 2018): 0–10. http://dx.doi.org/10.5604/01.3001.0012.2229.

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Introduction and aim: Patients with Liver Cirrhosis (LC) and Minimal Hepatic Encephalopaty have a higher accident rate. LC impairs the normal sleep-awake cycle and produces disturbances in behavior, cognition and motor skills. Abnormal melatonin (MT) levels have also been identified in LC. Administration of MT may regulate circadian rhythms and prevent the oxidative damage. We studied the effects of MT on spatial memory acquisition (SMA) and motor skills in a liver fibrosis model (LF)s. Materials and Methods: 45 rats, divided into 4 groups. (G1: LF; G2: LF+MT;G3:MT; G4:Healthy control (HC)). LF was induced by carbon tetrachloride intraperitoneal injection (0.2 ml/Kg) for 5 months. MT was administered during 5 weeks (0.4mg/Kg/day). SMA was evaluated by using the Morris Water Maze protocol where the escape latency (EL) and mean speed were measured. Data were registered by SMART®. Results: The EL measurement analyzed by two way ANOVA: cirrhosis presented a higher EL than controls or those treated with MT suggesting impaired memory acquisition which is rescued by MT treatment. The mean speed analysis revealed that LF presented higher speed than LF+MT or HC, suggesting that LF affects motor skills, which are improved by MT. To discard whether EL is affected by altered motor skills in LF treated with MT, we compared the average EL and speed between days 2 and 6 of the training protocol. Speed was not improved during the trials unlike EL, suggesting that memory acquisition is independent of motor skills. Conclusion: These findings suggest that MT improves cognition and motor skills in the LF model.

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14

Balzola, F., C. Sanna, A. Ottobrelli, M. Torrani, S. Martini, D. Leotta, A. Marchet, et al. "146 CHRONIC HEPATIC ENCEPHALOPATY (HE) IN PATIENTS WITH SEVERE LIVER CIRRHOSIS: EFFICACY OF THE WHEAT AND MILK PROTEIN FREE DIET IN THE REDUCTION OF CLINICAL EPISODES." Journal of Hepatology 54 (March 2011): S64. http://dx.doi.org/10.1016/s0168-8278(11)60148-7.

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15

L., Shevchenko, V. Bobrova, and V. Kalashnik. "The excitotoxic impairment of brain in patients with discirculatory encephalopathyand therapeutic correction." East European Journal of Neurology, no. 3(15) (September 20, 2018): 22–26. http://dx.doi.org/10.33444/2411-5797.2017.3(15).22-26.

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In view of the proved fact of influence of excitotoxicity on progressive course of dyscirculatory encephalopa- thy, clinical, neurophysiological investigation of the patients in dynamics of treatment with cytoflavin and cortexin. The positive clinical dynamics and partial normalization of electroencephalographic patterns were found out. Correlation analysis have proved ambiguous connection between clinical signs, focal changes in brain and therapeutic effectiveness. Results of investigation have proved the appropriateness of dyscirculatory encephalopathy therapy with cytoflavin and cortexin with the aim of inhibition of excitotoxicity. Multiplevalued connection between obtained parameters allow to assume the necessity of future investigations on this problem.

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16

Mamilla, Sarada Murali. "A case of PRES following intracranial hypotension, with spontaneous resolution with epidural blood patch." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 12 (November 26, 2018): 5190. http://dx.doi.org/10.18203/2320-1770.ijrcog20184992.

