Nutrition Issues in Gastroenterology
Nutrition Issues in Gastroenterology
Nutrition Issues in Gastroenterology
Brian E. Lacy
Burr J. Loew
Chronic intestinal pseudo-obstruction (CIP) is a rare, chronic disorder of the luminal gastrointestinal tract. Symptoms and signs suggest a mechanical bowel obstruction, although
in the evaluation of patients with CIP, both routine and specialized tests fail to identify
evidence of mechanical obstruction. Common symptoms include nausea, vomiting, bloating, abdominal distension, and involuntary weight loss. Unfortunately, these symptoms
are non-specific, frequently leading to either misdiagnosis or a delay in diagnosis. Many
patients require parenteral nutrition and a large number of patients require chronic opioids. This review will focus on the etiology, pathogenesis, diagnosis and treatment of
patients with CIP.
INTRODUCTION
hronic intestinal pseudo-obstruction (CIP) is a
rare and potentially life-threatening disorder of
the gastrointestinal tract characterized by symptoms and signs suggestive of mechanical obstruction
but in the absence of a true anatomical lesion. Normal
Brian E. Lacy, Ph.D., M.D. FACG, Associate Professor of Medicine, Dartmouth Medical School, Director,
GI Motility Laboratory, Dartmouth-Hitchcock Medical
Center, Lebanon, NH. Burr J. Loew, M.D., Fellow in
Gastroenterology, Division of Gastroenterology and
Hepatology, Dartmouth-Hitchcock Medical Center,
Lebanon, NH.
CASE 1
DB is a 43-year-old woman referred for further evaluation of abdominal pain, nausea, vomiting, and weight
loss. Her past medical history was notable for an
episode of volvulus 10 years earlier that required right
hemi-colectomy. After surgery, she had alternating
symptoms of constipation and diarrhea and was
labeled with the diagnosis of irritable bowel syndrome
(IBS). Two years ago she had a viral illness with symptoms of nausea, vomiting, diarrhea, fever, myalgias
and arthralgias. All of the symptoms except for her
nausea and vomiting resolved. Her weight dropped
from 100 to 70 lbs. She noticed difficulty swallowing
liquids and solids. She denied symptoms of anorexia
and bulimia, believed that her weight was too low, and
did not exercise. Physical examination revealed a
cachectic woman with a BMI of 13.3. Her abdomen
was moderately distended and tympanitic. Blood tests
were notable for an albumin of 2.2; her electrolytes
were normal as was a TSH. Her hemoglobin was 10
with a normal MCV. She was evaluated by multiple
physicians and underwent a variety of diagnostic tests:
Two separate upper endoscopies were normal
Two separate colonoscopies revealed a patent anastomosis without evidence of obstruction
An abdominal flat plate while acutely ill showed
dilated loops of small intestine with multiple air
fluid levels
A follow-up abdominal x-ray two weeks later
appeared normal
A right upper quadrant ultrasound showed evidence
of prior cholecystectomy but was otherwise normal
Two separate computed tomography (CT) scans of
the abdomen and pelvis were normal other than
demonstrating post-surgical changes
A small bowel follow-through did not show evidence of obstruction however transit was delayed at
four hours
Extensive blood tests, looking for evidence of a connective tissue disorder or autoimmune disorder, were
all normal
An MRI of the brain was normal as well
Esophageal manometry revealed normal lower
esophageal sphincter (LES) resting pressure of 17
mm Hg and complete LES relaxation, but failed peri10
CASE 2
GP is a 55-year-old man sent for a second opinion in
gastroenterology due to symptoms of nausea, vomiting, bloating, and diarrhea. He states that his symptoms began approximately seven years ago. His weight
at that time was 145 lbs. He does not recall any specific precipitating event, but noted the gradual onset of
bloating and diarrhea. He was told that he had lactose
intolerance, although avoiding all dairy products did
not seem to help. He was given the diagnosis of IBS
and was advised to use loperamide on a p.r.n. basis.
