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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric emptying delay is a rather frequent occurrence that may reveal itself with a broad spectrum of clinical manifestations, from slight dyspeptic symptoms up to alimentary vomiting. Once diagnosed with appropriate examinations, the treatment of this condition may be performed with a variety of means proportionate to the severity of the disease. In the first line there are dietetic measures and pharmacologic aids, that vary from currently available prokinetics drugs, drugs created for other therapeutical purposes, that reveal prokinetic properties, to new classes of prokinetics currently under clinical investigation or clinical trials. In more severe cases of gastroparesis, with vomiting and abdominal pain refractory to prokinetic therapy, other pharmacologic measures can be utilized, such as antiemetic and analgesic drugs. If the medical therapy is insufficient, endoscopic and surgical procedures are available, from the widening of the pyloric ring with botulinum toxin infiltrations or pneumatic dilatation, to the employment of various techniques of gastric electrical stimulation, up to partial or total gastric resection, when any other treatment fails and the patient is kept alive only with partial or total parenteral nutrition.
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PMID:Treatment of gastric emptying delay. 1982 88

Gastroparesis is a chronic disorder of gastric motility characterized by delayed gastric empting in the absence of mechanical obstruction, which can lead to symptoms of nausea, vomiting, bloating, abdominal pain, postprandial fullness and weight loss. Although there are many etiologies, the primary causes are diabetes or are idiopathic. The mainstay of treatment is dietary and drug therapies. However, many patients will continue to suffer intractable symptoms despite these treatments. Gastric neurostimulation with the Enterra Therapy system has been approved for use under the Humanitarian Device Exemption by the US FDA. The device produces pulses of electrical stimulation that are delivered to the stomach continuously. One randomized clinical trial and multiple nonrandomized unblinded clinical trials and case series have documented improvement of symptoms in intractable diabetic and idiopathic gastroparesis. The purpose of this article is to introduce the Enterra Therapy gastric neurostimulator. Gastroparesis and its pathophysiology will be discussed in this clinical context to enhance the understanding of the device and its development. We will analyze the device in detail, its placement and the results of studies evaluating its efficacy.
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PMID:Enterra Therapy: gastric neurostimulator for gastroparesis. 2042 May 55

Sphincter of Oddi dysfunction (SOD) is a poorly-understood disorder, typically presenting as postcholecystectomy, "biliary-type," right-sided abdominal and/or chest wall pain. Most patients referred to specialist clinics for work-up of presumed SOD do not, in fact, have anything wrong with their bile ducts or biliary sphincter mechanisms. A careful history and focused physical examination will often identify the true source of the pain syndrome, ranging from chest wall costochondritis and nerve injury at surgical trochar sites, to gastroparesis and visceral hypersensitivity ("irritable bowel"). The Rome III classification of functional gallbladder and biliary disorders defines SOD as episodic (not daily) pain lasting more than 30 min, which is disruptive of normal activities and not associated with bowel upset. It is not relieved by gastric acid suppression or antispasmodics. Other causes of abdominal pain must be excluded. Standard work-up includes endoscopic retrograde cholangiopancreatography (ERCP) with biliary manometry, which risks post-ERCP pancreatitis, especially in young women with normal bile ducts and liver serology. Noninvasive tests for SOD, such as timed ("gated") cholecystokinin (CCK)-stimulated hepatobiliary iminodiacetic acid (HIDA) scans and secretin-stimulated magnetic resonance cholangiopancreatography, are imperfect and still evolving. Although many doubt the very existence of SOD, a multidisciplinary approach to the management of pre- and postcholecystectomy abdominal pain syndromes is long overdue.
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PMID:Sphincter of Oddi dysfunction. 2042 85

Acute esophageal necrosis (AEN), commonly referred to as "black esophagus", is a rare clinical entity arising from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states. AEN may arise in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, thromboembolic phenomena, and malignancy. Clinical presentation is remarkable for upper gastrointestinal bleeding. Notable symptoms may include epigastric/abdominal pain, vomiting, dysphagia, fever, nausea, and syncope. Associated laboratory findings may reflect anemia and leukocytosis. The hallmark of this syndrome is the development of diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to involve variable length of the organ. Classic "black esophagus" abruptly stops at the gastroesophageal junction. Biopsy is recommended but not required for the diagnosis. Histologically, necrotic debris, absence of viable squamous epithelium, and necrosis of esophageal mucosa, with possible involvement of submucosa and muscularis propria, are present. Classification of the disease spectrum is best described by a staging system. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors. Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death. A high mortality of 32% seen in the setting of AEN syndrome is usually related to the underlying medical co-morbidities and diseases.
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PMID:Black esophagus: acute esophageal necrosis syndrome. 2061 76

