(1)
Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine and Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA
3.1 Introduction
Gastroparesis is defined as a chronic disorder characterized by delayed emptying of the stomach occurring in the absence of mechanical obstruction. It is a well-known and potentially serious complication of diabetes. Although gastroparesis was initially described in patients with type 1 diabetes, it is increasingly being recognized in patients with type 2 diabetes. Diabetic gastroparesis affects up to 40 % of patients with type 1 diabetes and up to 30 % of patients with type 2 diabetes [1, 2]. Diabetic gastroparesis generally affects patients with long-standing diabetes mellitus, and patients often have other diabetic complications such as retinopathy, neuropathy, or nephropathy. Gastroparesis can lead to poor glucose control, increased morbidity, and decreased quality of life. As the number of patients with diabetes increases, the number of diabetic patients with gastroparesis is increasing. For reasons that remain unclear, approximately 80 % of patients with gastroparesis are women [3]. Hospitalizations with gastroparesis as the primary diagnosis have increased 158 % from 1995 to 2004 [4]. Additionally, gastroparesis has the longest length of stay when compared with other upper gastrointestinal conditions [4]. This chapter will explore the clinical features, complications, diagnosis, management, and treatment options for gastroparesis.
3.2 Clinical Features
In diabetes, delayed gastric emptying can often be asymptomatic. Therefore, the term gastroparesis should only be reserved for patients that have both delayed gastric emptying and upper gastrointestinal symptoms. Additionally, discordance between the pattern and type of symptoms and the magnitude of delayed gastric emptying is a well-established phenomenon. Accelerating gastric emptying may not improve symptoms, and patients can have symptomatic improvement while gastric emptying time remains unchanged. Furthermore, patients with severe symptoms can have mild delays in gastric emptying.
Clinical features of gastroparesis include nausea, vomiting, bloating, abdominal pain, and malnutrition. In a tertiary care center of 146 patients, nausea was present in 92 %, vomiting in 84 %, abdominal bloating in 75 %, and early satiety in 60 % of patients [3]. Functional dyspepsia and gastroparesis have significant overlap, and up to 50 % of patients with dyspeptic symptoms can have delayed gastric emptying [5]. Abdominal pain is present in 46–89 % of patients and is often difficult to treat [3]. Impaired regulation of postprandial glycemia can also be an indication of gastroparesis. Gastroparesis affects oral drug absorption and can cause hyperglycemia that is challenging to manage, in addition to unexplained hypoglycemia. As a result, unstable glucose control can be a subtle sign of gastroparesis.
3.3 Complications
Gastroparesis can lead to poor nutrition and poor oral intake with subsequent malnutrition and vitamin and mineral deficiencies. Possible complications of gastroparesis include volume depletion with renal failure, malnutrition, electrolyte abnormalities, esophagitis, Mallory–Weiss tear (from vomiting), or bezoar formation. Patients with gastroparesis will often have other gastrointestinal manifestations of delayed motility.
3.3.1 Nutrition
Nutritional and caloric deficits are common in patients with gastroparesis, and patients should receive nutritional screening. In a study of 305 patients, 64 % of patients were found to have caloric deficient diets, defined as less than 60 % of daily total energy requirements [6]. One study of 45 patients found that foods provoking symptoms were generally fatty, acidic, spicy, and roughage based [7]. Additionally, patients were found to have several vitamin and mineral deficiencies specifically vitamins A, B6, C, and K, iron, potassium, and zinc [6]. Nutritional consultation increases the chances that daily total energy requirements will be met (odds ratio = 1.51, P = 0.08) [6]. Unfortunately, despite known nutritional and caloric deficiencies, nutritional consultation is often neglected, and only a minority receives a nutritional consultation [6].
3.3.2 Glycemic Control and Gastroparesis
It has been well documented that acute changes in blood glucose alter gastric emptying [8]. Additionally, acute hyperglycemia can attenuate the effect of prokinetics reducing their efficacy. Induction of acute hypoglycemia accelerates gastric emptying. Glucose control is often complicated in patients with diabetic gastroparesis as blood glucose levels both influence and are influenced by gastroparesis [9]. Long-term hyperglycemia is an independent risk factor for gastroparesis [8]. However, it has been shown that long-term glycemic control does not improve gastric emptying [8, 10].