This helped his diarrhea somewhat, although he still
had significant bloating. A low fiber diet did not
improve his bloating symptoms. Over the next two-tothree years he noticed the gradual onset of nausea and
vomiting. During the next several years he developed
new symptoms of pyrosis and dysphagia. He was
(continued on page 13)
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CLINICAL PRESENTATION
An analysis by Mann and colleagues found that the
median age of symptom onset was 17 years with a range
of two weeks to 59 years (4). The frequency and sever-
Table 1
Classification of Chronic Intestinal Pseudo-Obstruction
Primary
I. Myopathic
A. Congenital
B. Familial
C. Sporadic
II. Neuropathic
A. Congenital
B. Familial
C. Sporadic
Idiopathic **
Secondary
Collagen Vascular Disease
Primary Systemic Sclerosis
Systemic Lupus Erythematosus
Dermatomyositis/Polymyositis
Periarteritis nodosa
Mixed connective tissue disorder
Rheumatoid Arthritis
Endocrine Disorders
Hypothyroidism/hypoparathyroidism
Diabetes mellitus
Neurological Disorders
Parkinsons Disease
Hirschsprungs Disease
Chagas Disease
Intestinal Hypoganglionosis
Natural History
15
Esophageal involvement
Dysphagia
Esophageal reflux/heartburn
Atypical chest pain
Stomach
Early satiety
Extra-intestinal
Dysuria
Abnormal bladder function
Dilated ureter
Overall, only 11% of CIP patients are asymptomatic between subacute obstructive episodes and do
not require chronic medical treatment. Approximately
20% of patients develop intractable abdominal pain
and become opioid dependent (4).
19
Table 3
Histological differences between myopathic and
neuropathic CIP*
Myopathic
Muscle degeneration
Atrophy and fibrosis of one or both layers of the muscularis
propria
inflammatory cells
Neuropathic
Dense infiltrate of lymphocytes and plasma cells surrounding
myenteric plexus and axons
Fragmentation and loss of axons
Proliferation of glial cells
inflammatory cells
*Some cases may have mixed myopathic and neuropathic histological
findings
Diet
TREATMENT OPTIONS
Chronic intestinal pseudo-obstruction remains a challenge to treat. Therapy for secondary causes of CIP
(i.e., scleroderma) should focus on treating the underlying disorder. This often includes correcting electrolyte abnormalities, managing dehydration, treating
infections, using immunosuppressant agents for
patients with collagen vascular diseases, initiating a
20
Table 4
Treatment of Idiopathic or Primary CIP
Erythromycin, a macrolide antibiotic that acts as an agonist to
the motilin receptor, can be given either orally or intravenously.
Doses in the range of 50200 mg orally, or 50100 mg intravenously (iv), approximately 30 minutes before meals, have
been shown to be effective in accelerating gastric emptying and
improving symptoms of CIP (16).
Cisapride, a mixed 5HT-4 receptor agonist/5HT-3 receptor
antagonist, is not available for routine clinical use, although it
can be obtained in very limited circumstances. Cisapride was
removed from the market in July 2000 because of drug interactions leading to an increased risk of cardiac arrhythmias.
Metoclopramide, a commonly used anti-emetic, is a dopamine
antagonist that exerts its prokinetic effects by increasing acetylcholine release. Metoclopramide is commonly given as 1020
mg orally or IV 30 minutes before meals and at bedtime. Mild
adverse reactions include fatigue, somnolence, anxiety, jitteriness, or depression may occur. More severe adverse events
including extrapyramidal side effects (i.e., tardive dyskinesia) are
fortunately, uncommon.
Domperidone is similar to metoclopramide in that it acts as an
antagonist at dopamine receptors. Domperidone does not readily cross the blood-brain-barrier, and therefore, does not have
the potential for the central nervous system side affects that
metoclopramide have. Doses range between 1020 mg orally 30
minutes before meals and at bedtime. Domperidone is not FDA
approved for use in the United States.
Octreotide, a long acting somatostatin analogue, stimulates
small intestine motility when given in low doses. It is most effective in patients who have a neuropathic process as the underlying etiology of their CIP, since it requires the presence of smooth
muscle in order to be effective. It is usually given in doses of
2550 g subcutaneously after both the morning and evening
meals.
Tegaserod, a specific 5-HT4 receptor agonist, improves gastric
emptying, colonic transit, and orocecal transit time, and was
approved for use only in women with irritable bowel syndrome
and constipation (17). Unfortunately, tegaserod is now available
only for life-threatening emergencies due to concerns that it may
increase the risk of cardiovascular complications (18).
Lubiprostone, a chloride channel activator approved for the
treatment of chronic constipation and women with IBS and constipation, has not been studied in CIP patients (19).
Nutrition Support
Enteral Feeding. If dietary changes are unsuccessful
resulting in unmet nutritional requirements and continued weight loss, then enteral nutrition support is the next
step. In a retrospective study, Scolapio and colleagues
demonstrated that patients with CIP can generally be
managed with EN using a standard formula (13). A trial
of nasogastric or nasojejunal feeding should be tried
prior to placement of a more permanent percutaneous
feeding tube. If patients are able to tolerate fiber-free EN
with few symptoms and regular bowel movements (it is
important for the clinician to find out the normal stool
habits of the individual patient), then consideration can
be given for placement of a percutaneous gastrostomy
or gastro-jejunostomy tube, or direct placement of a
jejunostomy tube, to bypass a dysfunctional stomach. If
delayed gastric emptying is present, then direct feeding
of the small intestine is preferred, unless the patient
would benefit from having a gastric venting port. Continuous or cycled EN (1012 hours overnight) is often
better tolerated than bolus feedings. A trial of elemental
feeding prior to PN is warranted.
