scholarly journals Hyperammonemia Is Associated with Increasing Severity of Both Liver Cirrhosis and Hepatic Encephalopathy

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Abidullah Khan ◽  
Maimoona Ayub ◽  
Wazir Mohammad Khan
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Ammonia Level ◽  
Chronic Viral Hepatitis ◽  
The Body ◽  
Chronic Liver ◽  
Chi Squared ◽  
Serum Ammonia Level ◽  
The Mean ◽  
Serum Ammonia

Background. Hyperammonemia resulting from chronic liver disease (CLD) can potentially challenge and damage any organ system of the body, particularly the brain. However, there is still some controversy regarding the diagnostic or prognostic values of serum ammonia in patients with over hepatic encephalopathy, especially in the setting of acute-on-chronic or chronic liver failure. Moreover, the association of serum ammonia with worsening Child-Pugh grade of liver cirrhosis has not been studied. Objective. This study was conducted to solve the controversy regarding the association between hyperammonemia and cirrhosis, especially hepatic encephalopathy in chronically failed liver. Material and Methods. In this study, 171 cirrhotic patients had their serum ammonia measured and analyzed by SPSS version 16. Chi-squared test and one-way ANOVA were applied. Results. The study had 110 male and 61 female participants. The mean age of all the participants in years was 42.33±7.60. The mean duration (years) of CLD was 10.15±3.53 while the mean Child-Pugh (CP) score was 8.84±3.30. Chronic viral hepatitis alone was responsible for 71.3% of the cases. Moreover, 86.5% of participants had hepatic encephalopathy (HE). The frequency of hyperammonemia was 67.3%, more frequent in males (N=81, z-score = 2.4, and P<0.05) than in females (N=34, z-score = 2.4, and P<0.05), and had a statistically significant relationship with increasing CP grade of cirrhosis (χ2(2) = 27.46, P<0.001, Phi = 0.40, and P<0.001). Furthermore, serum ammonia level was higher in patients with hepatic encephalopathy than in those without it; P<0.001. Conclusion. Hyperammonemia is associated with both increasing Child-Pugh grade of liver cirrhosis and hepatic encephalopathy.

scholarly journals Factors associated with non-response to lactulose therapy in cirrhotic patients with minimal hepatic encephalopathy

2018 ◽  
Vol 12 (1) ◽  
pp. 15-21
Author(s):  
Shireen Ahmed ◽  
Md Golam Azam ◽  
Indrajit Kumar Datta ◽  
Md Nazmul Hoque ◽  
Tareq M Bhuiyan
Keyword(s):  
Hepatic Encephalopathy ◽  
Arterial Pressure ◽  
Minimal Hepatic Encephalopathy ◽  
Ammonia Level ◽  
Response To Treatment ◽  
Psychometric Tests ◽  
Cirrhotic Patients ◽  
Serum Ammonia Level ◽  
The Mean ◽  
Serum Ammonia

Background and objectives: Minimal hepatic encephalopathy (MHE) impairs health related quality of life and predicts overt hepatic encephalopathy (HE) in cirrhotic patients. Lactulose is effective in the treatment of MHE. But the response to lactulose treatment depends on several factors. This study was aimed to find out the contributing factors to non-response to lactulose therapy.Materials and methods: The study was carried out at the BIRDEM general hospital from September, 2013 to March, 2015. Sixty patients were enrolled to assess the response of lactulose therapy in cirrhotic patients with MHE. MHE was diagnosed based on abnormal psychometric tests namely, number connection test (NCT), digit symbol test (DST) and high serum ammonia level. A daily dose of 30-60 ml of lactulose was given to all patients for one month. The response to treatment with regard to MHE was determined after one month using defined criteria. The response was graded as responder and non-responder.Results: The mean age of the study population was 57.0±10.3 years. Out of 60 cases, 46 (77%) were male and 39 (65%) had diabetes. Out of 60 enrolled MHE cases, 16 (27%) had Child-Turcotte-Pugh-A (CTP-A) score and 44 (73%) belonged to CTP-B & C category. Out of 60 MHE cases, 23 (38.3%) showed improvement in their MHE status based on normalization of psychometric tests and reduction of serum ammonia level to ≤32 μmol/L. Age, gender and diabetes were not associated with the response to lactulose therapy. Low baseline arterial pressure was significantly (p=0.003) associated with non-response to lactulose treatment. The mean baseline ammonia level was higher significantly among the nonresponders compared to the responders (83.6±21.4 μmol/L vs 58.8±19.8 μmol/L, p<0.001). Compared to responders, low serum sodium and potassium and raised serum bilirubin levels of non-responders at baseline were found significantly (p<0.05) associated with non-response to one month of lactulose treatment. Initial hemoglobulin, peripheral leucocyte and platelet counts did not have any effect on the response to lactulose treatment in MHE cases.Conclusions: The status of MHE in patients with cirrhosis improved by one-month treatment with lactulose. Baseline low arterial pressure, hyperammonemia, hypokalemia and hyponatremia were major contributors to non-response to lactulose therapy. The findings of the study would be useful in treating patients of cirrhosis with MHE.IMC J Med Sci 2018; 12(1): 15-21

