| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Clinical Observations |
1 Department of Radiology, Hospital of the University of Pennsylvania, 3400
Spruce St., Philadelphia, PA 19104.
2 Present address: Department of Radiology, University of California, San
Francisco, Medical Center, San Francisco, CA.
Received October 17, 2007;
accepted after revision December 14, 2007.
Address correspondence to M. S. Levine
(marc.levine{at}uphs.upenn.edu).
Abstract
 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
CONCLUSION. The hyperirritable stomach was characterized on barium studies in 15 patients by rapid emesis of ingested barium, a collapsed stomach with little or no retained debris or fluid, and normal emptying of residual barium into nondilated duodenum and proximal jejunum. Fourteen (93%) of these 15 patients had extraintestinal causes of nausea and vomiting, and 13 (93%) of 14 with clinical follow-up had marked improvement or resolution of symptoms after treatment. Radiologists therefore should evaluate the stomach and duodenum even after rapid emesis of ingested barium in patients with nausea and vomiting to differentiate a hyperirritable stomach from mechanical or functional gastrointestinal obstruction.
Keywords: barium studies • fluoroscopy • hyperirritable stomach • nausea • vomiting
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
We have encountered a subset of patients with severe nausea and vomiting in whom barium studies caused early and rapid emesis of much of the ingested barium, and subsequent images revealed a collapsed stomach with normal emptying of residual barium into nondilated duodenum and proximal jejunum. We have termed this constellation of findings the "hyperirritable" stomach, postulating that it results from extraintestinal causes of nausea and vomiting. The purpose of our study was to characterize the clinical and radiographic features of a hyperirritable stomach and to determine whether this condition is associated with extraintestinal causes of nausea and vomiting in the absence of gastric outlet obstruction, gastroparesis, or intestinal obstruction or ileus.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
All 15 patients with nausea and vomiting had single-contrast upper gastrointestinal tract examinations to determine if their symptoms were caused by mechanical gastric outlet obstruction or small-bowel obstruction, and all of the studies were terminated prematurely because of rapid emesis of much of the ingested barium from the stomach. Thus, only a limited number of views were obtained. The studies were performed by residents or fellows or by one of three experienced gastrointestinal radiology attending physicians and all were interpreted by the radiology attending physicians. All of the studies were performed with 50% weight/volume (w/v) barium (Entrobar, Lafayette Pharmaceuticals) and digital fluoroscopic equipment (Diagnost 76, Philips Medical Systems, or Sirescope, Siemens Medical Solutions) and all included fluoroscopic evaluation and digital spot images. IV glucagon was not administered to any of these patients.
The images from these examinations were reviewed retrospectively by two of the authors (both gastrointestinal radiologists with 24 and 22 years of experience, respectively) to determine the degree of gastric distention (distended, normal caliber, or collapsed), the presence or absence of retained debris or fluid in the stomach, and the presence or absence of barium in the duodenum or proximal jejunum (if barium was present, the duodenum and proximal jejunum were classified as dilated or normal in caliber). A collapsed stomach was defined as a considerably less than normal-caliber stomach with conspicuous rugal folds, whereas a distended stomach was defined as a greater than normal-caliber stomach with a smooth, bowed contour and effaced rugal folds. The available images were also reviewed for evidence of gastric outlet obstruction or small-bowel obstruction and for large ulcers, masses, or other gross abnormalities in the stomach, duodenum, or proximal small bowel.
Medical records were reviewed by one author to determine the character (bilious vs nonbilious, bloody vs nonbloody, and relationship to meals), severity, and duration of nausea and vomiting and the presence or absence of other associated symptoms. Medical records were also reviewed to determine if these patients were taking medications or had extraintestinal conditions that predispose to the development of nausea and vomiting. Six patients (40%) underwent upper endoscopy a mean interval of 20 days (range, 1-30 days) before or after the barium studies, and the endoscopic findings were also reviewed. Finally, treatment and patient course were reviewed to determine whether correction of the underlying conditions responsible for nausea and vomiting led to improvement or resolution of symptoms in these patients during their initial hospital admission. Long-term follow-up data were not available.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
Radiographic Findings
Spot images from the upper gastrointestinal tract examinations in these 15
patients—after rapid emesis of much of the ingested barium—showed
residual barium outlining the rugal folds of a collapsed stomach with varying
amounts of barium in nondilated duodenum and proximal jejunum (Figs.