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Posterior reversible encephalopathy syndrome (PRES (also known as reversible posterior leukoencephalopathy syndrome)) presents with rapid onset of symptoms including headache, seizures, altered consciousness, and visual disturbance. It is often but by no means always associated with acute hypertension. Diffusion-weighted MRI is the most sensitive exam to confirm the diagnosis of PRES. If promptly recognized and treated, the clinical syndrome usually resolves within a week, and the changes seen in magnetic resonance imaging (MRI) resolve over days to weeks. Posterior reversible encephalopathy syndrome is an increasingly recognized disorder, with a wide clinical spectrum of both symptoms and triggers, and yet it remains poorly understood. Differential diagnosis includes venous sinus thrombosis, cerebral haemorrhage, encephalitis, vasculititis and metabolic encephalopathys. No clinical trials have evaluated the management of PRES, but rapid withdrawal of the trigger appears to hasten recovery and to avoid complications: for example, aggressive blood pressure management, withdrawal of the offending drug, or delivery in eclampsia. We report a case of women presenting with severe headache, tonic clonic convulsions 7 days after spinal anaesthesia for caesarean delivery, MRI showed evidence of intracranial hypotension and posterior reversible encephalopathy syndrome. She was treated with Blood patch which lead to complete resolution of symptoms and radiological findings. The possible pathogenetic relationship between intracranial hypotension, secondary to the inadvertent dural puncture, and PRES is discussed. Prompt diagnosis and proper treatment results in complete cure without permanent neurological sequelae.

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17

Yatoo, Hilal, Kishalay Datta, Jitesh Bhandarkar, Indranil Das, and Monil Patel. "Metronidazole Induced Encephalopathy." Indian Journal of Emergency Medicine 3, no. 1 (2017): 152–54. http://dx.doi.org/10.21088/ijem.2395.311x.3117.25.

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18

Correia, Rita. "RESLES: Encefalopatia por 5-Fluorouracil." Sinapse 20, no. 1 (June 30, 2020): 68–70. http://dx.doi.org/10.46531/sinapse/cc/200003/2020.

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19

Shaikh, Dr Safiya I., and Dr C. Govindaraju Dr. C Govindaraju. "Posterior Reversible Encephalopathy Syndrome." Indian Journal of Applied Research 3, no. 9 (October 1, 2011): 424–25. http://dx.doi.org/10.15373/2249555x/sept2013/126.

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20

Archit, Dahiya, and Nandy Parvati. "Recurrent Posterior Reversible Encephalopathy Syndrome." Indian Journal of Emergency Medicine 2, no. 1 (2016): 37–39. http://dx.doi.org/10.21088/ijem.2395.311x.2116.7.

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21

Ochiai, Atsushi, and Hideaki Naganuma. "Wernicke's encephalopathy with upbeat nystagmus." Equilibrium Research 75, no. 6 (2016): 505–10. http://dx.doi.org/10.3757/jser.75.505.

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22

R Gomes, Richmond. "Enteric Encephalopathy: An Old Archenemy." General Medicine and Clinical Practice 5, no. 1 (May 31, 2022): 01–04. http://dx.doi.org/10.31579/2639-4162/055.

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Typhoid fever is the name given to the illness caused by the bacterium Salmonella Typhi, a member of the Salmonella family. Typhoid fever is spread through food and water contaminated by animal and human feces. Typhoid fever is very rare in the United States and other developed nations, and it is more common in underdeveloped nations, particularly Latin America, Asia, and Africa. Typhoid fever has a wide variety of presentations that range from an overwhelming multisystemic illness to relatively minor cases of diarrhea with low-grade fever. The classic presentation is fever, malaise, diffuse abdominal pain, and constipation. Untreated typhoid fever may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications. Here, we present a 30 years old nurse who presented with fever, constipation and diagnosed as typhoid fever. While on treatment, she developed abnormal behavior. CSF was sterile. Neuro imaging was normal. Considering typhoid encephalopathy she was treated with high dose pulse steroid. She showed significant improvement. Thus, all clinicians should keep in mind the possibility of typhoid encephalopathy as a rare complication of typhoid fever.

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23

Montagnese, Sara, Carlo Merkel, and Piero Amodio. "Encephalopathy or hepatic encephalopathy?" Journal of Hepatology 57, no. 4 (October 2012): 928–29. http://dx.doi.org/10.1016/j.jhep.2012.04.042.

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24

Shimizu, Naoki. "“Iatrogenic encephalopathy” vs. “pathogenic encephalopathy”." Nihon Shuchu Chiryo Igakukai zasshi 13, no. 4 (2006): 405–7. http://dx.doi.org/10.3918/jsicm.13.405.

