scholarly journals Fatal Nonhepatic Hyperammonemia in ICU Setting: A Rare but Serious Complication following Bariatric Surgery

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Gyanendra Acharya ◽  
Sunil Mehra ◽  
Ronakkumar Patel ◽  
Simona Frunza-Stefan ◽  
Harmanjot Kaur
Keyword(s):  
Bariatric Surgery ◽  
Normal Liver ◽  
Liver Function Tests ◽  
Altered Mental Status ◽  
Ammonia Level ◽  
Gastric Bypass Procedure ◽  
History Of ◽  
Serum Ammonia Level ◽  
Pedal Edema ◽  
Serum Ammonia

Bariatric surgery is well established in reducing weight and improving the obesity-associated morbidity and mortality. Hyperammonemic encephalopathy following bariatric surgery is rare but highly fatal if not diagnosed in time and managed aggressively. Both macro- and micronutrients deficiencies play a role. A 42-year-old Hispanic female with a history of Roux-en-Y Gastric Bypass Procedure was brought to ED for progressive altered mental status. Physical exam was remarkable for drowsiness with Glasgow Coma Scale 11, ascites, and bilateral pedal edema. Labs showed elevated ammonia, low hemoglobin, low serum prealbumin, albumin, HDL, and positive toxicology. She remained obtunded despite the treatment with Narcan and flumazenil and the serum ammonia level fluctuated despite standard treatment with lactulose and rifaximin. Laboratory investigations helped to elucidate the etiology of the hyperammonemia most likely secondary to unmasking the functional deficiency of the urea cycle enzymes. Hyperammonemia in the context of normal liver function tests becomes diagnostically challenging for physicians. Severe hyperammonemia is highly fatal. Early diagnosis and aggressive treatment can alter the prognosis favorably.

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.

scholarly journals Recurrent noncirrhotic hyperammonemia causing acute metabolic encephalopathy in a patient with a continent ileocecal pouch: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
T. M. Skipina ◽  
S. Macbeth ◽  
E. L. Cummer ◽  
O. L. Wells ◽  
S. Kalathoor
Keyword(s):  
Emergency Department ◽  
Metabolic Acidosis ◽  
Mental Status ◽  
Rare Case ◽  
Liver Function Tests ◽  
Altered Mental Status ◽  
Potassium Citrate ◽  
Metabolic Encephalopathy ◽  
History Of ◽  
Normal Urine

Abstract Introduction Acute encephalopathy, while a common presentation in the emergency department, is typically caused by a variety of metabolic, vascular, infectious, structural, or psychiatric etiologies. Among metabolic causes, hyperammonemia is relatively common and typically occurs in the setting of cirrhosis or liver dysfunction. However, noncirrhotic hyperammonemia is a rare occurrence and poses unique challenges for clinicians. Case presentation Here we report a rare case of a 50-year-old Caucasian female with history of bladder cancer status post chemotherapy, radical cystectomy, and ileocecal diversion who presented to the emergency department with severe altered mental status, combativeness, and a 3-day history of decreased urine output. Her laboratory tests were notable for hyperammonemia up to 289 μmol/L, hypokalemia, and hyperchloremic nonanion gap metabolic acidosis; her liver function tests were normal. Urine cultures were positive for Enterococcus faecium. Computed tomography imaging showed an intact ileoceal urinary diversion with chronic ileolithiasis. Upon administration of appropriate antibiotics, lactulose, and potassium citrate, she experienced rapid resolution of her encephalopathy and a significant reduction in hyperammonemia. Her hyperchloremic metabolic acidosis persisted, but her hypokalemia had resolved. Conclusion This case is an example of one of the unique consequences of urinary diversions. Urothelial tissue is typically impermeable to urinary solutes. However, when bowel segments are used, abnormal absorption of solutes occurs, including exchange of urinary chloride for serum bicarbonate, leading to a persistent hyperchloremic nonanion gap metabolic acidosis. In addition, overproduction of ammonia from urea-producing organisms can lead to abnormal absorption into the blood and subsequent oversaturation of hepatic metabolic capacity with consequent hyperammonemic encephalopathy. Although this is a rare case, prompt identification and treatment of these metabolic abnormalities is critical to prevent severe central nervous system complications such as altered mental status, coma, and even death in patients with urinary diversions.

