Gastrointestinal Issues Which Impede Successful Weight Restoration in Anorexia Nervosa and ARFID

By Philip S. Mehler, MD, FACP, FAED, CEDS

Nutritional rehabilitation and weight restoration are primary goals of the overall treatment for patients with anorexia nervosa (AN) and Avoidant/Restrictive Food Intake Disorder (ARFID). Therefore, medical conditions which interfere with this goal must be considered and successfully treated if a favorable outcome is to be achieved. Three such common gastrointestinal complications, which develop as a result of the marked weight loss of AN and ARFID, are gastroparesis, superior mesenteric artery (SMA) syndrome, and diarrhea. They will be reviewed in order to enable clinicians, caring for these patients, to definitively address these potential impediments to successful weight restoration.

Gastroparesis

Gastroparesis refers to delayed emptying of the stomach due to impairment of the antral portion of the stomach’s normal contractions. This in turn, causes reduced grinding of the food and an overall slowing of the normal rate of the egress of food from the stomach. Therefore, as the food eaten during the course of a day abnormally accumulates in the stomach, the patient with gastroparesis experiences predictable feelings of fullness, nausea, bloating and early satiety during meals along with non-descript mild left upper quadrant abdominal discomfort which may impede refeeding.  While weight restoration will almost always resolve this problem, medications can be temporarily utilized to hasten gastric emptying. Some commonly used medications to treat gastroparesis are metoclopramide and azithromycin. Metoclopramide has the additional benefit of being an antiemetic but is associated rarely with the development of tardive dyskinesia. Azithromycin can prolong the QTc interval on the EKG. Therefore, before starting it and a few days later, it is recommended to repeat the EKG to ensure a normal QTc interval. A nuclear medicine gastric emptying study, which is the gold standard for the diagnosis of gastroparesis, can be obtained to confirm the diagnosis of gastroparesis, but is not often needed given how common this complaint is in patients with AN and ARFID, with moderate or greater degrees of weight loss.

A second gastrointestinal issue which develops in patients with AN and ARFID and can impede refeeding is known as the superior mesenteric artery (SMA) syndrome. This develops as a direct result of the weight loss which accompanies AN and ARFID. SMA syndrome causes compression of the third portion of the duodenum. The compression occurs with weight loss because normally there is a fat pad which cushions the SMA and presents its lateral movement in the abdominal cavity.  When there is significant weight loss, there is atrophy of the fat pad; this in turn allows for medial migration of the SMA, which in turn now constricts the lumen of the duodenum and blocks the passage of food through the small intestine on its normal path to the large intestine.  As food then backs up from this point of obstruction, the patient experiences crampy upper abdominal pains, bloating, nausea and even vomiting of undigested food within approximately fifteen minutes of initiating their eating.

SMA syndrome should be suspected when a patient with anorexia nervosa, of moderately severe weight loss or greater, complains of the aforementioned symptoms during the early stages of their refeeding program.  One can presumptively make the diagnosis in the proper clinical setting, but it might be best to definitively prove its presence by obtaining a CT scan of the abdomen with oral and intravenous contrast, and specifically requesting that the radiologist carefully look at the angle size between the SMA and the aorta.  Normally, the SMA forms an approximately 45°angle (range 38°-65°) as it branches off the aorta.  When the angle decreases to less than 25°, due to loss of the fat pad and the third portion of the duodenum is compressed, SMA syndrome symptoms ensue.

Treatment for SMA syndrome is a temporary change in the patients diet toward softer and more liquid calories.  Surgical intervention is rarely, if ever, indicated.  The treatment also includes close collaboration with a registered dietician to amend the dietary plan.  Specifically, this involves dividing the dairy caloric prescription into smaller more frequent meals in addition to the softer foods or it may involve changing to an entirely oral liquid diet.  Passage of a nasogastric (NG) tube may at times be necessary, or even less commonly, insertion of a nasojejunal (NJ) tube past the point of obstruction.  Generally with just 5-10 pounds of weight gain, the fat pad is reconstituted and the SMA is again pushed back to its more lateral normal position, removing the compression on the duodenum.

An additional gastrointestinal factor which can impede and frustrate the refeeding plan, for patients with AN and ARFID, is the advent of diarrhea during the early stages of refeeding. Certainly in this day and age, first and foremost, an infectious etiology must be excluded. Parasites, such as Giardia, are the most common infectious agents causing diarrhea of 1 week or less and must also be excluded. Parasitic diarrhea is much less common in industrialized countries. C. difficile causes recurrent diarrhea among patients taking antibiotics in health care settings and must always be considered, especially with its increasing virulence worldwide.

Once infectious causes have been thoughtfully ruled out, other noninfectious pathologies to consider include celiac disease, irritable bowel syndrome and other forms of functional bowel disease. The evaluation for persistent diarrhea early on in the refeeding period includes a complete history and physical examination and diagnostic testing for infectious and noninfectious etiologies responsible for the patients’ symptoms. But, in the end a common additional cause to consider, which is really a diagnosis of exclusion, is a malabsorption state which accompanies marked weight loss in patients with A.N. Basically, it is directly caused by the weight loss and subsequent loss of small intestinal absorptive surface. Therefore, in essence, a new state of short-gut syndrome ensues due to the reduced intestinal absorptive area from villous atrophy, wherein calories are normally absorbed. There is actually one blood test which can be done to confirm the diagnosis, called a diamine oxidase level; it will be abnormally low in patients with AN, if the diarrhea is due to malabsorption. The treatment for this malabsorption state, which ultimately will correct itself with weight gain and nutritional rehabilitation, is to alter the diet so that the reduced absorptive area does not adversely impact weight restoration. Once again, this requires a close working relationship with an informed registered dietician to add more complex carbohydrates, to increase the protein content of the diet to reduce the amount of liquid ingested during the meal and to substitute six smaller meals instead of the traditional larger breakfast, lunch and dinner meals.