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Charmaine A Stewart

Publications and source records attributed to Charmaine A Stewart.

5 recordsLinked to original sources
PubMed2005

Hepatic encephalopathy: a dynamic or static condition.

Hepatic encephalopathy (HE) is a neuropsychiatric disorder associated with portal hypertension. The mechanism of this disorder is still being characterized and the management has relied primarily on lowering the amount of ammonia present in the gastrointestinal tract or reversing liver disease by replacing the diseased liver. It is, however, not established that all the effects of hepatic encephalopathy are reversed by liver transplantation. In this review, we have outlined the mechanisms underlying HE and the pros and cons of reversibility of HE.

Cognition Disorders↗
PubMed2005

Neuroimaging in hepatic encephalopathy.

Hepatic encephalopathy (HE) is a poorly defined, complex neuropsychological disorder that often accompanies portal hypertension. Although the mechanisms underlining HE and the characterization of HE are still under investigation, the information derived from functional neuroimaging of patients with HE complemented by laboratory investigation and neuropsychological and neurophysiological studies have clarified much of the neuroanatomical defects. In this review, we have provided an outline of the understood mechanisms of HE and the associated findings on neuroimaging.

Ammonia↗
PubMed2004

Ascites after liver transplantation--a mystery.

Ascites after liver transplantation, although uncommon, presents a serious clinical dilemma. The hemodynamic changes that support the development of ascites before liver transplantation are resolved after transplant; therefore, persistent ascites (PA) after liver transplantation is unexpected and poorly characterized. The aim of this study was to define the clinical factors associated with PA after liver transplantation. This was a retrospective case-control analysis of patients who underwent liver transplantation at the University of Pennsylvania. PA occurring for more than 3 months after liver transplantation was confirmed by imaging studies. PA was correlated with multiple recipient and donor variables, including etiology of liver disease, preoperative ascites, prior portosystemic shunt (PS), donor age, and cold ischemic (CI) time. There were 2 groups: group 1, cases with PA transplanted from November 1990 to July 2001, and group 2, consecutive, control subjects who underwent liver transplantation between September 1999 and December 2001. Both groups were followed to censoring, May 2002, or death. Twenty-five from group 1 had ascites after liver transplantation after a median follow-up of 2.6 years. In group 1 vs group 2 (n = 106), there was a male predominance 80% vs 61% (P =.10) with similar age 52 years; chronic hepatitis C virus (HCV) was diagnosed in 88% vs 44% (P <.0001); preoperative ascites and ascites refractory to treatment were more prevalent in group 1 (P =.0004 and P =.02, respectively), and CI was higher in group 1, (8.5 hours vs 6.3 hours, P =.002). Eight of the 25 (group 1) had portal hypertension with median portosystemic gradient 16.5 mm Hg (range, 16-24). PS was performed in 7 of 25 cases, which resulted in partial resolution of ascites. The development of PA after liver transplantation is multifactorial; HCV, refractory ascites before liver transplantation, and prolonged CI contribute to PA after liver transplantation.

Ascites↗
PubMed2003

Grading portal gastropathy: validation of a gastropathy scoring system.

OBJECTIVES: The specific aim of this study was to independently evaluate the reproducibility and validity of the Baveno portal hypertensive gastropathy (PHG) grading system. METHODS: This is a prospective study of 100 consecutive patients with cirrhosis and portal gastropathy. An endoscopy was performed at entry on all subjects and on 70 patients during follow-up (median 15 months). Interobserver reproducibility was assessed by the kappa statistic. Patients with PHG-related bleeding were compared with those without bleeding. The relationship of PHG-related bleeding to the PHG score was assessed by a receiver operating characteristic curve and by multiple logistic regression analysis. RESULTS: Interobserver agreement about the presence of the mosaic pattern and red marks was high (kappa >0.75). However, the agreement about the extent of the lesion was poorer (kappa = 0.4-0.45). There was a stepwise increase in PHG-related bleeding risk with increasing PHG scores. Multiple logistic regression confirmed that the PHG score independently correlated with PHG-associated bleeding (OR = 2.5, 90% CI = 1.4-4.6, p < 0.009). During follow-up, red marks developed de novo in one of 70 patients. The severity of red marks worsened in five of 25 patients, whereas they disappeared in eight of 62 individuals. Nodular lesions in the antrum were found in five subjects. The risks of recurrent bleeding during follow-up were related to severe PHG scores (>4), presence of gastric antral vascular ectasia, and nodular lesions in the antrum. CONCLUSIONS: The PHG scoring system is reproducible and accurately reflects the risks of PHG-related bleeding in patients with cirrhosis.

Adult↗