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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastroparesis is characterized by delayed gastric emptying in the absence of obstruction. Common symptoms include nausea, vomiting, and abdominal pain. Severe gastroparesis might result in recurrent hospitalizations, malnutrition, and significant mortality. Patients failing medical therapy are often considered for a variety of surgical interventions, the efficacy of which is not well studied. This review summarizes available literature on surgical interventions in gastroparesis. A MEDLINE search for the period from 1966 to 2002 was performed to identify all English language literature regarding surgical interventions in gastroparesis. Therapies reviewed were gastrostomy, jejunostomy, gastric pacing/stimulation, and gastrectomy or surgical drainage procedures. Candidate studies involved human subjects and included surgical series or trials. The search was conducted independently by two authors and discrepancies resolved by consensus opinion. Seventeen articles met inclusion criteria. These included series reporting on gastrostomy (2), jejunostomy (3), gastric stimulation (2), and gastrectomy for postsurgical (6), diabetic (3), and idiopathic (1) gastroparesis. All trials were unblinded, uncontrolled case series or retrospective reviews. Methodologic differences did not allow for pooled analysis. Completion gastrectomy seems to provide symptom relief in postsurgical gastroparesis. Benefits of gastric surgery for other forms of gastroparesis are not adequately studied. Gastrostomy might provide symptom improvement, but only 26 subjects in two trials were evaluable. Jejunostomy improved symptoms and nutrition in 32 evaluable subjects in three trials but had significant complications. Gastric neurostimulation improves symptoms of nausea and vomiting, but therapeutic gain beyond placebo has not been demonstrated. Limited data exist concerning surgical therapies of gastroparesis. Completion gastrectomy seems effective for postsurgical gastroparesis, but a cautious approach is warranted before surgical therapies in diabetic or idiopathic gastroparesis are used.
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PMID:A systematic review of surgical therapy for gastroparesis. 1457 55

Currently, electrical stimulation is utilized to treat morbid obesity, gastroparesis, and diaphragmatic paralysis. Although this technology is in its infancy, numerous case reports and small series appear throughout the literature. Furthermore, electrical stimulation is not relegated to only academic centers and tertiary referral centers. As these technologies continue to evolve and alter the treatment of several different pathophysiologic processes, the general surgeon needs to understand the technical aspects of these devices and their potential complications. This paper presents the management of a gastroparetic patient with chronic abdominal pain following the successful placement of gastric pacing wires. A 45-year-old female with idiopathic gastroparesis underwent laparoscopic placement of gastric pacing wires without complications. Four months postoperatively, she presented with chronic left upper quadrant abdominal pain. Her nausea and vomiting had dissipated and she was tolerating a regular diet. Abdominal and pelvic computed tomography (CT) was normal except for the presence of a generator and pacing wires. Ultimately, she required a diagnostic laparoscopy and an upper endoscopy. The upper endoscopy was normal. The diagnostic laparoscopy showed a wide adhesive band from the seromuscular tunnel of the pacing wires to the abdominal wall in the left upper quadrant. The band was lysed and an omental patch was sutured over the insertion site of the wires. On postoperative day 1, the patient was pain-free and discharged home on a regular diet. This case presents an unusual complication of electrical pacing wires. This patient experienced somatic pain due to an adhesive band from her pacing wires to the abdominal wall. Based on the findings of this case, an omental patch was placed on top of the seromuscular electrode tunnel in order to prevent adhesions and potentially persistent abdominal wall pain.
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PMID:Laparoscopic revision of gastric pacing wires. 1524 74

