[Dysphagia] reflux

[hillivie423 at adelphia.net (hillivie423@adelphia.net)]

Sorry for such a long post, but I wanted to be thorough in giving you as much information as possible.

I'm working with a 52 year old gentleman who has severe to profound MR, and experiences GERD.  Lately there has been an increase in symptoms.  We hear "wet burps" and he hits his throat with his fist.  Staff members who are most familiar with him suggest that at times this appears to be a behavioral issue, doing it on purpose.  Most of the time, however, he seems uncomfortable and probably not doing it on purpose.  

I am his SLP, and I work closely with the dietician to offer him the best nourishment we can.  The man is fed by staff because he tries to eat too fast and in overly large bite sizes.  He lunges into each bite, and I suspected some aerophagia because of that.  To decrease his hunger and to increase hydration, I recommended offering him free water throughout the day, and a glass of water before coming to the dining room.  The dietician suggested that this might actually be aggrevating the GERD.

Neurological history:  Jacksonian seizures since early childhood.  In June 1999 he suffered a CVA, leaving him with spastic hemiplegia on the right arm and leg.  

GI history:  Initial diagnosis of patulous GE junction with reflux was made in 1982.  A barium swallow in 1993 revealed a normal upper GI with GE reflux again demonstrated.  He consistently demonstrated behavior which would strongly suggest pain associated with ingestion of food.  This included his hitting his throat and chest, with very little evidence of frank aspiration.  An OPMS done in 1993 and in 1996 showed dysphagia with a trace of silent aspiration.  An EGD done in 1993 showed an esophageal web which was dilated.  The stomach and duodenal at that time were described as normal.  Ultrasound of the gallbladder on several occasions have been normal.  In 1995, repeated an EGD which revealed esophagitis and gastritis which was positive for H. pylori.  He was treated for this infestation.  A repeat Upper G.I. Series done in November, 1996, revealed GE reflux with no evidence of hiatal hernia but possible esophageal varices noted on that study.  Another EGD in July, 1997 failed to reveal the presence of esophageal varices but did demonstrate mild gastritis and the presence of a hiatal hernia with biopsy proving Barrett?s esophagus noted at that time.
Early in 1997 he began to demonstrate weight loss and had several episodes of prolonged seizure activity with aspiration pneumonia requiring admission to hospital on three occasions.  EGD revealed the presence of esophagitis and an OPMS showed very little aspiration.  It was felt that the primary problem was that of GERD and a recommendation for Nissen fundoplication was made.
On September 23, 1999, a Nissen fundoplication, incidental appendectomy, jejunal and gastric feeding tube insertion were carried out.  Subsequently he had continued to have some choking with meals and a barium swallow revealed the presence of a very tight Nissen wrap.  An EGD with dilatation of the fundoplication was carried out in February, 2000.  Gastritis was observed on this study.  Subsequent to this dilatation of the Nissen, he had no further choking with his meals and began to eat quite well.  Upper G.I. Series done in January, 2000, and a persistent significant GE reflux was demonstrated on that study.
The jejunostomy tube was left in place following surgery and as he began to eat progressively well he was given supplemental feedings of Jevity Plus through the jejunal feeding tube.  On this regimen he steadily gained weight.  On February 14, 2000, all enteral feeding was discontinued and he was maintained on a pureed bland diet with extra fluid and prune juice.  NOTE:  although extra fluids were ordered, his SLP at that time who was working with his eating skills put him on "pudding thickness liquids."  The J-tube and G-tube were subsequently removed.  He had a gallbladder ultrasound in November 2000 due to an elevated alkaline phosphatase which was normal.  
             In the calendar year 2001-2002 the staff reported ?wet burps? and a consultation was obtained with GI physician.  An EGD was performed in June 2002.  This study revealed a hiatal hernia with an incompetent fundoplication, and biopsies failed to reveal the presence of Barrett?s, and no H.pylori was identified.  With the negative biopsies for Barrett?s, GI physician recommended follow up on a p.r.n. basis and no further surveillance EGDs were indicated.  He advised continuing the post-prandial positioning and Prevacid.  Revision of the fundoplication was discussed, but the client?s general status remains quite good and this revision is not under consideration at present time.   
	Over the calendar year 2003-2004 there were no significant problems associated with GERD such as weight loss or aspiration.  He did have an OPMS in May 2003 which demonstrated normal chewing abilities and called for an upgraded diet texture to include diced diet with ground meat and salads along with soft vegetables and changing from pudding thickness to regular thin liquids.  He tolerated this diet seemingly without any problems, but he changed to a ground diet within a year when he stopped chewing foods.  He had also been changed from Prevacid to Prilosec to meet formulary requirements.

                For the past several months there has been a gradual increase in GERD symptoms, and now the physician has prescribed (1) d/c Boniva, Calcium+ D for a month, then re-evaluate; (2) d/c Prilosec; (3) Prevacid 30 mg, 1 p.o. b.i.d. for GERD ongoing; (4) Mylanta 30cc p.o. now and q.d. at 11 a.m., ongoing; (5) no coffee, caffeine or chocolate; (6) stool OB x 3.

My question:  are we missing anything?  Could we be doing anything more for this gentleman?