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HIGHLIGHTS FROM MEDICAL GRAND ROUNDS EDY E. SOFFER, MD Dr. Soffer is a member of the Department of Gastroenterology at the Cleveland Clinic. His major clinical and research interests are in the area of motor dysfunction of the stomach, small bowel, and colon Gastric and intestinal dysmotility syndromes Rule out mechanical obstruction before considering a diagnosis of gastroparesis D isorders of motility of the stomach and small intestine are common, and patients often present with a variety of nonspecific symptoms, including nau- sea, abdominal pain, bloating, and vomiting. The challenge for the internist is determine the nature and extent of motility dysfunction. GASTRIC DYSMOTILITY Gastric motor dysfunction comprises two main disorders: accelerated and delayed gastric emp- tying. Accelerated gastric emptying is seen almost without exception after gastric surgery, specifically vagotomy and drainage procedures that result in dumping. Typical symptoms occur after meals and include nausea, bloating, pain, diarrhea, and vasomotor symptoms such as syncope, flushing, and palpitations. Most office-based internists are more like- ly to encounter delayed gastric emptying (also known as gastroparesis). Typical symptoms of gastroparesis include early satiety, nausea and vomiting (mostly postprandial), abdominal pain, and weight loss. Individually, none of these symptoms indicates delayed gastric emp- tying, but when they occur together, the like- lihood of gastroparesis is strong. However, before one considers a diagnosis of gastroparesis, mechanical obstruction must be ruled out. Benign or malignant pancreatic disease or mesenteric ischemia should be sus- pected if weight loss and pain are the predom- inant symptoms. Causes of gastroparesis Gastroparesis can be a feature of many disor- ders and syndromes, such as collagen vascular diseases and metabolic and endocrine disor- ders, and an effect of medications such as anti- cholinergics or narcotics. However, most cases encountered in clinical practice arc caused by vagotomy, diabetes, or unknown factors. Vagotomy. Postsurgical gastroparesis occurs less frequently now that antibiotic treatment for Helicobacter pylori infection and potent acid-suppressing medicines have replaced surgery for treating peptic ulcer. Most patients who undergo a vagotomy and a pyloroplasty or gastroenterostomy experience little alteration in gastric emptying of solids, although the initial phase of liquid emptying can be accelerated, resulting in dumping. Fewer than 3% of postgastrectomy patients experience clinically significant gastroparesis. Diabetic gastroparesis. Altered gastroin- testinal function is common among patients with longstanding type 1 diabetes mellitus, par- ticularly those with complications such as retinopathy, peripheral neuropathy, or nephropathy. Delayed emptying of solids is common in diabetic patients and is frequently asymptomatic. Among symptomatic patients, gastroparesis frequently runs a fluctuating course, with episodes of pronounced symptoms interspersed with relatively symptom-free intervals. Detecting gastroparesis is especially important in patients with diabetes because it interferes with nutrient delivery to the small intestine and can result in fluctuating blood glucose levels. CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 64 • NUMBER 2 FEBRUARY 1997 6 9

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Page 1: Gastric and intestinal dysmotility syndromes...Gastric and intestinal dysmotility syndromes Rule out mechanical obstruction before considering a diagnosis of gastroparesis D isorders

HIGHLIGHTS FROM MEDICAL GRAND ROUNDS

EDY E. SOFFER, MD Dr. Soffer is a member of the Department of Gastroenterology at the Cleveland Clinic. His major clinical and research interests are in the area of motor dysfunction of the stomach, small bowel , and colon

Gastric and intestinal dysmotility syndromes

Rule out mechanical obstruction before considering a diagnosis of gastroparesis

Disorders of motility of the stomach and small intestine are common, and patients often present with a variety of nonspecific symptoms, including nau-sea, abdominal pain, bloating, and

vomiting. T h e challenge for the internist is determine the nature and extent of motility dysfunction.

GASTRIC DYSMOTILITY

Gastric motor dysfunction comprises two main disorders: accelerated and delayed gastric emp-tying.

Accelerated gastric emptying is seen almost without exception after gastric surgery, specifically vagotomy and drainage procedures that result in dumping. Typical symptoms occur after meals and include nausea, bloating, pain, diarrhea, and vasomotor symptoms such as syncope, flushing, and palpitations.

Most office-based internists are more like-ly to encounter delayed gastric emptying (also known as gastroparesis). Typical symptoms of gastroparesis include early satiety, nausea and vomiting (mostly postprandial), abdominal pain, and weight loss. Individually, none of these symptoms indicates delayed gastric emp-tying, but when they occur together, the like-lihood of gastroparesis is strong.

However, before one considers a diagnosis of gastroparesis, mechanical obstruction must be ruled out. Benign or malignant pancreatic disease or mesenteric ischemia should be sus-pected if weight loss and pain are the predom-inant symptoms.

Causes of gastroparesis Gastroparesis can be a feature of many disor-ders and syndromes, such as collagen vascular diseases and metabolic and endocrine disor-ders, and an effect of medications such as anti-cholinergics or narcotics. However, most cases encountered in clinical practice arc caused by vagotomy, diabetes, or unknown factors.