Celiac axis compression syndrome has generated much controversy since its original description in 1963. The main symptoms are postprandial epigastric abdominal pain, regurgitation of undigested food, and weight loss, all of which are caused by gastric ischemia from impingement of the celiac axis by the median arcuate ligament of the diaphragm. These symptoms are seen in other common disorders such as chronic mesenteric ischemia and gastroparesis. This makes the diagnosis of celiac axis compression syndrome a true challenge for the clinician. We present data on three patients successfully treated. The pre- and postoperative studies clearly demonstrate a resolution of the condition. The duplex ultrasound images clearly show variable compression on the celiac axis. The angiogram presented shows a classic image of the disease. A review of the data has enabled us to develop an algorithm for the diagnosis of this disease.
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PMID:Reversible gastroparesis: functional documentation of celiac axis compression syndrome and postoperative improvement. 1667 60

Gastroparesis, or delayed gastric emptying, is a common cause of chronic nausea and vomiting as seen in a gastroenterology practice. Diabetic, postsurgical, and idiopathic causes remain the three most common forms of gastroparesis. In addition to nausea and vomiting, symptoms of gastroparesis may include early satiety, postprandial fullness, and abdominal pain. Physiologic changes that may explain symptoms in patients with gastroparesis, in addition to delayed gastric emptying, include impaired fundic accommodation, antral hypomotility, gastric dysrhythmias, pylorospasm, and perhaps visceral hypersensitivity. Diagnosis of gastroparesis is best determined using a radioisotope-labeled solid meal with scintigraphic imaging for at least 2 hours, and preferably 4 hours, postprandially. Most commonly, a 99mTc sulfur colloid-labeled egg sandwich with imaging at 0, 1, 2, and 4 hours is used. Extension of the gastric emptying test to 4 hours improves the accuracy of the test, but unfortunately, this is not commonly performed at many centers. Emptying of liquids remains normal until the late stages of gastroparesis and is less useful. The aims of treatment should be to control symptoms and maintain adequate nutrition and hydration. Patients should be advised to eat small meals and to limit their intake of fat and fiber. Additional dietary recommendations may include increasing caloric intake in the form of liquids. For diabetic patients, control of blood glucose levels is important, as symptom exacerbation is frequently associated with poor glycemic control. Specific treatment often begins with metoclopramide, 10 mg, up to four times daily, after a discussion of possible side effects with the patient. An antiemetic agent, such as prochlorperazine, 5 to 10 mg orally or 25 mg by suppository, can be added on an as-needed basis every 4 to 6 hours to control nausea. If these antiemetic medications are not effective, or if side effects develop, orally dissolving ondansetron, 8 mg every 8 to 12 hours, can be tried on an as-needed basis. If this regimen is unsuccessful, then alternative prokinetic agents--erythromycin, 125 mg, or tegaserod, 6 mg, prior to meals--can be tried. For cases refractory to these treatments, referral to a center with US Food and Drug Administration permission to use domperidone should be considered. Alternatively, symptom modulators such as low-dose tricyclic antidepressants can be tried to reduce symptoms, but these do not improve gastric emptying. In patients for whom all medical therapy fails, other options that are tried at experienced centers include the injection of botulinum toxin into the pylorus, placement of a feeding jejunostomy, and/or placement of a gastric electrical stimulator.
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PMID:Delayed gastric emptying: whom to test, how to test, and what to do. 1683 48

Hemolysis is something that occurs to a small degree with every dialysis treatment. As we monitor our patients and the equipment we use, we hope that we have looked at everything and that our patients will be safe. We were extremely fortunate that we did not have a mortality related to this event. All of the hospitalized patients recovered and HP went on to receive her kidney transplant and is doing well. CG came back to dialyze in our unit after his physician was satisfied that our problem had been solved. In retrospect, we did not realize that we had an instrument in use that picked up the hemolysis long before we did. Our blood volume monitors showed us the increase in blood volume as the cells were lysed and vascular volume increased as the intracellular fluids were released. The concurrent rise in BP with these patients was also indicative of increased vascular volume. The blood volume monitor also showed the drop in hematocrit as red cells were lysed. We are now more experienced in interpreting these parameters and we are grateful to have this monitor on all of our patients and to have a new parameter to watch for to help forestall any further problems. Our patients' symptoms were baffling at the time because there were no overt signs of hemolysis. There was no "cherry pop" or brown colored blood in the lines or dialyzers which are what we have been taught to look for. Patients #1 and #3 essentially had no symptoms till the next day. Patient #2 exhibited nausea and some mild abdominal pain, which was also not new for him with his diabetic gastroparesis. Our nursing staff was very "gun shy" following this episode and some staff members seriously considered a change in profession. Fortunately they did not and opted to stay. It was brought home to all that dialysis, though it may seem to be a routine procedure, is inherently risky. Diligence and careful monitoring of all of our patients during their runs needs to be our utmost priority. Hemolysis to this degree is fortunately rare and we are grateful to have had an education with a positive outcome for all concerned.
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PMID:Hemolysis: a hidden danger. 1748 53

