1.
The relationship between serum ammonia level and neurologic complications in patients with acute glufosinate ammonium poisoning: A prospective observational study.
Cha, YS, Kim, H, Lee, Y, Choi, EH, Kim, HI, Kim, OH, Cha, KC, Lee, KH, Hwang, SO
Human & experimental toxicology. 2018;(6):571-579
Abstract
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.
2.
Submucosal hematoma: a new distinctive sign during emergency upper digestive endoscopy for ammonia ingestion.
Gelu-Simeon, M, Chuong, AP, Saliba, F, Thiery, G, Laurent, M, Vilain, C, Borel, M, Amaral, L, Alexis, M, Saint-Georges, G, et al
BMC gastroenterology. 2018;(1):92
Abstract
BACKGROUND Submucosal hematoma has never been associated with caustic injuries. Long-term follow-up of patients who ingested ammonia is not well known and ammonia ingestion is rare. METHODS In a Single-center observational study, prospective data were collected from 2009 to 2013, in patients over the age of 14 years old referred for ammonia ingestion. The emergency and follow-up endoscopic data and the outcome were reported. RESULTS Ammonia ingestion occurred in 43 patients. Submucosal hematoma of the gastric wall was a distinctive endoscopic sign observed in 15 (34.8%) cases. Oropharyngeal lesions were present in 30 (69.8%) patients, which was associated with ingestion with suicidal intent in 18 cases. Mild and severe endoscopic lesions (grade IIB to IIIB) were found in 16 (37.2%) cases with 10 (23.3%) cases presenting submucosal hematoma at initial endoscopy. A complete spontaneous gastric healing was frequently observed in 36 (83.7%) cases. In 11 cases with submucosal hematoma, a favourable outcome was observed with a medical treatment, however 6 of these patients had severe endoscopic lesions initially. CONCLUSIONS Submucosal hematoma of the gastric wall is an endoscopic sign occurring frequently in ammonia ingestion. Submucosal hematoma should be distinguished from necrosis in order to avoid false misclassification in favour of more severe lesions, which would lead to an abusive surgery.
3.
Predictors of infection in viral-hepatitis related acute liver failure.
Shalimar, , Kedia, S, Sharma, H, Vasudevan, S, Sonika, U, Upadhyaya, AD, Acharya, SK
Scandinavian journal of gastroenterology. 2017;(12):1413-1419
Abstract
OBJECTIVE Infections are common and associated with complications and mortality in acute liver failure (ALF). The temporal relationship between ammonia and infection in ALF patients is unclear. We aimed to evaluate the predictors of infection and its relationship with arterial ammonia levels. MATERIALS AND METHODS Consecutive ALF patients hospitalized between January 2004 and December 2015, without signs of infection at/within 48 h of admission, were included. Occurrence of infection after 48 h was documented and ammonia levels were estimated for five consecutive days. Multivariate logistic regression analysis was used to assess factors associated with development of infection. Generalized estimating equations (GEE) were used to evaluate five-day time trend of ammonia in patients with and without infection. RESULTS Of 540 consecutive patients, 120 were infected at admission/within 48 h and were excluded. Of the rest 420 patients, 144 (34.3%) developed infection after 48 h and 276 (65.7%) remained non-infected. Infected patients had higher mortality than non-infected patients (61.8% vs 40.0%, p < .001). On multivariate analysis, presence of cerebral edema(HR 2.049; 95%CI, 1.30-3.23), ammonia level on day 3 of admission (HR 1.006; 95%CI, 1.003-1.008), and model for end stage liver disease (MELD) score (HR 1.051; 95%CI, 1.026-1.078) were associated with development of infection. GEE showed group difference in serial ammonia values between infected and non-infected patients indicating lack of ammonia decline in infected patients. CONCLUSIONS Cerebral edema, elevated ammonia on day 3, and higher MELD score predict the development of infection in ALF. Ammonia persists at high levels in infected patients, and elevated ammonia on day 3 is associated with complications and death.