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25

Samala, Renato V., and Mellar P. Davis. "Encephalopathy." Xiangya Medicine 1 (July 7, 2016): 9. http://dx.doi.org/10.21037/xym.2016.06.10.

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26

Russ, Jeffrey B., Roxanne Simmons, and Hannah C. Glass. "Neonatal Encephalopathy: Beyond Hypoxic-Ischemic Encephalopathy." NeoReviews 22, no. 3 (March 2021): e148-e162. http://dx.doi.org/10.1542/neo.22-3-e148.

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27

Molloy, Eleanor J., and Cynthia Bearer. "Neonatal encephalopathy versus Hypoxic-Ischemic Encephalopathy." Pediatric Research 84, no. 5 (September 7, 2018): 574. http://dx.doi.org/10.1038/s41390-018-0169-7.

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28

Durand, François, Pere Ginès, Faouzi Saliba, and Javier Fernández. "Reply to: “Encephalopathy or hepatic encephalopathy?”." Journal of Hepatology 57, no. 4 (October 2012): 929–30. http://dx.doi.org/10.1016/j.jhep.2012.06.002.

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29

Nardone, R., M. McCoy, A. B. Kunz, J. Kraus, W. Staffen, G. Ladurner, and S. M. Golaszewski. "Hyponatremic Encephalopathy Mimicking Hypoxic-Ischemic Encephalopathy." Clinical Neuroradiology 20, no. 4 (July 14, 2010): 243–46. http://dx.doi.org/10.1007/s00062-010-0017-6.

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30

Schendel, Diana, Karin B. Nelson, and Eve Blair. "Neonatal encephalopathy or hypoxic-ischemic encephalopathy?" Annals of Neurology 72, no. 6 (December 2012): 984–85. http://dx.doi.org/10.1002/ana.23753.

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31

Ridola, Lorenzo, Oliviero Riggio, Stefania Gioia, Jessica Faccioli, and Silvia Nardelli. "Clinical management of type C hepatic encephalopathy." United European Gastroenterology Journal 8, no. 5 (February 26, 2020): 536–43. http://dx.doi.org/10.1177/2050640620909675.

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Type-C hepatic encephalopathy is a complex neurological syndrome, characteristic of patients with liver disease, causing a wide and complex spectrum of nonspecific neurological and psychiatric manifestations, ranging from a subclinical entity, minimal hepatic encephalopathy, to a deep form in which a complete alteration of consciousness can be observed: overt hepatic encephalopathy. Overt hepatic encephalopathy occurs in 30–40% of patients. According to the time course, hepatic encephalopathy is subdivided into episodic, recurrent and persistent. Diagnostic strategies range from simple clinical scales to more complex psychometric and neurophysiological tools. Therapeutic options may vary between episodic hepatic encephalopathy, in which it is important to define and treat the precipitating factor and hepatic encephalopathy and secondary prophylaxis, where the standard of care is non-absorbable disaccharides and rifaximin. Grey areas and future needs remain the therapeutic approach to minimal hepatic encephalopathy and issues in the design of therapeutic studies for hepatic encephalopathy.

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32

Premal, Travedi, Kriss Michael, Biggins Scott, and Johnson Thor. "Splenic Embolization for Recalcitrant Post-TIPS Encephalopathy." Journal of Clinical Cases & Reports 1, no. 3 (October 30, 2018): 122–25. http://dx.doi.org/10.46619/joccr.2018.1-1025.

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Encephalopathy in the setting of transjugular portosystemic shunts (TIPS) is a difficult clinical problem. Shunt reduction often improves encephalopathy but increases the risk of portal hypertension related complications. In this case we describe the use of partial splenic artery embolization in a 60-year-old female who presented with both TIPS dysfunction and refractory encephalopathy. Prior to treatment the patient had an elevated TIPS gradiant, visible varices by endoscopy, and encephalopathy that was severe and refractory enough to be considered for hospice. Following 60% splenic volume embolization, encephalopathy resolved, varices decompressed, and patient was able to be discharged home. This demonstrates that splenic embolization may be considered as a potential alternative to TIPS reduction in the setting of TIPS dysfunction and encephalopathy.