Persistently raised aspartate aminotransferase (AST) due to macro-AST in a rheumatology clinic

Diagnosis ◽  
2015 ◽  
Vol 2 (2) ◽  
pp. 137-140 ◽  
Author(s):  
Wycliffe Mbagaya ◽  
Joanne Foo ◽  
Ahai Luvai ◽  
Claire King ◽  
Sarah Mapplebeck ◽  
...  
Keyword(s):  
Liver Function ◽  
Aspartate Aminotransferase ◽  
Normal Liver ◽  
Abdominal Ultrasound ◽  
Liver Function Tests ◽  
Analytical Investigation ◽  
Normal Liver Function ◽  
Rheumatology Clinic ◽  
History Of ◽  
Liver Biopsies

AbstractMacrocomplexes between immunoglobins and aspartate aminotransferase (macro-AST) may result in persistently increased AST concentration. The presence of macro-AST in patients has been implicated in unnecessary investigations of abnormal liver function tests. We report the case of a 44-year-old female who presented to the rheumatology clinic with a 12-months’ history of constant widespread pain affecting her limbs and was found to have an elevated AST concentration. Further information from her GP revealed a 14-years’ history of elevated AST with otherwise normal liver function. Previous abdominal ultrasound and two liver biopsies carried out 2 years apart were normal. This prompted further analytical investigation by the biochemistry department which identified macro-AST as the cause. This case illustrates that persistently raised isolated AST concentration with no other abnormal indices may warrant macroenzyme analysis potentially avoiding unnecessary invasive investigations.

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.

scholarly journals Oxaliplatin-Induced Hyperammonemic Encephalopathy in a Patient with Metastatic Pancreatic Cancer: A Case Report

2017 ◽  
Vol 10 (3) ◽  
pp. 885-889 ◽  
Author(s):  
Takatsugu Ogata ◽  
Hironaga Satake ◽  
Misato Ogata ◽  
Yukimasa Hatachi ◽  
Hisateru Yasui
Keyword(s):  
Pancreatic Cancer ◽  
Nutritional Supplement ◽  
Ammonia Level ◽  
High Concentration ◽  
Hyperammonemic Encephalopathy ◽  
Consciousness Disorder ◽  
Serum Ammonia Level ◽  
Branched Chain ◽  
Gcs Score ◽  
Serum Ammonia

Oxaliplatin-based chemotherapy is widely used to treat advanced cancer. Oxaliplatin-induced hyperammonemic encephalopathy is rarely reported. Here, we report a case of oxaliplatin-induced hyperammonemic encephalopathy occurring after gemcitabine plus oxaliplatin (GEMOX) chemotherapy in a patient with pancreatic cancer. A 76-year-old man received GEMOX regimen as first-line treatment for pancreatic adenocarcinoma with peritoneal dissemination. GEMOX consists of gemcitabine (1,000 mg/m2) and oxaliplatin (100 mg/m2) on day 1, repeated every 2 weeks. The second cycle of GEMOX was administered as planned. However, he appeared to have difficulties with daily activities. Two days later, he visited the emergency room complaining of drowsiness. On examination, the patient had a Glasgow Coma Scale (GCS) score of 14 (E4V4M6), and asterixis was not present. Blood examination revealed a serum ammonia level of 202 µg/dL. The levels of serum hepatic enzymes were only mildly elevated, and the hemoglobin level was typical for this patient. Computed tomography, magnetic resonance imaging, lumbar puncture test, and blood culture showed no abnormality. Based on these results, he was diagnosed with oxaliplatin-induced hyperammonemia. One day after hospitalization, GCS score had significantly decreased to 6 (E1V1M4). His consciousness disorder improved after administration of a nutritional supplement containing a high concentration of branched-chain amino acids for 5 days, and the level of serum ammonia improved to 79 µg/dL. He stated that he could not remember the episode. The findings of this case suggest the importance of examining serum ammonia levels in patients receiving an oxaliplatin-containing regimen who develop disordered consciousness.

The relationship between serum ammonia level and neurologic complications in patients with acute glufosinate ammonium poisoning: A prospective observational study

2017 ◽  
Vol 37 (6) ◽  
pp. 571-579 ◽  
Author(s):  
YS Cha ◽  
H Kim ◽  
Y Lee ◽  
EH Choi ◽  
HI Kim ◽  
...  
Keyword(s):  
Observational Study ◽  
Prospective Observational Study ◽  
Latency Period ◽  
Ammonia Level ◽  
Control Group ◽  
Neurologic Complication ◽  
Neurologic Complications ◽  
Glufosinate Ammonium ◽  
Serum Ammonia Level ◽  
Serum Ammonia