A case of synchronous adrenocortical carcinoma (ACC) and renal cell carcinoma (RCC) has not yet been described in the English medical literature, to our knowledge. We report a first such case of adrenocortical and renal cell carcinomas occurring simultaneously in a 53-year-old male. He presented with history of vague abdominal pain. Ultrasound followed by a computed tomography (CT) scan and a magnetic resonance imaging (MRI) examination revealed a 6.4 cm left adrenal mass and a 3.5 cm right renal mass. The patient had complaints of gastroparesis manifesting with constant nausea as well as intermittent abdominal bloating and abdominal pain. He also had history of profuse intermittent sweating. There was no history of palpitations or fluctuations in blood pressure. The patient's urinary vanillylmandelic acid (VMA) levels and serum cortisol levels were normal. His 24-hour urine metanephrine levels were slightly elevated. Left adrenalectomy and right partial nephrectomy were performed. In this case, it is important to determine whether these tumors represent metastases or two synchronous tumors, as this has implications on the patient's management and prognosis. Clinical and pathological clues that led to the diagnosis are discussed in detail.
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PMID:Synchronous renal cell carcinoma and adrenocortical carcinoma: a rare case report and clinicopathologic approach. 1840 53

Gastrointestinal complications of diabetes include gastroparesis, intestinal enteropathy (which can cause diarrhea, constipation, and fecal incontinence), and nonalcoholic fatty liver disease. Patients with gastroparesis may present with early satiety, nausea, vomiting, bloating, postprandial fullness, or upper abdominal pain. The diagnosis of diabetic gastroparesis is made when other causes are excluded and postprandial gastric stasis is confirmed by gastric emptying scintigraphy. Whenever possible, patients should discontinue medications that exacerbate gastric dysmotility; control blood glucose levels; increase the liquid content of their diet; eat smaller meals more often; discontinue the use of tobacco products; and reduce the intake of insoluble dietary fiber, foods high in fat, and alcohol. Prokinetic agents (e.g., metoclopramide, erythromycin) may be helpful in controlling symptoms of gastroparesis. Treatment of diabetes-related constipation and diarrhea is aimed at supportive measures and symptom control. Nonalcoholic fatty liver disease is common in persons who are obese and who have diabetes. In persons with diabetes who have elevated hepatic transaminase levels, it is important to search for other causes of liver disease, including hepatitis and hemochromatosis. Gradual weight loss, control of blood glucose levels, and use of medications (e.g., pioglitazone, metformin) may normalize hepatic transaminase levels, but the clinical benefit of aggressively treating nonalcoholic fatty liver disease is unknown. Controlling blood glucose levels is important for managing most gastrointestinal complications.
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PMID:Gastrointestinal complications of diabetes. 1861 80