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33

Yadav, Dr Shashibala J. "Imaging of Postpartum Encephalopathy: A Pictoral Essay." Journal of Medical Science And clinical Research 05, no. 03 (March 8, 2017): 18599–608. http://dx.doi.org/10.18535/jmscr/v5i3.55.

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34

Conkar, Secil, Caner Kabasakal, and Sevgi Mir. "Tacrolimus-Induced Posterior Reversible Encephalopathy Syndrome (PRES)." Turkish Nephrology Dialysis Transplantation 23, no. 3 (September 2, 2014): 265–68. http://dx.doi.org/10.5262/tndt.2014.1003.17.

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35

Tamai, Yasuyuki, Motoh Iwasa, Yuichi Yoshida, Jun Nomoto, Takahiro Kato, Hiroe Asuke, Akiko Eguchi, Yoshiyuki Takei, and Hayato Nakagawa. "Development of a New Index to Distinguish Hepatic Encephalopathy through Automated Quantification of Globus Pallidal Signal Intensity Using MRI." Diagnostics 12, no. 7 (June 29, 2022): 1584. http://dx.doi.org/10.3390/diagnostics12071584.

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Hyperintensities within the bilateral globus pallidus on T1-weighted magnetic resonance images were present in some liver cirrhosis patients with hepatic encephalopathy. The symptoms of covert hepatic encephalopathy are similar to those of mild dementia. We aimed to develop a new diagnostic index in which to distinguish hepatic encephalopathy from dementia. The globus pallidus signal hyperintensity was quantified using three-dimensional images. In addition, the new index value distribution was evaluated in a cohort of dementia patients. Signal intensity of globus pallidus significantly increased in liver cirrhosis patients with hepatic encephalopathy compared to those without hepatic encephalopathy (p < 0.05), healthy subjects (p < 0.05) or dementia patients (p < 0.001). Only 12.5% of liver cirrhosis patients without hepatic encephalopathy and 2% of dementia patients exceeded the new index cut-off value of 0.994, which predicts hepatic encephalopathy. One dementia patient in our evaluation had a history of liver cancer treatment and was assumed to have concomitant hepatic encephalopathy. The automatic assessment of signal intensity in globus pallidus is useful for distinguishing liver cirrhosis patients with hepatic encephalopathy from healthy subjects and liver cirrhosis patients without hepatic encephalopathy. Our image analyses exclude possible cases of hepatic encephalopathy from patients with neurocognitive impairment, including dementia.

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36

Abdaal, Maham, Zafeer-ul-Hassan Iqbal, Numan Ghafoor, Muhammad Usman, Saqib Hussain, and Mehi Naqvi. "Determine the Frequency of Factors Leading to Hepatic Encephalopathy in Patients with Liver Cirrhosis." Pakistan Journal of Medical and Health Sciences 16, no. 12 (December 30, 2022): 197–99. http://dx.doi.org/10.53350/pjmhs20221612197.