Glufosinate ammonium poisoning can cause neurological complications even after a symptom-free period. We prospectively investigated the predictors of neurologic complications in acute glufosinate ammonium poisoning and the change of serum ammonia level as a predictor of patient’s presence and recovery of neurologic complication. This prospective observational study collected data from consecutive patients diagnosed with acute glufosinate ammonium poisoning between September 2014 and June 2016. Serum ammonia was serially measured. The patients were divided into two groups: the neurologic complication group and the nonneurologic complication group. We also defined 25 other insecticide- or herbicide-poisoned patients as controls. The neurologic complication group included 18 patients (72.0%). The latency period for neurologic complications was within 48-h postingestion. The peak ammonia level was statistically higher in the neurologic complication group than in the control group ( p < 0.001) and the nonneurologic complication groups ( p = 0.001). There was a statistical difference between the nonneurologic complication group and the neurologic complication group ( p = 0.0085) in terms of ingested amount. The peak ammonia was the only predictor for the development of neurologic complications (the optimal cutoff: 90 μg/dL). In patients with mental changes, the mean serum ammonia levels before and after recovery of the mental changes were statistically different ( p = 0.0019). In acute glufosinate ammonium poisoning, serial serum ammonia level measurements are needed and a serum peak ammonia level greater than 90 μg/dL is a predictor of neurologic complications. Also, it is important to treat the hyperammonemia in acute glufosinate ammonium poisoning.

Serum ammonia as an early predictor of in-hospital mortality in patients with glufosinate poisoning

2019 ◽  
Vol 38 (9) ◽  
pp. 1007-1013 ◽  
Author(s):  
J Lee ◽  
Y Lee ◽  
YS Kim ◽  
JG Choi ◽  
TH Go ◽  
...  
Keyword(s):  
Hospital Mortality ◽  
Academic Medical Center ◽  
Multiple Logistic Regression Analysis ◽  
Ammonia Level ◽  
Apache Ii ◽  
Hospital Death ◽  
Glufosinate Ammonium ◽  
Serum Ammonia Level ◽  
Serum Ammonia ◽  
Early Predictor

Background: The mortality rate associated with human glufosinate poisoning is high. We evaluated the usefulness of serum ammonia and sequential organ failure assessment (SOFA) and acute physiology and chronic health evaluation II (APACHE II) scores for early prediction of in-hospital mortality in glufosinate ammonium poisoning. Methods: A prospectively collected pesticide poisoning registry at a single academic medical center was retrospectively analyzed. Data were collected from consecutive patients diagnosed with glufosinate ammonium poisoning between May 2007 and February 2018. The initial serum ammonia level was defined as the highest serum ammonia level measured within 12 h after emergency department (ED) arrival. The SOFA and APACHE II scores were calculated using data obtained within the first 12 h after ED arrival. The patients were divided into survivor and nonsurvivor groups by in-hospital death status. Results: In total, 110 patients were included. Ten patients (9.1%) died in the hospital despite treatment. Median initial serum ammonia level was significantly higher in the nonsurvivor group than in the survivor group (219 (range: 158–792) versus 100.5 (range: 25–317) µg/dL, p < 0.001). Median SOFA and APACHE II scores in the survivor and nonsurvivor groups were 2 (range: 0–10) versus 5 (range: 1–8) ( p = 0.044) and 7 (range: 0–28) versus 16 (range: 8–22) ( p = 0.001), respectively. In the multiple logistic regression analysis, the initial serum ammonia level was the only independent predictor (cutoff value: 151 µg/dL). Conclusion: An initial serum ammonia level >151 µg/dL was an independent early predictor of in-hospital mortality in glufosinate ammonium poisoning.

Hepatitis C infection and chemotherapy toxicity

2017 ◽  
Vol 25 (2) ◽  
pp. 474-480 ◽  
Author(s):  
Amy Ly ◽  
Heather H Cheng ◽  
Laura Alwan
Keyword(s):  
Hepatitis C ◽  
Viral Infection ◽  
Case Reports ◽  
Normal Liver ◽  
Liver Function Tests ◽  
Solid Organ ◽  
Hepatitis C Infection ◽  
Chemotherapy Toxicity ◽  
Palliative Intent ◽  
History Of

There exists little guidance on chemotherapy toxicity management in patients with a history of or active hepatitis C viral infection. We report four cases of patients with solid organ tumors and hepatitis C viral infection, who have experienced severe or unexpected toxicities with chemotherapy. Based on the four case reports, we recommend increased laboratory monitoring for toxicities, initial dose reductions for chemotherapy given with palliative intent, or pre-emptive use of growth factor support, even if the patient presents with normal liver function tests. In this patient population, we also recommend treating active hepatitis C viral infection prior to chemotherapy treatment when possible.

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