Superior mesenteric artery (SMA) syndrome is a rare acquired disorder in which acute angulation of SMA causes compression of the third part of the duodenum between the SMA and the aorta, leading to obstruction. Loss of fatty tissue as a result of a variety of debilitating conditions is believed to be the etiologic factor causing the acute angulation. We report a case of 30 years old lady who presented with postprandial abdominal pain at the epigastric region, colic type without radiation accompanied by nausea, postprandial vomiting and weight loss. Esophageal gastric series revealed an abrupt interruption in the contrast medium flow at the level of the junction of third portion (midpart) of the duodenum in barium studies. Adiverticula is noted just proximal to the site of obstruction. High resolution ultrasound and color Doppler sonography showed narrowing of the aortomesenteric angle to 220. Duodenojejunostomy was performed in the patient. Unfortunately the patient later was admitted in the hospital for refractory gastroparesis associated with superior mesenteric artery syndrome. Although open and laparoscopic duodenojejunostomy have been described as the best surgical treatment options for Wilkie's syndrome, but further attention is needed to the management of patients with refractory symptoms of gastroparesis after corrective surgery.
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PMID:Superior mesenteric artery syndrome: case report. 1882 43

Gastroparesis is a relatively common and often disabling condition that is characterized by a broad range of clinical presentation ranging from dyspeptic symptoms to nausea, vomiting, abdominal pain, malnutrition, frequent hospitalizations and incapacitation. The treatment of gastroparetic symptoms can be challenging to the gastroenterologist and the intensity of therapy varies with the physician's knowledge. Hence the determination that a patient is refractory to 'standard medical therapy' is an assessment that is subspeciality-based and could differ around the world depending on medications available. In this article, we review the use of available prokinetics, antiemetic agents, the approach for analgesia in the context of gastroparesis, and also discuss potential and evolving pharmacotherapies. The progress has been relatively limited as far as availability of new medications for gastroparesis is concerned; however, active research in developing newer prokinetics holds great promise for the future of management of this challenging entity.
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PMID:Pharmacotherapy of gastroparesis. 1919 82

A common gastrointestinal complication of diabetes is gastroparesis, and patients with gastroparesis may present with early satiety, nausea, vomiting, bloating, postprandial fullness, or upper abdominal pain. However, the pathogenesis is not clear yet. A recent study indicated that atrial natriuretic peptide (ANP) was secreted from the gastric mucosa and the ANP family plays an inhibitory role in the regulation of gastrointestinal motility, but the effect of the natriuretic peptide signal pathway on diabetic gastroparesis has not been reported. The study investigated the effect of C-type natriuretic peptide (CNP) particulate guanylyl cyclase (pGC) cyclic guanosine monophosphate (cGMP) signaling on gastroparesis in streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley rats were divided into two groups; group I: normal control rats; group II: STZ-induced diabetic rats; 4 weeks after induction, the experiments were performed. The spontaneous contraction of gastric smooth muscle strips was recorded by using physiographs in control and diabetic rats. The pGC activity in response to CNP and cGMP production in gastric smooth muscle were measured by using radioimmunoassay (RIA) in normal and diabetic rats. CNP induced a longer lasting relaxation of gastric antral circular smooth muscle strips in STZ-induced diabetic rats. The inhibitory effect of CNP on spontaneous contraction revealed a dose-dependency, and the inhibitory percentages were 25.5 +/- 1.7%, 43.6 +/- 3.2%, 85.1 +/- 2.5% in diabetic rats and 20.5 +/- 1.5%, 31.1 +/- 1.7%, 58.9 +/- 3.7% in the control group at the concentrations of 0.01, 0.03, and 0.1 mumol/l, respectively. The cGMP production and pGC activity in response to CNP in gastric muscle tissues were significantly potentiated in STZ-induced diabetic rats. Natriuretic peptide receptor type B (NPR-B) gene was expressed in the gastric smooth muscles of normal and diabetic rats, and the expression was increased in diabetic rats. The results suggest that natriuretic peptide-dependent pGC-cGMP signal is upregulated and may contribute to diabetic gastroparesis in STZ-induced diabetic rats.
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PMID:Natriuretic peptide-dependent cGMP signal pathway potentiated the relaxation of gastric smooth muscle in streptozotocin-induced diabetic rats. 1926 96


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