scholarly journals Serum ammonia is a strong prognostic factor for patients with acute-on-chronic liver failure

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chenxia Hu ◽  
Kaizhou Huang ◽  
Lingfei Zhao ◽  
Fen Zhang ◽  
Zhongwen Wu ◽  
...  
Keyword(s):  
Prognostic Factor ◽  
Liver Failure ◽  
Ammonia Level ◽  
Chronic Liver ◽  
Hbv Reactivation ◽  
Chronic Liver Failure ◽  
Short Term ◽  
Plasma Ammonia ◽  
Serum Ammonia Level ◽  
Serum Ammonia

Abstract Ammonia is thought to be central to the pathogenesis of hepatic encephalopathy (HE), but its prognostic role in acute-on-chronic liver failure (ACLF) is still unknown. We aimed to determine the association between serum ammonia level and short-term prognosis in ACLF. Furthermore, we performed an in-depth evaluation of the independent effect of serum ammonia level on the short-term prognosis of hepatitis B virus (HBV) reactivation-induced ACLF patients. We identified 174 patients as part of prospective observational studies in patients with ACLF. Plasma ammonia levels were measured on admission, and several prognostic scores were used to determine the prognostic effect of ammonia. The 28-day patient survival was determined. Receiver operating characteristic analysis was used to identify the cut-off points for ammonia values, and multivariable analysis was performed using the Cox proportional hazard regression model. Plasma ammonia was significantly higher in nonsurvivors (83.53 ± 43.78 versus 67.13 ± 41.77 µmol/L, P = 0.013), and ACLF patients with hyperammonemia had significantly higher 28-day mortality than those without hyperammonemia. Ammonia was also closely related to ACLF grade (P < 0.001) and organ failure, including liver (P = 0.048), coagulation (P < 0.001) and brain (P < 0.001). HBV reactivation serves as the main precipitating factor in the ACLF population. Subgroup analysis showed that ammonia is also a strong prognostic factor in the HBV reactivation-induced ACLF population. Ammonia level is closely correlated with failure of other organs and is an independent risk factor for mortality in ACLF and the special population defined as HBV reactivation-related ACLF. Based on the results from our study, we measured serum ammonia in the population with ACLF, which strongly indicates their prognosis. It serves as an important biomarker and a therapeutic target.

Serum Ammonia Level for the Evaluation of Hepatic Encephalopathy

JAMA ◽  
2014 ◽  
Vol 312 (6) ◽  
pp. 643 ◽  
Author(s):  
Phillip S. Ge ◽  
Bruce A. Runyon
Keyword(s):  
Hepatic Encephalopathy ◽  
Ammonia Level ◽  
Serum Ammonia Level ◽  
Serum Ammonia

scholarly journals Hepatic Encephalopathy due to Congenital Multiple Intrahepatic Portosystemic Venous Shunts Successfully Treated by Percutaneous Transhepatic Obliteration

2016 ◽  
Vol 10 (3) ◽  
pp. 701-705 ◽  
Author(s):  
Shinsuke Takenaga ◽  
Kenichi Narita ◽  
Yo Matsui ◽  
Kunihiko Fukuda
Keyword(s):  
Hepatic Encephalopathy ◽  
Conservative Therapy ◽  
Transcatheter Embolization ◽  
Ammonia Level ◽  
Hepatic Trauma ◽  
Underlying Liver Disease ◽  
Consciousness Disorder ◽  
Serum Ammonia Level ◽  
Serum Ammonia

Hepatic encephalopathy due to intrahepatic portosystemic venous shunts (IPSVS) in a non-cirrhotic condition is rare. Here we report a rare case of a patient with congenital multiple IPSVS successfully treated by percutaneous transhepatic obliteration. The patient was a 67-year-old woman who presented to our hospital with progressive episodes of consciousness disorder and vomiting. Laboratory tests revealed hyperammonemia (192.0 μg/dL), and computed tomography revealed multiple IPSVS in both lobes. There was no evidence of underlying liver disease or hepatic trauma. Transcatheter embolization for IPSVS was performed because conservative therapy was not sufficiently effective. After endovascular shunt closure, hepatic encephalopathy improved. The serum ammonia level normalized during the 5-year follow-up period. Thus, transcatheter embolization may be an effective therapy for patients with symptomatic and refractory IPSVS. Careful follow-up is necessary for portal hypertension-related complications after transcatheter embolization for IPSVS.