1 and
2). None of the patients had
findings of gastric outlet obstruction (i.e., gastric dilatation with retained
debris or fluid diluting residual barium in the stomach) before or after
emesis of barium, and none had findings of small-bowel obstruction (i.e.,
dilated proximal small bowel). No large ulcers or masses were seen in the
stomach or duodenum on these limited views. Finally, no major discrepancies
were found between the original radiologic reports and our retrospective
review of the images.
|
|
Predisposing Factors for Nausea and Vomiting
Four patients (27%) were taking pharmacologic agents that cause nausea and
vomiting, including narcotics in two (oxycodone and acetaminophen [Percocet,
Endo Pharmaceuticals] in one and an unspecified narcotic in the other) and
chemotherapy in two (mitomycin [Mutamycin, Bristol-Myers Squibb]) for bladder
cancer in one and antiviral agents (interferon alfa-2b [Intron A, Schering]
and ribavirin [Rebetol, Schering]) after a liver transplant in one. Five
patients (33%) had acute infectious conditions associated with nausea and
vomiting, including Candida species fungemia in one, a psoas abscess
related to Crohn's disease in one, Clostridium difficile colitis in
one, Escherichia coli cystitis in one, and soft-tissue cellulitis in
one. The latter two patients also were taking phenytoin (Dilantin,
Parke-Davis) for seizure disorders. Five patients (33%) had other conditions
associated with nausea and vomiting, including acute intermittent porphyria in
one, renal calculi with colic in one, acute renal failure in one, progressive
liver metastases in one, and acute gastroenteritis in one. The remaining
patient (7%) had nausea and vomiting of unknown cause.
Treatment and Course
Treatment with pharmacologic agents was stopped in the four patients who
were being treated with narcotics and chemotherapy that had been thought to be
causing nausea and vomiting; two of these patients were also treated with
antiemetic agents (promethazine [Phenergan, Wyeth Pharmaceuticals] in one and
ondansetron [Zofran, GlaxoSmithKline] in one). The nausea and vomiting
resolved in three of these four patients and markedly improved in one. The
five patients with acute infectious conditions underwent treatment with
antimicrobial agents (caspofungin [Cancidas, Merck] for Candida
species fungemia, fluconazole [Diflucan, Pfizer] for a psoas abscess,
vancomycin [Vancocin, ViroPharma] and metro nidazole [Flagyl, Pfizer] for
C. difficile colitis, sulfamethoxazole-trimethoprim [Bactrim, Roche]
for E. coli cystitis, and doxycycline [Vibramycin, Pfizer] for
soft-tissue cellulitis); three of these five patients were also treated with
antiemetic agents (promethazine, ondansetron, and prochlorperazine [Compazine,
Glaxo SmithKline]). The nausea and vomiting resolved after treatment in two of
these five patients and markedly improved in three. The patient with renal
calculi underwent mechanical lithotripsy of the stones, and the patients with
acute intermittent porphyria, acute renal failure, progressive liver
metastases, and acute gastroenteritis were treated with antiemetic agents
(prochlorperazine in two, prochlorperazine and ondansetron in one, and
ondansetron and metoclopramide [Reglan, Wyeth] in one).
The nausea and vomiting resolved after treatment of the patients with acute intermittent porphyria, renal calculi, and progressive liver metastases, and markedly improved after treatment of the patient with acute renal failure, but no further clinical follow-up was available for the patient with acute gastroenteritis after discharge from the emergency department. Finally, the patient with nausea and vomiting of unknown cause had no improvement in symptoms after treatment with antiemetic and hyperkinetic agents (prochlorperazine and metoclopramide). Thus, nausea and vomiting markedly improved (n = 5) or resolved (n = 8) in 13 (93%) of the 14 patients in whom clinical follow-up was available. Twelve (86%) of the 14 patients were discharged from the hospital on a solid diet and two (14%) on a liquid diet.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
In our study, however, we have described a subset of 15 patients with severe nausea and vomiting in which barium examinations revealed a typical constellation of findings that we have designated as the "hyperirritable" stomach. This condition is characterized by rapid (within 30 seconds) emesis of much of the ingested barium, with residual barium in a collapsed stomach and varying amounts of barium in nondilated duodenum and proximal jejunum (Figs. 1 and 2). No patients in this group had findings of gastric outlet obstruction (i.e., gastric dilatation with retained debris or fluid diluting residual barium in the stomach) before or after emesis of barium, and none had findings of small-bowel obstruction.
When this constellation of findings is encountered on barium studies, gastric outlet obstruction and gastroparesis are extremely unlikely because such conditions are usually associated with a dilated rather than a collapsed stomach, often with retained fluid or debris (or even a conglomerate mass of debris, or bezoar) and delayed emptying of barium into the duodenum. Small-bowel obstruction or adynamic ileus is also unlikely because such conditions are usually associated with barium filling dilated jejunal loops rather than normal-caliber or collapsed jejunal loops, as in our patients. Thus, despite rapid emesis of ingested barium from the stomach, mechanical or functional obstruction of the gastrointestinal tract is extremely unlikely when a hyperirritable stomach is encountered on barium studies.