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Aim: To determine the frequency of factors leading to hepatic encephalopathy in patients with liver cirrhosis. Study design: Retrospective study Place and duration of study: Department of Internal Medicine, Rawalpindi Medical Universityfrom 01-07-2021 to 30-06-2022 Methodology: One hundred patients were included and divided into two groups. One group was those which developed hepatic encephalopathy while the other group was of those which did not develop any hepatic encephalopathy. Various risk factors and their frequencies were measured through a modelled hepatic encephalopathy pharmacological, clinical as well as demographic data. Comparison on the frequency of the variable seen in hepatic encephalopathy patients with non-hepatic encephalopathy was conducted for better assessment of the frequency of risk factors. Results: Seventy patients did not develop hepatic encephalopathy while 30 patients did develop hepatic encephalopathy. Fifteen patients had developed alcoholic liver cirrhosis followed by hepatitis C and non-alcoholic cirrhosis. Age greater than 60 years had a percentage of 60% within cases of hepatic encephalopathy only. Prevalence of hepatitis C cirrhosis in 36.6%, diabetes in 49%, cardiovascular disease in 51%, hepatocellular carcinoma in 6.6%, use of proton pump inhibitor in 63.3% were presented and were higher than who did not develop hepatic encephalopathy. Benzodiazepines, gamma aminobutyric acid [GABA]ergics, opioids and proton pump inhibitors each of them was associated with increased chances of hepatic encephalopathy. Conclusion: Hepatic encephalopathy was more commonly observed in older patients (60%) and more specifically in male population. Higher frequency of comorbidities (hypertension, diabetes, cardiovascular disease, ascites, alcoholic cirrhosis), CCI score and pharmacological drugs were identifiable risk factors for hepatic encephalopathy. Key words: Neurotoxicity; Cirrhosis, Complications, Hepatitis C, Deteriorate

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37

Imataka, George, Shigeko Kuwashima, and Shigemi Yoshihara. "A Comprehensive Review of Pediatric Acute Encephalopathy." Journal of Clinical Medicine 11, no. 19 (October 7, 2022): 5921. http://dx.doi.org/10.3390/jcm11195921.

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Acute encephalopathy typically affects previously healthy children and often results in death or severe neurological sequelae. Acute encephalopathy is a group of multiple syndromes characterized by various clinical symptoms, such as loss of consciousness, motor and sensory impairments, and status convulsions. However, there is not only localized encephalopathy but also progression from localized to secondary extensive encephalopathy and to encephalopathy, resulting in a heterogeneous clinical picture. Acute encephalopathy diagnosis has advanced over the years as a result of various causes such as infections, epilepsy, cerebrovascular disorders, electrolyte abnormalities, and medication use, and new types of acute encephalopathies have been identified. In recent years, various tools, including neuroradiological diagnosis, have been developed as methods for analyzing heterogeneous acute encephalopathy. Encephalopathy caused by genetic abnormalities such as CPT2 and SCN1A is also being studied. Researchers were able not only to classify acute encephalopathy from image diagnosis to typology by adjusting the diffusion-weighted imaging/ADC value in magnetic resonance imaging diffusion-weighted images but also fully comprehend the pathogenesis of vascular and cellular edema. Acute encephalopathy is known as a very devastating disease both medically and socially because there are many cases where lifesaving is sometimes difficult. The overall picture of childhood acute encephalopathy is becoming clearer with the emergence of the new acute encephalopathies. Treatment methods such as steroid pulse therapy, immunotherapy, brain hypothermia, and temperature control therapy have also advanced. Acute encephalopathy in children is the result of our predecessor’s zealous pursuit of knowledge. It is reasonable to say that it is a field that has advanced dramatically over the years. We would like to provide a comprehensive review of a pediatric acute encephalopathy, highlighting advancements in diagnosis and treatment based on changing disease classification scenarios from the most recent clinical data.

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Wang, Kevin Y., Harvey S. Singer, Barbara Crain, Sachin Gujar, and Doris D. M. Lin. "Hypoxic-Ischemic Encephalopathy Mimicking Acute Necrotizing Encephalopathy." Pediatric Neurology 52, no. 1 (January 2015): 110–14. http://dx.doi.org/10.1016/j.pediatrneurol.2014.09.009.

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Golzari, Samad EJ, and Ata Mahmoodpoor. "Sepsis-associated encephalopathy versus sepsis-induced encephalopathy." Lancet Neurology 13, no. 10 (October 2014): 967–68. http://dx.doi.org/10.1016/s1474-4422(14)70205-4.

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Allampati, Sanath K., and Kevin D. Mullen. "Understanding the impact of neurologic complications in patients with cirrhosis." SAGE Open Medicine 7 (January 2019): 205031211983209. http://dx.doi.org/10.1177/2050312119832090.