Diabetic gastroparesis is a disorder that occurs in both type 1 and type 2 diabetes. It is associated with considerable morbidity among these patients and with the resultant economic burden on the health system. It is primarily a disease seen in middle-aged women, although the increased predisposition in women still remains unexplained. Patients often present with nausea, vomiting, bloating, early satiety and abdominal pain. The pathogenesis of this complex disorder is still not well understood but involves abnormalities in multiple interacting cell types including the extrinsic nervous system, enteric nervous system, interstitial cells of Cajal (ICCs), smooth muscles and immune cells. The primary diagnostic test remains gastric scintigraphy, although other modalities such as breath test, capsule, ultrasound, MRI and single photon emission CT imaging show promise as alternative diagnostic modalities. The mainstay of treatment for diabetic gastroparesis has been antiemetics, prokinetics, nutritional support and pain control. In recent years, gastric stimulation has been used in refractory cases with nausea and vomiting. As we better understand the pathophysiology, newer treatment modalities are emerging with the aim of correcting the underlying defect. In this review, what has been learned about diabetic gastroparesis in the past 5 years is highlighted. The epidemiology, pathogenesis, diagnosis and treatment of diabetic gastroparesis are reviewed, focusing on the areas that are still controversial and those that require more studies. There is also a focus on advances in our understanding of the cellular changes that underlie development of diabetic gastroparesis, highlighting new opportunities for targeted treatment.
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PMID:Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years. 2087 Nov 31

Abdominal pain can be disabling in patients with gastroparesis. The pathogenesis of pain in these individuals is poorly understood. Agents commonly used in clinical practice, including tricyclic antidepressants, gabapentin, and pregabalin, have remained largely unsatisfactory in treating this pain. We report the case of a 50-year-old woman presenting with chronic unrelenting abdominal pain due to severe diabetic gastroparesis that was managed successfully with coeliac plexus block with local anaesthesia and steroid injection. Adequate analgesia was achieved and maintained for 10 weeks following the coeliac plexus block, which allowed elimination of opiate requirements for pain management (and avoidance of narcotic associated constipation), continuation of percutaneous endoscopy jejunostomy tube feedings, and avoidance of long term parenteral nutrition.
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PMID:Coeliac plexus block in the management of chronic abdominal pain due to severe diabetic gastroparesis. 2212 92

This guideline presents recommendations for the evaluation and management of patients with gastroparesis. Gastroparesis is identified in clinical practice through the recognition of the clinical symptoms and documentation of delayed gastric emptying. Symptoms from gastroparesis include nausea, vomiting, early satiety, postprandial fullness, bloating, and upper abdominal pain. Management of gastroparesis should include assessment and correction of nutritional state, relief of symptoms, improvement of gastric emptying and, in diabetics, glycemic control. Patient nutritional state should be managed by oral dietary modifications. If oral intake is not adequate, then enteral nutrition via jejunostomy tube needs to be considered. Parenteral nutrition is rarely required when hydration and nutritional state cannot be maintained. Medical treatment entails use of prokinetic and antiemetic therapies. Current approved treatment options, including metoclopramide and gastric electrical stimulation (GES, approved on a humanitarian device exemption), do not adequately address clinical need. Antiemetics have not been specifically tested in gastroparesis, but they may relieve nausea and vomiting. Other medications aimed at symptom relief include unapproved medications or off-label indications, and include domperidone, erythromycin (primarily over a short term), and centrally acting antidepressants used as symptom modulators. GES may relieve symptoms, including weekly vomiting frequency, and the need for nutritional supplementation, based on open-label studies. Second-line approaches include venting gastrostomy or feeding jejunostomy; intrapyloric botulinum toxin injection was not effective in randomized controlled trials. Most of these treatments are based on open-label treatment trials and small numbers. Partial gastrectomy and pyloroplasty should be used rarely, only in carefully selected patients. Attention should be given to the development of new effective therapies for symptomatic control.
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PMID:Clinical guideline: management of gastroparesis. 2400 61