Vagotomy. Postsurgical gastroparesis occurs less frequently now that antibiotic treatment for Helicobacter pylori infection and potent acid-suppressing medic ines have replaced surgery for treating peptic ulcer. Most patients who undergo a vagotomy and a pyloroplasty or gastroenterostomy experience little alteration in gastric emptying of solids, although the initial phase of liquid emptying can be accelerated, resulting in dumping. Fewer than 3 % of postgastrectomy patients experience clinically significant gastroparesis.

Diabetic gastroparesis. Altered gastroin-testinal function is common among patients with longstanding type 1 diabetes mellitus, par-ticularly those with complications such as retinopathy, peripheral neuropathy, or nephropathy. Delayed emptying o f solids is common in diabetic patients and is frequently asymptomatic.

Among symptomatic patients, gastroparesis frequently runs a fluctuating course, with episodes of pronounced symptoms interspersed with relatively symptom-free intervals. Detecting gastroparesis is especially important in patients with diabetes because it interferes with nutrient delivery to the small intestine and can result in fluctuating blood glucose levels.

CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 64 • NUMBER 2 FEBRUARY 1997 6 9

Page 2: Gastric and intestinal dysmotility syndromes...Gastric and intestinal dysmotility syndromes Rule out mechanical obstruction before considering a diagnosis of gastroparesis D isorders

HIGHLIGHTS FROM MEDICAL GRAND ROUNDS n

Gastroparesis in diabetic patients interferes with nutrient delivery and can result in fluctuating blood glucose levels

Gastric motor abnormalities in diabetes include loss or disruption of antral migrating motor complex ( M M C ) activity, fasting and postprandial antral hypomotility, and abnor-malities of the proximal small intestine. The etiology of gut dysmotility in diabetes is not clear, but evidence exists for autonomic ner-vous system and enteric nervous system dys-function, in addition to the metabolic effects of hyperglycemia.

Idiopathic gastroparesis. Many patients with gastroparesis have no primary abnormali-ty. Most are young women. Some of these patients report having a viral-like illness before the onset of gastric symptoms. Specific viral infections, such as cytomegalovirus and herpes simplex, are known to cause gastropare-sis in immunocompromised patients; the gas-troparesis resolves quickly following antiviral therapy.

Diagnosis T h e most important diagnostic step for a patient who presents with nausea, vomiting, bloating, or postprandial abdominal pain is to rule out mechanical obstruction, either of the stomach or the small intestine. After mechan-ical obstruction has been ruled out, gastric motor function is best evaluated by a radioscintigraphic solid-emptying study. This test, in which the patient consumes a meal that contains a radioisotope, allows for a sim-ple, sensitive, quantitative, noninvasive mea-sure of solid-phase emptying.

TREATMENT OF GASTRIC DYSMOTILITY

Dietary changes If radioscintigraphy reveals delayed gastric emptying, the initial phase of treatment should be directed toward dietary changes.

Small, frequent meals, preferably in liq-uid form, are encouraged because gastric emp-tying is volume-dependent, and liquids empty faster than solids.

A low-fat diet is helpful because fat is the most potent inhibitor of gastric emptying.

A low'residue diet is also important because the disturbed motor activity prevents

nondigestable food from emptying, and can result in bezoar formation.

Pharmacologic therapy Available agents that stimulate gastric empty-ing are not ideal, because they have an incon-sistent effect on the motor function of the stomach. T h e ideal prokinetic agent for gas-troparesis would target the defined pathophys-iology, enhance stomach function (rather than contractions), and cause few side effects.

Cisapride is the most commonly used pro-kinetic agent because of its good safety profile. It is usually given at 10 mg four times a day at least 30 minutes before meals and at bedtime. Cisapride has a very good safety profile and minimal side effects.

Metoclopramide, a dopamine agonist, has efficacy equal to that of cisapride. However, up to 2 0 % of patients have side effects, the most troubling of which are related to extrapyrami-dal manifestations and mood changes.

Erythromycin is not particularly effective as a prokinetic agent when given in oral form.

Cholinergic agents are rarely used because of their high incidence of side effects.

If tolerance develops to one of these pro-kinetic agents, I would increase the dose or add another prokinetic agent.

Surgical therapy If dietary and pharmacologic methods fail in patients with medical causes of gastroparesis, a feeding jejunostomy may be attempted.

Subtotal gastrectomy and Roux-en-Y gas-trojejunostomy can be helpful in severe post-surgical cases of gastroparesis, but are not effec-tive in cases caused by medical diseases.

Gastric pacing, which requires the place-ment of stimulating electrodes on the stom-ach, is experimental and its value has yet to be established.