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Patients with cirrhosis may experience neurologic complications, including hepatic encephalopathy. Hepatic encephalopathy may be classified as covert (mild symptoms (e.g. lack of awareness)) or overt (moderate to severe symptoms (e.g. confusion or coma)), and symptoms may overlap with other neurologic conditions (e.g. epilepsy, stroke). Managing hepatic encephalopathy includes identifying and treating precipitating factors (e.g. dehydration). First-line treatment for patients with overt hepatic encephalopathy is typically lactulose; to reduce the risk of overt hepatic encephalopathy recurrence, lactulose plus the nonsystemic antibiotic rifaximin is recommended. Rifaximin reduced the risk of breakthrough overt hepatic encephalopathy by 58% versus placebo over 6 months (p < 0.001; 91% of patients in each group were on concomitant lactulose). However, neither pharmacologic hepatic encephalopathy treatment nor liver transplantation may completely reverse neurologic impairment in patients with hepatic encephalopathy. Additional neurologic considerations for patients with cirrhosis include preventing falls, as well as managing sleep-related issues, hyponatremia, and cerebral edema. Thus, monitoring neurologic impairment is an important component in the management of patients with cirrhosis.

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Rauf, Amna, and Sidra Rauf. "Assessment of Serum Biochemical Changes in Hepatic Encephalopathy." Pakistan Armed Forces Medical Journal 72, no. 5 (November 4, 2022): 1690–93. http://dx.doi.org/10.51253/pafmj.v72i5.6802.

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Objective: To analyze the association of various biochemical changes with different grades of hepatic encephalopathy among patients of hepatitis C-related decompensated liver disease presenting at Pak Emirates Military Hospital. Rawalpindi, Pakistan. Study Design: Comparative cross-sectional study. Place and Duration of Study: Medicine and Gastroenterology Department of Pak Emirates Military Hospital (PEMH), Rawalpindi Pakistan, from Mar 2020 to Feb 2021. Methodology: This study was conducted on 100 patients with hepatitis C-related decompensated liver. A consultant medical specialist or gastroenterologist graded hepatic encephalopathy according to the West Haven criteria. Serum urea, creatinine, albumin and international normalized ratio were performed in all the patients at the time of grading of encephalopathy and derangement in the level of these parameters was analyzed with Grades of encephalopathy. Results: Out of 100 patients, in the final analysis, 66 were males, and 44 were females. The commonest aetiology of hepatic encephalopathy was Infection (33%) followed by Constipation (29%). 15 patients had Grade-1 encephalopathy, 43 had Grade-2, 26 had Grade-3 while 16 had Grade-4 encephalopathy. Deranged serum creatinine, international normalized ratio and albumin levels were significantly associated with a higher grade of hepatic encephalopathy (p-value<0.05) in our study participants. Conclusion: Biochemical markers studied in patients with hepatic encephalopathy secondary to hepatitis C-related decompensated chronic liver disease were deranged. In addition, creatinine, albumin and International normalized ratio were found to be more deranged in higher grades of encephalopathy.

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Martin, Thomas C. S., Sean Chow, Scott T. Johns, and Sanjay R. Mehta. "Ceftaroline-associated Encephalopathy in Patients With Severe Renal Impairment." Clinical Infectious Diseases 70, no. 9 (August 29, 2019): 2002–4. http://dx.doi.org/10.1093/cid/ciz857.

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Abstract Encephalopathy complicates beta-lactam therapy, particularly with impaired renal function, though no studies have reported ceftaroline-associated encephalopathy. Among 28 patients with estimated glomerular filtration rates <30 mL/min who received ≥5 days of ceftaroline, 3 developed encephalopathy. Ceftaroline, when dosed supra-therapeutically for serious infections, may be a cause of antibiotic-associated encephalopathy.

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Aladdin, Yasser, and Bader Shirah. "Hashimoto's Encephalopathy Masquerading as Rapidly Progressive Dementia and Extrapyramidal Failure." Journal of Neurosciences in Rural Practice 13, no. 01 (January 2022): 101–4. http://dx.doi.org/10.1055/s-0041-1741487.