We describe a 13-year-old female with abrupt onset urinary retention progressing rapidly to pandysautonomia with symptoms of postural orthostatic tachycardia syndrome, gastroparesis, anhidrosis, pupillary dysfunction, and abdominal pain. Pandysautonomia has been reported frequently in adults, but is less commonly described in children. Autonomic nervous system dysfunction usually has a self-limiting course with gradual near-complete or complete recovery. Most patients with pure pandysautonomia produce an antibody targeted against the ganglionic nicotinic acetylcholine receptor and titers have been shown to correlate with symptom severity. The clinical presentation described in this report is consistent with a progressive form of acute autoimmune autonomic neuropathy, but she was initially seronegative for known autoantibodies. She responded promptly to plasmapheresis. This case report emphasizes the importance of recognizing features of autonomic nervous system dysfunction and discusses the medical evaluation and treatment options for pediatric patients based on symptom severity.
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PMID:A pediatric case of severe pandysautonomia responsive to plasmapheresis. 2335 30

Abdominal pain physiology may be better understood studying electrophysiology, histology, and symptom scores in patients with the symptoms of gastroparesis (Gp) treated with gastric electrical stimulation (GES). Ninety-five Gp patients' symptoms were recorded at baseline and during temporary and permanent GES. Gastric-emptying times and cutaneous, mucosal, and serosal electrogastrograms were obtained. S100-stained, full-thickness gastric biopsies were compared with autopsy controls. Sixty-eight patients reported severe pain at baseline. Severe pain patients' mean pain scores decreased with temporary GES from 3.62 to 1.29 (P < 0.001) and nonsevere pain from 1.26 to 0.67 (P = 0.01). With permanent GES, severe mean pain scores fell to 2.30 (P < 0.001); nonsevere pain changed to 1.60 (P = 0.221). Mean follow-up was 275 days. Mean cutaneous, mucosal, and serosal frequencies and frequency-to-amplitude ratios were markedly higher than literature controls. For patients with Gp overall and subdivided by etiology and severity of pain, S-100 neuronal fibers were significantly reduced in both muscularis propria layers. GES improved severe pain associated with symptoms of Gp. This severe pain is associated with abnormal electrogastrographic activity and loss of S100 neuronal fibers in the stomach's inner and outer muscularis propria and, therefore, could be the result of gastric neuropathy.
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PMID:Gastric electrical stimulation for abdominal pain in patients with symptoms of gastroparesis. 2363 79

Diabetes mellitus affects virtually every organ system in the body and the degree of organ involvement depends on the duration and severity of the disease, and other co-morbidities. Gastrointestinal (GI) involvement can present with esophageal dysmotility, gastro-esophageal reflux disease (GERD), gastroparesis, enteropathy, non alcoholic fatty liver disease (NAFLD) and glycogenic hepatopathy. Severity of GERD is inversely related to glycemic control and management is with prokinetics and proton pump inhibitors. Diabetic gastroparesis manifests as early satiety, bloating, vomiting, abdominal pain and erratic glycemic control. Gastric emptying scintigraphy is considered the gold standard test for diagnosis. Management includes dietary modifications, maintaining euglycemia, prokinetics, endoscopic and surgical treatments. Diabetic enteropathy is also common and management involves glycemic control and symptomatic measures. NAFLD is considered a hepatic manifestation of metabolic syndrome and treatment is mainly lifestyle measures, with diabetes and dyslipidemia management when coexistent. Glycogenic hepatopathy is a manifestation of poorly controlled type 1 diabetes and is managed by prompt insulin treatment. Though GI complications of diabetes are relatively common, awareness about its manifestations and treatment options are low among physicians. Optimal management of GI complications is important for appropriate metabolic control of diabetes and improvement in quality of life of the patient. This review is an update on the GI complications of diabetes, their pathophysiology, diagnostic evaluation and management.
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PMID:Gastrointestinal complications of diabetes mellitus. 2377 73


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