Type B hepatic encephalopathy due to a congenital superior mesenteric-caval shunt: clinical scenario and therapeutic approach

MedPharmRes ◽  
2020 ◽  
Vol 4 (4) ◽  
pp. 10-14
Author(s):  
Hoang Huu Bui ◽  
Van Huy Vo ◽  
Viet Khac Doan Tran ◽  
Viet Quoc Dang ◽  
Long Duy Cong Tran ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Hepatic Encephalopathy ◽  
Neuropsychiatric Symptoms ◽  
Elevated Serum ◽  
Rare Condition ◽  
Ammonia Level ◽  
Type B ◽  
Serum Ammonia Level ◽  
Computed Topography ◽  
Serum Ammonia

Type B Hepatic encephalopathy (HE) due to a congenital extra-hepatic porto-systemic shunt is an extremely rare condition. We report the case of a 57-year-old woman, with recurrent episodes of confusion and neuropsychiatric symptoms, who had an elevated serum ammonia level and a superior mesenteric-caval shunt documented on abdominal computed topography (CT) scan. There was no evidence of cirrhosis or portal hypertension. A diagnosis of non-cirrhotic, non-portal hypertension hepatic encephalopathy was made after excluding other causes of confusion and cognitive impairment. The patient was successfully treated by radiologically guided endovascular shunt closure and during 9 months follow up, her neuropsychiatric symptoms did not recur and repeated serum ammonia level results were normal.

scholarly journals A Hepatitis C Virus-Associated Decompensated Cirrhotic Patient Who Showed the Disappearance of Hepatic Encephalopathy, Ascites, and Pleural Effusion by Antiviral Therapy with Sofosbuvir/Velpatasvir

2021 ◽  
Vol 15 (1) ◽  
pp. 436-442
Author(s):  
Kazuo Tarao ◽  
Akito Nozaki ◽  
Hirokazu Komatsu
Keyword(s):  
Liver Cirrhosis ◽  
Hepatitis C Virus ◽  
Hepatic Encephalopathy ◽  
Hepatitis C ◽  
Pleural Effusion ◽  
Ammonia Level ◽  
Albumin Level ◽  
Hcv Rna ◽  
Direct Acting ◽  
Serum Ammonia

Oral direct-acting antivirals (DAAs) are the main therapy for hepatitis C virus (HCV)-associated liver disease in Japan. Moreover, many DAAs include an indication for compensated liver cirrhosis. However, patients with decompensated HCV-associated cirrhosis have hitherto not been indicated for therapy with DAAs. Recently, a new DAA, sofosbuvir/velpatasvir (SOF/VEL), was indicated for decompensated HCV-associated cirrhotic patients. Actually, it has been shown to eradicate HCV in many cases. However, it is not clear whether hepatic encephalopathy, ascites, and pleural effusion in patients with decompensated HCV-associated cirrhosis disappear by SOF/VEL treatment. Recently, we encountered a decompensated HCV-associated cirrhosis patient who showed the disappearance of hepatic encephalopathy, ascites, and pleural effusion with marked improvement of serum ammonia level, albumin level, prothrombin time, and platelet count after the eradication of HCV by the administration of SOF/VEL. Her consciousness was cloudy and it took many hours for the preparation of each meal just before SOF/VEL treatment, but after the disappearance of HCV-RNA by the therapy, her consciousness became clear and she could prepare meals in a short time. This case suggests the possibility of improvement from decompensated HCV-associated liver cirrhosis to compensated liver cirrhosis with disappearance of hepatic encephalopathy, ascites, and pleural effusion by SOF/VEL therapy.

scholarly journals Seizure Disorder Exacerbated by Hepatic Encephalopathy: A Case Report

2019 ◽  
Vol 7 (10) ◽  
pp. 1669-1671 ◽  
Author(s):  
Aneesa Rahman Chowdhury ◽  
Erin Marcus
Keyword(s):  
Hepatic Encephalopathy ◽  
Ammonia Level ◽  
Seizure Disorder ◽  
Unique Case ◽  
Case Presentation ◽  
Liver Decompensation ◽  
History Of ◽  
Serum Ammonia Level ◽  
Ct Brain ◽  
Serum Ammonia

