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Diabetes with evidence of gastroparesis on objective testing has been associated with increased health-care costs, including increased clinic. Gastroparesia Diabética – Relevância clínica e actuação médica. Authors. Ana Isabel Branco, Miguel Azevedo. Read article. Get treatment to help you manage gastroparesis, so that you can be as healthy and comfortable as possible.

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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.

Treatment of Patients With Diabetic Gastroparesis

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 exemptiondo 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 termand 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. This clinical guideline addresses the definition, diagnosis, differential diagnosis, and treatment of gastroparesis, including nutritional supplementation, glycemic control, pharmacological, endoscopic, device, and surgical therapy. Each section of this document will present the key recommendations related to the section topic and a subsequent summary of the evidence supporting those recommendations.

An overall summary will be presented in the first table. We used systematic reviews and meta-analyses for each topic when available, followed by a review of clinical trials. The GRADE system was used to evaluate the strength of the recommendations and the overall quality of evidence 1 Table 1. Gastroparesis is defined as a syndrome of objectively delayed gastric emptying in the absence of mechanical obstruction and cardinal symptoms including early satiety, postprandial fullness, nausea, vomiting, bloating, and upper abdominal pain 2 ; the same constellation of complaints may be seen with other etiologies, including gastritis secondary to Heli-cobacter pylori infection, peptic ulcer, and functional dyspepsia.

Symptoms have not been well correlated with gastric emptying. Nausea, vomiting, early satiety, and postprandial fullness correlate better with delayed gastric emptying than upper abdominal pain and bloating 34. The epidemiology and impact of gastroparesis are reviewed elsewhere 2. More community-based data are required to confirm or enhance the published figures.

Gastroparesis significantly impacts quality of life 67increases direct health-care costs through hospitalizations, emergency room, or doctor visits, and is associated with morbidity and mortality 89.

The symptoms are often the same with the different etiologies of gastroparesis: In patients from the NIH Gastroparesis Registry, symptoms prompting evaluation more often included vomiting for diabetic gastroparesis DG and abdominal pain for idiopathic gastroparesis IG.

Patients with IG have more early satiety and abdominal pain compared with patients with DG who have more severe retching; all the patients included in these multicenter studies had documentation of delayed gastric emptying in their medical record 11 Abdominal pain is an often under-appreciated symptom in gastro paresis. Severity ranking of abdominal pain was in the same range as other symptoms e. The presence of anxiety or depression has been associated with more severe symptoms 14 The combination of symptoms and delayed gastric emptying is required to establish the diagnosis of gastroparesis as the epidemiology, natural history, pathophysiology, and treatment of gastroparesis which are reviewed in detail elsewhere 2 are typically based on combined criteria.


Diabetes with evidence of gastroparesis on objective testing has been associated with increased health-care costs, including increased clinic visits, emergency room visits, hospitalizations, overall morbidity and mortality 89. Since accelerated gastric emptying and functional dyspepsia can also present with symptoms similar to gastroparesis, documentation of delayed gastric emptying 316 is necessary before selecting therapy with prokinetics agents or GES.

Diabetes mellitus is the most commonly recognized systemic disease associated with gastroparesis. In the NIH consortium cohort, delayed gastric emptying was more pronounced in patients with type 1 DG The year incidence of gastroparesis has been reported to be 5. Idiopathic gastroparesis refers to a symptomatic patient from delayed gastric empting with no detectable primary underlying abnormality for the delayed gastric emptying.

This may represent the most common form of gastroparesis 10 Most patients with IG are women; typically young or middle aged.

Clinical Guideline: Management of Gastroparesis

Symptoms of IG overlap with those of functional dyspepsia; it may be difficult to provide a definitive distinction between the two based on symptoms, and many regard IG and functional dyspepsia with delayed gastric emptying as the same condition. Therefore, measurement of gastric emptying is important, as therapies differ if gastric emptying is delayed, normal, or rapid.

A subset of patients with gastroparesis report sudden onset of symptoms after a viral prodrome, suggesting a potential viral etiology for their symptoms, and the diagnosis of postviral gastroparesis 18 Previously, healthy subjects have developed the sudden onset of nausea, vomiting, diarrhea, fever, and cramps suggestive of a systemic viral infection. However, instead of experiencing resolution of symptoms, these individuals note persistent nausea, vomiting, and early satiety.

Over a period of about a year, the gastroparesis often improves. Diavetica general, this course is typical of postviral gastroparesis that is not associated with autonomic neuropathy. On the other hand, a minority of patients with infections due to viruses such as cytomegalovirus, Epstein — Barr virus, and ddiabetica zoster may develop a form of autonomic neuropathy generalized or selective cholinergic dysautonomia that includes gastroparesis.

These patients with autonomic dysfunction may have slower resolution of their symptoms that may take several years and the prognosis is worse than in postviral gastroparesis without autonomic disorders 20 Postsurgical gastroparesis PSGoften with vagotomy or vagus nerve injury, represents the third most common etiology of gastroparesis. In the past, most cases resulted from vagotomy performed in combination with gastric drainage to correct medically refractory or complicated peptic ulcer disease.

Since the advent of laparoscopic techniques for the treatment of GERD, gastroparesis has become a recognized complication of fundoplication possibly from vagal injury during the surgery or bariatric surgery that involves gastroplasty or bypass procedures. The combination of gatsroparesia, distal gastric resection, and Roux-en-Y gastrojejunostomy gastrpparesia to slow emptying from the gastric remnant and delayed transit in the denervated Roux efferent limb. The Roux-en-Y stasis syndrome — characterized by postprandial abdominal pain, bloating, nausea, and vomiting — is particularly difficult to manage, and its severity may be proportional to the length of the Roux limb generally, 25 cm is ideal to avoid stasis.