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AbstractHashimoto's encephalopathy is a rare immune-mediated disorder characterized by subacute encephalopathy with elevated thyroid antibodies. Hashimoto's encephalopathy is also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis. We report a rare presentation of Hashimoto's encephalopathy presenting with acute neuropsychiatric disturbances, rapidly progressive dementia, seizures, and extrapyramidal failure. Neuroimaging revealed multifocal vasculitides of major cerebral vessels that support the autoimmune vasculitic theory as the underlying pathogenesis for Hashimoto's encephalopathy. Unfortunately, permanent irreversible cerebral damage has already ensued before her presentation to our center, which rendered steroid therapy ineffective. Serological testing for Hashimoto's thyroiditis must be in the investigation of all rapidly progressive dementias as early diagnosis and timely management of autoimmune thyroiditis may salvage sizable and eloquent cerebral tissues. The rarity of the condition should not preclude the investigation of Hashimoto's disease even in the presence of normal levels of thyroid hormones. Delayed diagnosis may result in irreversibly catastrophic encephalopathy in patients who once presented with potentially curable dementia.

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Nasreen, Ali. "Infantile Spasm-Rare Presentation of “Vitamin B12 Encephalopathy”." Journal of Medical Science And clinical Research 05, no. 05 (May 8, 2017): 21583–86. http://dx.doi.org/10.18535/jmscr/v5i5.56.

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Ximena Fernández, María, Juan Manuel Calderón N., and Sebastián Ben. "Síndrome de Encefalopatía Posterior Reversible y Embarazo: Reporte de un caso." Horizonte Médico (Lima) 15, no. 3 (September 17, 2015): 68–73. http://dx.doi.org/10.24265/horizmed.2015.v15n3.13.

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Tanuma, Naoyuki, Rie Miyata, Keisuke Nakajima, Akihisa Okumura, Masaya Kubota, Shin-ichiro Hamano, and Masaharu Hayashi. "Changes in Cerebrospinal Fluid Biomarkers in Human Herpesvirus-6-Associated Acute Encephalopathy/Febrile Seizures." Mediators of Inflammation 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/564091.

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To determine the involvement of oxidative stress in the pathogenesis of acute encephalopathy associated with human herpesvirus-6 (HHV-6) infection, we measured the levels of oxidative stress markers 8-hydroxy-2′-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct (HEL), tau protein, and cytokines in cerebrospinal fluid (CSF) obtained from patients with HHV-6-associated acute encephalopathy (HHV-6 encephalopathy)(n=16)and complex febrile seizures associated with HHV-6 (HHV-6 complex FS)(n=10). We also examined changes in CSF-8OHdG and CSF-HEL levels in patients with HHV-6 encephalopathy before and after treatment with edaravone, a free radical scavenger. CSF-8-OHdG levels in HHV-6 encephalopathy and HHV-6 complex FS were significantly higher than in control subjects. In contrast, CSF-HEL levels showed no significant difference between groups. The levels of total tau protein in HHV-6 encephalopathy were significantly higher than in control subjects. In six patients with HHV-6 infection (5 encephalopathy and 1 febrile seizure), the CSF-8-OHdG levels of five patients decreased after edaravone treatment. Our results suggest that oxidative DNA damage is involved in acute encephalopathy associated with HHV-6 infection.

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Arif, Kanwal, Nauman Ismat Butt, Farman Ali, Fahmina Ashfaq, Osama Habib, and Aniqa Anser Tufail Khan Kakar. "Frequency of Recurrence of Hepatic Encephalopathy in Patients of Chronic Liver Disease Treated With Rifaximin." Pakistan Journal of Medical and Health Sciences 16, no. 10 (October 30, 2022): 150–52. http://dx.doi.org/10.53350/pjmhs221610150.