• INTESTINAL DYSMOTILITY

Small-bowel motor activity and its control mechanisms are quite similar to those of the antrum of the stomach. Normal small bowel motility serves to mix nutrients with digestive

7 0 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 64 • NUMBER 2 FEBRUARY 1997

Page 3: Gastric and intestinal dysmotility syndromes...Gastric and intestinal dysmotility syndromes Rule out mechanical obstruction before considering a diagnosis of gastroparesis D isorders

enzymes, allows sufficient time for absorption, and propels undigestible parts of the chyme distally to the colon. Symptoms of intestinal dysmotility can be quite similar to those of gas-troparesis, though abdominal distention and changes in bowel habits indicate small-bowel disease. T h e disease is typically chronic.

Diagnosis There is no adequate functional study of the small bowel that is analogous to solid phase gastric emptying studies of the stomach. A diagnosis of intestinal dysmotility must rely on symptoms, plain abdominal radiographs, bari-um studies, and intestinal manometry. As in gastric dysmotility, mechanical obstruction should be ruled out in the evaluation of patients with symptoms of intestinal dysmotil-ity-

Flat abdominal radiographs are not sensi-tive enough to distinguish obstruction from pseudo-obstruction, and contrast studies may be needed to exclude mechanical obstruction. If pseudo-obstruction is suspected, I would pro-ceed to manometry.

Manometry. Certain abnormal patterns on abdominal manometry (eg, lack of response to food) are consistent with visceral neuropathy. Manometry has particular value in patients with unexplained symptoms and a negative work-up. In such cases, normal findings on manometry help to exclude dysmotility.

Treatment Treatment of intestinal dysmotility includes a low-fat diet, antibiotics (cycled to prevent bac-terial overgrowth), and prokinetic agents. In

general, prokinetic agents are less effective in treating intestinal dysmotility than in gastro-paresis.

In refractory or severe, intermittent intestinal dysmotility, a venting jejunostomy is helpful. Every attempt should be made to use the small bowel by infusion of liquid formulas including elemental preparations. Total par-enteral nutrition may be required with bowel failure. Intestinal transplantation and pacing are still experimental. •

• SUGGESTED READING

A n u r a s S . I n t e s t i n a l p s e u d o o b s t r u c t i o n s y n d r o m e . A n n u R e v M e d 1 9 8 8 ;

3 9 : 1 - 1 5 .

C h a u d h u r i T K , F ink S . U p d a t e : p h a r m a c e u t i c a l s a n d gastr ic e m p t y i n g .

A m J G a s t r o e n t e r o l 1 9 8 0 ; 8 5 : 2 2 3 - 2 3 0 .

J a n s s e n s J , P e e t e r s T L , V a n t r a p p e n G , e t al. I m p r o v e m e n t ol gastric e m p -

tying in d i a b e t i c gastroparesis by e r y t h r o m y c i n . N Engl J M e d 1 9 9 0 ;

3 2 2 : 1 0 2 8 - 1 0 3 1 .

M a l a g e l a d a J R , R e e s W D W , Mazzotta L J , G o V L W . G a s t r i c m o t o r abnor -

mal i t i e s i n d i a b e t i c a n d p o s t v a g o t o m y gastroparesis : Effect ol m e i o c l o -

p r a m i d e a n d b e t h a n e c h o l . G a s t r o e n t e r o l o g y 1 9 8 0 ; 7 8 : 2 8 6 - 2 9 3 .

M a l m u d L S , F i sher R S , K n i g h t L C , R o c k E . S c i n i t ¡ g r a p h i c e v a l u a t i o n ol

gas t r i c e m p t y i n g . S e m N u c l M e d 1 9 8 2 ; 12:1 1 6 - 1 2 6 .

M i n a m i H . M c C a l l u m RW. T h e physiology a n d p a t h o p h y s i o l o g y of gas-

t r i c e m p t y i n g in h u m a n s . G a s t r o e n t e r o l o g y 1 9 8 9 ; 8 6 : 1 5 9 2 - 1 6 1 0 .

S c h u f f l e r M D , Baird H W , F l e m i n g C R , et al. I n t e s t i n a l p s e u d o o b s t r u c t i o n

as t h e p r e s e n t i n g m a n i f e s t a t i o n of smal l cel l c a r c i n o m a of t h e lung. A n n

I n t e r n M e d 1 9 8 3 ; 9 8 : 1 2 9 - 1 34.

S o f f e r E E , T h o n g s a w a t S . T h e c l i n i c a l value of d u o d c n a l - j c j u n a l m a n o m -

etry: Its usefulness in t h e diagnosis a n d m a n a g e m e n t of pa t i en ts with gas-

t r o i n t e s t i n a l s y m p t o m s . Dig Dis S c i 1 9 9 6 ; 4 1 : 8 5 9 - 8 6 3 .

S u m m e r s R W , A n u r a s S , G r e e n J . J e j u n a l m a n o m e t r y p a t t e r n s in h e a l t h ,

par t ia l i n t e s t i n a l o b s t r u c t i o n , a n d p s e u d o o b s t r u c t i o n . G a s t r o e n t e r o l o g y

1 9 8 3 ; 8 5 : 1 2 9 0 - 1 3 0 0 .

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