The precise role of the antireflux surgery itself is not clearly demonstrated in the published literature.

Thus, while symptoms suggesting gastric stasis are extremely common in the first 3 months after fundoplication, they persist in a minority of patients at 1 year post surgery. In a series of patients who underwent laparoscopic Nissen fundoplication, all had symptoms during the first 3 postoperative months e.

The precise role of fundoplication is therefore difficult to determine unless the patient diabetiica testing for abdominal vagal dysfunction, such as the plasma pancreatic polypeptide response to modified sham feeding; such tests are described elsewhere In patients with refractory symptoms of GERDinvestigation for delayed gastric emptying should be considered, since delayed gastric emptying can be associated with GERD and possibly aggravate symptoms of heartburn, regurgitation, and other symptoms gastroparfsia with GERD.

Known causes of iatrogenic gastroparesis include surgical vagal disruption, which may be due to vagal nerve injury e. The second major category of iatrogenic gastroparesis is induced by pharmacological agents as may occur with narcotic opiate analgesics, anticholinergic agents, and some diabetic medications. These include agents such as morphine 25as well as oxycodone and tapentadol 26but less with tramadol Therefore, patients receiving such agents should first undergo withdrawal of the agent before assuming a diagnosis of gastroparesis.


GLP-1 analogs, such as exenatide, used for treatment of type 2 diabetes mellitus 28 can delay gastric emptying. The antirejection drug, cyclosporine, can delay gastric emptying. Thus, in patients with prior pancreatic transplantation treated with antirejection treatment with cyclosporine, there may be delay in gastric emptying This does not apply to another calcineurin inhibitor, tacrolimus, which is derived from a macrolide molecule and retains prokinetic properties Other rarer causes of gastroparesis include diseases affecting the extrinsic neural control such as Parkinsonism, amyloidosis, and paraneoplastic disease or disorders that result in infiltration or degeneration of the muscle layer of the stomach such as scleroderma.

Mesenteric ischemia should also be considered as a rare cause of gastroparesis that is potentially reversible. There are three tests to objectively demonstrate delayed gastric emptying: For any type of gastric emptying test, patients should discontinue medications that may affect gastric emptying.

For most medications, this will be 48 — 72 h. These include medications that can delay gastric emptying, such as narcotic opioid analgesics and anticholinergic agents.

These agents may give a falsely delayed result. Medications that accelerate gastric emptying, such as metoclopramide, domperidone, and erythromycin, may give a falsely normal result. The conventional test for measurement of gastric emptying is scintigraphy 33 Gastric emptying scintigraphy of a solid-phase meal is considered as the standard for diagnosis of gastroparesis, as it quantifies the emptying of a physiologic caloric meal.

For solid-phase testing, most centers use a 99m Tc sulfur colloidlabeled egg sandwich as the test meal, with standard imaging at 0,1,2, and 4h.

Assessment of gastric emptying over 4 h is necessary Shorter duration solid emptying or sole liquid emptying by scintigraphy is associated with lower diagnostic sensitivity. On the other hand, the clinical significance of selectively delayed gastric emptying of liquids has not been assessed, for example, in terms of its value in predicting response of symptoms to treatment. There is evidence that the effect of hyperglycemia on gastric emptying in diabetics is more clearly demonstrated in the retardation of the gastric emptying of liquids The most reliable parameter to report gastric emptying is the gastric retention at 4 h.

However, it is also important to assess emptying at least 1 and 2 h after radiolabeled meal ingestion, since prolongation of the early phases of emptying may also be associated with symptoms of gastroparesis, even though the gastric retention at 4 h is normal or mildly delayed. A WMC that measures pH, pressure, and temperature can assess gastric emptying by the acidic gastric residence time of the capsule. Gastric emptying is determined when there is a rapid increase in the pH recorded indicating emptying from the acidic stomach to the alkaline duodenum.

The gastric residence time of the WMC e. The overall correlation between gastric emptying time of the WMC and gastric emptying at 4 h by scintigraphy was 0. Breath testing has been used in both clinical and clinical research studies for determining gastric emptying These breath tests using 13 C-octanoate or -spirulina 44 provide reproducible results that correlate with results on gastric emptying scintigraphy, including responsiveness to pharmacological therapy.

The optimization of mathematical models for measurement of gastric emptying derived from breath excretion profiles has been thoroughly examined in the literature Both WMC and breath testing require further validation before they can be considered as alternates to scintigraphy for diagnosis of gastroparesis.

Gastroparesis: American Diabetes Association®

The vomiting symptom of a patient can be difficult to differentiate from the regurgitation seen in GERD or the regurgitation seen in rumination syndrome. Rumination syndrome is a condition characterized by the repetitive, effortless regurgitation of recently ingested food into gasstroparesia mouth followed by re-chewing and re-swallowing or expectorating gastropagesia food.

Although initially described in infants and the gastorparesia disabled, rumination syndrome is now widely recognized at all ages and cognitive abilities; the condition is more frequent in females, but it is recognized in adolescent and adult males 46 Rumination can become a habit, often initiated by a belch, a swallow, or by stimulation of the palate with the tongue. Abdominal muscle contraction with lower esophageal sphincter relaxation in the early postprandial period is responsible for regurgitation.

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