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Aim: To determine the frequency of recurrence of hepatic encephalopathy in patients treated with Rifaximin. Study design: Observational cross-sectional study. Setting & duration: Department of Medicine, Services institute of Medical Sciences Lahore for duration of 12 months. Methodology: Hepatic encephalopathy was diagnosed using West-Haven classification in patients of chronic liver disease. Recurrence was considered if a new episode of hepatic encephalopathy occurred within 3 months after initiation of treatment. A total 120 patients of chronic liver disease having had an episode of recent hepatic encephalopathy within the last 3 months, of both genders, above 20 years of age with hepatic encephalopathy were included in the study. The patients were followed for 3 months after initiation of therapy and any episode of recurrence of hepatic encephalopathy was recorded. Results: Mean age was 51.5±12.2 years and 52.3±12.8 years respectively in Rifaximin and Placebo groups. Fourteen (23.3%) patients in Rifaximin group and 17(28.3%) in placebo group were younger than 40 years of age. Thirty-three (55%) patients in Rifaximin group were male versus 29(48.3%) patients in Placebo group. Fifteen (25%) patients in Rifaximin Group developed hepatic encephalopathy by 3 months of follow up as compared to 31(51.7%) patients in Placebo Group Conclusion: Frequency of recurrence of hepatic encephalopathy is significantly lower in Rifaximin treated patients. Keywords: Hepatic Encephalopathy, Recurrence, Rifaximin.

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Sharma, Sanjeev Kumar, Dharma Choudhary, Anil Handoo, Gaurav Dhamija, Gaurav Kharya, Vipin Khandelwal, Mayank Dhamija, and Sweta Kothari. "An unusual cause of anemia and encephalopathy." Mediterranean Journal of Hematology and Infectious Diseases 7 (April 24, 2015): e2015036. http://dx.doi.org/10.4084/mjhid.2015.036.

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The authors present here an interesting case of recent onset anemia that was associated with an encephalopathy of the unusual cause.Although severe anemia can theoretically result in anemic hypoxia and can then lead to hypoxic encephalopathy, it is not a primary cause of encephalopathy. More frequently anemia can contribute together with other multiple causes of encephalopathy, such as infections, metabolic abnormalities, trauma, hepatic dysfunction, hypertension, toxins.

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Lazzari, Jacqueline Mori, Maria Gabriela Lang, and Henrique Luiz Staub. "Posterior reversible encephalopathy syndrome and primary Sjögren's syndrome." Scientia Medica 28, no. 2 (February 27, 2018): 29837. http://dx.doi.org/10.15448/1980-6108.2018.2.29837.

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Posterior reversible encephalopathy syndrome is a nebulous disorder triggered by a number of conditions, mostly hypertensive crisis, renal insufficiency, and immunosuppressive therapy. Other possible etiologies include eclampsia, transplantation and infections. The association of posterior reversible encephalopathy syndrome with autoimmune diseases has been rather intriguing. We herein describe an unusual case of posterior reversible encephalopathy syndrome in a patient with primary Sjögren's syndrome, hypertension and lung infection. This is probably the second reported case associating posterior reversible encephalopathy syndrome and primary Sjögren's syndrome. If the posterior reversible encephalopathy syndrome was triggered by primary Sjögren's syndrome itself or by its comorbidities remains an open question.

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Ciećko-Michalska, Irena, Małgorzata Szczepanek, Agnieszka Słowik, and Tomasz Mach. "Pathogenesis of Hepatic Encephalopathy." Gastroenterology Research and Practice 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/642108.

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Hepatic encephalopathy can be a serious complication of acute liver failure and chronic liver diseases, predominantly liver cirrhosis. Hyperammonemia plays the most important role in the pathogenesis of hepatic encephalopathy. The brain-blood barrier disturbances, changes in neurotransmission, neuroinflammation, oxidative stress, GABA-ergic or benzodiazepine pathway abnormalities, manganese neurotoxicity, brain energetic disturbances, and brain blood flow abnormalities are considered to be involved in the development of hepatic encephalopathy. The influence of small intestine bacterial overgrowth (SIBO) on the induction of minimal hepatic encephalopathy is recently emphasized. The aim of this paper is to present the current views on the pathogenesis of hepatic encephalopathy.

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