Conversely, clinical follow-up revealed extraintestinal causes of nausea and vomiting in 14 (93%) of our 15 patients with a hyperirritable stomach on barium studies. Major causes included pharmacologic agents (narcotics, chemotherapy, and anticonvulsants) as well as a variety of acute infectious conditions (Candida species fungemia, psoas abscess, C. difficile colitis, E. coli cystitis, and soft-tissue cellulitis), renal calculi, acute gastroenteritis, acute renal failure, progressive liver metastases, and acute intermittent porphyria. In 13 (93%) of the 14 patients with clinical follow-up, the nausea and vomiting markedly improved (n = 5) or resolved (n = 8) after successful treatment of the underlying cause or withholding of the responsible pharmacologic agents combined with antiemetic medications. Our findings therefore suggest that severe nausea and vomiting in patients with a hyperirritable stomach on barium studies results from extraintestinal causes and that successful treatment of the underlying cause almost always leads to marked improvement or resolution of symptoms in these patients.
It is well recognized that nausea and vomiting can result from a host of extraintestinal causes that affect the central nervous system by stimulation of peripheral afferent pathways to the brain or release of neurotransmitters such as serotonin [1, 2]. Some of the most frequent classes of pharmacologic agents causing nausea and vomiting include narcotics, analgesics, anticonvulsants, and chemotherapy [1, 2]. Nausea and vomiting occur in 40-70% of patients on narcotics for pain control and in 20% of patients on chemotherapy (especially cisplatinum) [1, 3]. Other extraintestinal causes of nausea and vomiting include infectious conditions, hormonal disorders, labyrinthine disorders, increased intracranial pressure, seizures, Ménière's disease, metastatic disease, uremia, acute intermittent porphyria, radiation, motion sickness, pregnancy, and psychogenic vomiting [1, 2, 4-8].
Affected individuals are thought to develop nausea and vomiting as a result of various neurologic pathways leading to the area postrema, a chemoreceptor trigger zone (CTZ) in the brain [9]. Because the CTZ is located in the medulla adjacent to the floor of the fourth ventricle, it is exposed to emetic toxins in the blood and CSF. As a result, various neurotransmitters and neuromodulators in these toxins could stimulate the CTZ, which in turn triggers the emetic center in the brain, causing the patient to experience nausea and vomiting [1, 9].
We believe that the hyperirritable stomach is most likely related to sudden disturbances in gastric myoelectric activity and marked gastric contraction similar to that documented in patients with nausea and vomiting caused by motion sickness [10, 11], pregnancy [12], and chemotherapy [13] and in patients with idio-pathic nausea and vomiting [14]. A hyperirritable stomach may therefore develop in a subset of patients with severe nausea and vomiting of extraintestinal origin. Whatever the pathophysiology, rapid emesis of barium on upper gastrointestinal tract examinations in the absence of structural lesions should be considered a positive finding suggesting an extraluminal cause for the patient's nausea and vomiting.
It may seem surprising that we did not encounter more patients with a hyperirritable stomach on barium studies, given that extraintestinal causes of nausea and vomiting are so common. However, many patients with conditions known to cause nausea and vomiting are treated empirically for their symptoms with antiemetic and hyperkinetic agents without undergoing barium studies or other diagnostic tests. Even when these patients are evaluated with barium studies, they may not have a hyperirritable stomach if their symptoms are intermittent or if the neural pathways that stimulate emesis are unrelated to gastric distention.
Our investigation has the inherent limitations of a retrospective study, including selection bias and interpretation bias. It also is limited by lack of adequate clinical follow-up in all patients with a hyperirritable stomach on barium studies. The retrospective nature of our study design also meant that we had to rely on the findings on spot images rather than direct observation at fluoroscopy. A large prospective study is therefore needed to corroborate our observations.
In summary, the hyperirritable stomach is characterized on barium studies by a constellation of findings, including rapid emesis of much of the ingested barium, a collapsed stomach with little or no retained debris or fluid, and normal emptying of residual barium into nondilated duodenum and proximal jejunum. None of our 15 patients with this constellation of findings had gastric outlet obstruction, gastroparesis, or intestinal obstruction or ileus, 14 (93%) of 15 had extraintestinal causes of nausea and vomiting, and 13 (93%) of 14 with clinical follow-up had marked improvement or resolution of symptoms after successful treatment of the underlying condition responsible for the nausea and vomiting. Our experience indicates that a hyperirritable stomach can be diagnosed on barium studies despite rapid emesis of much of the ingested barium and that the appropriate constellation of findings should be highly suggestive of extraintestinal causes of nausea and vomiting. Radiologists therefore should evaluate the stomach and duodenum even after rapid emesis of ingested barium in patients with nausea and vomiting to differentiate a hyperirritable stomach from mechanical or functional gastrointestinal obstruction.
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