BACKGROUND: Hepatic encephalopathy is a serious complication of cirrhosis that presents with a variety of neuropsychiatric abnormalities, including disorientation, asterixis, and coma. Seizures are an uncommon and potentially dangerous complication of hepatic encephalopathy. We present a unique case of a 42-year-old female with a history of well-controlled seizure disorder suddenly become refractory to anticonvulsant therapy following the development of hepatic encephalopathy secondary to liver decompensation. CASE PRESENTATION: A 42-year-old female presented to our hospital following a seizure accompanied by loss of consciousness, urinary incontinence, and the prolonged postictal state. She reports her seizures were initially well-controlled with Levetiracetam 500 mg twice a day but recently began experiencing seizures every other day despite up-titration of Levetiracetam to 1500 mg twice a day over a few weeks. On arrival, her serum ammonia level was 116 μmol/L. CT brain was negative while CT liver was consistent with cirrhotic morphology. An electroencephalogram revealed irregular, diffuse, delta/theta slowing consistent with mild to moderate encephalopathy. The patient was started on lactulose 40mg and Rifaximin 550 mg twice a day. Her symptoms of disorientation and lethargy resolved over 3 days. CONCLUSION: Though uncommon, hepatic encephalopathy should be considered in patients presenting with convulsions, especially if there is a known history of liver disease. Until the underlying liver issues are addressed, patients may not respond to traditional anti-convulsant therapy for their seizures.

Hepatic Encephalopathy

2017 ◽  
Author(s):  
Bret Alvis ◽  
Amy Robertson
Keyword(s):  
Hepatic Encephalopathy ◽  
Elevated Serum ◽  
Hepatic Function ◽  
Ammonia Level ◽  
Definitive Treatment ◽  
Deep Coma ◽  
Anesthetic Considerations ◽  
Serum Ammonia Level ◽  
Serum Ammonia ◽  
Rule Out

Hepatic encephalopathy is a complication of both acute and chronic liver failure. The disease can range from mild cognitive deficits to deep coma. Ammonia accumulation and inflammation are the two most accepted causes of hepatic encephalopathy. It is important to confirm an elevated serum ammonia level and rule out alternative causes of neurological derangements. Nonabsorbable disaccharides are the mainstay of treatment; however, the only definitive treatment is liver transplantation. Pertinent anesthetic considerations include avoiding benzodiazepines, understanding the implications of diminished hepatic function, and recognizing factors that may contribute to increased intracranial cerebral pressure. Proper assessment and management of the patient presenting with hepatic encephalopathy will be discussed.

scholarly journals Splenic Vein Embolization Using Coil Anchors and Prophylactic Occlusion of a Hepatofugal Collateral for Hepatic Encephalopathy due to Splenorenal Shunt: Technical Note and Literature Review

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Masayoshi Inoue ◽  
Toshihiro Tanaka ◽  
Hiroyuki Nakagawa ◽  
Tetsuya Yoshioka ◽  
Kimihiko Kichikawa
Keyword(s):  
Hepatic Encephalopathy ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Treatment Strategies ◽  
Ammonia Level ◽  
Technical Note ◽  
Splenorenal Shunt ◽  
Interventional Treatment ◽  
Serum Ammonia Level ◽  
Serum Ammonia

Purpose. Interventional treatment strategies for patients with encephalopathy due to splenorenal shunt remain controversial. Portosplenic blood flow separation by occluding the splenic vein could avoid the complication of severe portal hypertension, but it would require repeated reintervention due to recurrence of symptoms. This paper describes occlusion of the splenic vein using coil anchors and prophylactic embolization of a collateral hepatofugal vessel with no recurrence of hyperammonemia.Materials and Methods. A 51-year-old woman with severe cirrhosis had hepatic encephalopathy due to a large splenorenal shunt. The serum ammonia level was 132 μg/dL. Via a transileocolic approach, the splenic vein was completely embolized with 0.035-inch metallic coils using coil anchors while preserving the splenorenal shunt. In addition, one of the collateral vessels of the portal vein, the retrogastric vein, was also embolized prophylactically.Results. After this procedure, the serum ammonia level decreased immediately to 24 μg/dL. The portal venous pressure increased by only 1.5 mmHg. Hepatic encephalopathy had not been observed for 25 months after the procedure, and neither retention of ascites nor worsening of esophageal varices and liver function was observed.Conclusion. This procedure appears to be safe and effective for hepatic encephalopathy caused by a splenorenal shunt.

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