21
Table 5
Medications Commonly Used to Treat Nausea in CIP
Antihistamines
Dimenhydrinate (Dramamine)
Promethazine (Phenergan)
Meclizine (Antivert)
Cyclizine (Marezine)
Diphenhydramine (Benadryl)
Anticholinergics
Scopolamine
Phenothiazines
Prochlorperazine (Compazine)
Chlorpromazine (Thorazine)
Promethazine (Phenergan)
Butyrophenones
Haloperidol (Haldol)
Droperidol (Inapsine)
Dopaminergic Antagonists
Metoclopramide (Reglan)
Domperidone (Motilium)
Serotonin Receptor Antagonists
Ondansetron (Zofran)
Granisetron (Kytril)
Dolasetron (Anzemet)
Miscellaneous
Lorazepam (Ativan)
Prednisone
Dexamethasone
Dronabinol (Marinol)
Trimethobenzamide (Tigan)
Ginger
Prokinetic Agents
Regardless of whether the underlying process is myopathic or neuropathic in nature, all patients with CIP
have disordered gastrointestinal tract motility. Multiple prokinetic agents have been used in an attempt to
promote normal intestinal motility; however, there are
few investigational studies available to demonstrate
the efficacy of any of these agents in CIP (Table 4).
Antibiotics
Intestinal stasis may lead to small intestine bacterial
overgrowth and diarrhea, with resultant malabsorption,
weight loss and the development of multiple vitamin
deficiencies. Rotating antibiotics may relieve symptoms of diarrhea and bloating and improve the nutritional status in many patients with CIP. No controlled
trials have been performed to determine which antibiotics are best, however many clinicians have patients
use a different antibiotic every month for seven-to-10
days over a five-to-six month cycle. (Please see the
following review for more information about small
bowel bacterial overgrowth: DiBaise JK. Small Intestinal Bacterial Overgrowth: Nutritional Consequences
and Patients at Risk. Practical Gastroenterology,
2008;32(12):15).
Antiemetics
Decompression Measures
Decompression of distended intestinal segments via
intermittent nasogastric suction, rectal tubes, or
endoscopy is helpful for many patients. Given a lack
of clinical studies addressing this issue, there are no
firm guidelines on when such intervention should be
undertaken. Decompression of the distended intestinal
segment may include a venting enterostomy. These
are typically placed in the stomach, although some
patients with feeding J-tubes also use them for venting
22
CONCLUSION
CIP is a rare, disabling, and potentially life-threatening
neuromuscular disorder of the digestive tract simulating mechanical obstruction in the absence of an
anatomical lesion. As demonstrated by the two cases
provided above, it often goes unrecognized and misdiagnosed for long periods of time given its nonspecific
symptoms, clinical overlap with more common conditions, and the absence of a biological marker of disease. Maintaining a high index of suspicion together
with a careful history and physical examination can
guide appropriate further diagnostic testing to arrive at
the correct diagnosis. Unfortunately, except for cases
in which a secondary cause can be identified, management is largely supportive. Ensuring appropriate nutrition and managing complications from CIP or its
associated treatments is paramount. n
PRACTICAL
GASTROENTEROLOGY
R E P R I N T S
References
1. Dudley HAF, Sinclair ISR, McLaren IF, et al. Intestinal pseudoobstruction. J R Coll Surg Edin, 1958;3:206-217.
2. Di Lorenzo C. Pseudo-obstruction: Current Approaches. Gastroenterology, 1999;116: 980-987.
3. Schwankovsky L, Mousa H, Rowhani A, et al. Quality of life outcomes in congenital chronic intestinal pseudo-obstruction. Dig
Dis Sci, 2002;47:1965-1968.
4. Mann SD, Debinski HS, Kamm MA. Clinical characteristics of
chronic idiopathic intestinal pseudo-obstruction in adults. Gut,
1997;41:675-681.
5. Krishnamurthy S, Schuffler MD. Pathology of neuromuscular
disorders of the small intestine and colon. Gastroenterology,
1987;93:610-639.
6. Debinski HS, Kamm MA, Talbot IC, et al. DNA viruses in the
pathogenesis of sporadic chronic idiopathic intestinal pseudoobstruction. Gut, 1997;41:100-106.
7. Stanghellini V, Camilleri M, Malagelada JR. Chronic idiopathic
intestinal pseudo-obstruction: clinical and intestinal manometric
findings. Gut, 1987;28:5-12.
24
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