3.4 Diagnosis
A diagnosis of gastroparesis should only be made in patients that have both upper gastrointestinal symptoms and objective evidence of delayed gastric emptying. Diabetic gastroparesis is diagnosed by demonstrating delayed gastric emptying in a symptomatic patient after the exclusion of other etiologies of symptoms and exclusion of mechanical obstruction. An upper endoscopy is important to exclude the presence of ulcer, stricture, or mass.
Initial investigation should include a complete blood count, complete metabolic profile, and thyroid-stimulating hormone. Additionally, a pregnancy test should be obtained in women of childbearing age. If vomiting or pain is acute or severe, consider an abdominal obstruction series. If abdominal pain is a significant symptom, workup may include a right upper quadrant ultrasound, amylase, and lipase. Once mechanical obstruction has been excluded, gastroparesis is diagnosed by demonstrating delayed gastric emptying with solid phase gastric emptying scintigraphy, wireless motility capsule (SmartPill), or stable isotope breath test.
3.4.1 Gastric Emptying Scintigraphy
The gold standard to evaluate delayed gastric emptying is a solid phase gastric emptying scintigraphy over 4 h. The Society of Nuclear Medicine and American Neurogastroenterology and Motility Society (ANMS) has a standardized protocol for gastric emptying scintigraphy [11]. It is important that it is performed with a solid meal because liquid emptying may remain normal despite advanced disease. The standardized meal for testing is 99-m technetium sulfur-colloid labeled low fat, egg white. The scan should be performed with the patient in an upright position 1, 2, and 4 h after the test meal to identify both rapid and slow gastric emptying. Prior to testing, medications that can impair or promote gastric emptying should be held at least 48–72 h in advance. Patients already taking prokinetics should stop taking them prior to testing. Medications that delay gastric emptying and should be held include narcotic analgesics, tricyclic antidepressants, lithium, and calcium channel blockers. Serotonin receptor antagonists, such as ondansetron, can be given during testing for severe symptoms of nausea and vomiting because they do not alter gastric emptying. Table 3.1 provides a more complete list of medications that affect gastric emptying.
Table 3.1
Medications that affect gastric emptying
Delay gastric emptying | Accelerate gastric emptying |
|---|---|
Opiates (e.g., oxycodone, acetaminophen–codeine) | Macrolide antibiotics (e.g., erythromycin, azithromycin, clarithromycin) |
Anticholinergics (e.g., dicyclomine, hyoscyamine, tricyclic antidepressants such as amitriptyline) | Metoclopramide |
Aluminum-containing antacids | Diazepam |
Dopamine, levodopa | Bulk laxatives |
Calcium channel blockers (e.g., diltiazem, verapamil, nifedipine) | |
GLP analogue (e.g., exenatide) |
Interpreting the results of a gastric emptying study can be challenging in patients with diabetes. Hyperglycemia has been shown to result in delayed gastric emptying on scintigraphy, and gastric emptying normalized when euglycemia was achieved prior to testing [12]. It may be advisable to check glucose levels prior to a gastric emptying study to ensure that glucose levels are within normal range [13]. Ideally blood glucose levels in patients with diabetes should be <275 mg/dL on the day of the test because hyperglycemia significantly delays gastric emptying [13, 14].
One disadvantage of gastric emptying scintigraphy is that it is often not performed in a standardized manner in many medical centers. Despite strong guidelines that scintigraphy be performed over 4 h, many medical centers continue to extrapolate gastric emptying using data after 90–120 min. Results from scintigraphy tests under 4 h long should not be used to diagnose gastroparesis. Another disadvantage of this test is radiation exposure. The amount of exposure with testing is equivalent to approximately one-third of the average annual radiation exposure in the United States from natural sources [13].
3.4.2 Wireless Motility Capsule
The SmartPill® GI Monitoring System (SmartPill Corporation, NY, USA) is an ingested capsule that can also be used to diagnose gastroparesis. The pill is swallowed after ingesting a standardized meal and delivers information on pressure, pH, and temperature wirelessly to a data recorder worn by the patient. The data estimates gastric emptying time, combined small and large bowel transit time, and total transit time and studies pressure patterns in the stomach, small bowel, and colon. The capsule is approved by the US Food and Drug Administration for use in studying gastroparesis. In a study of 87 healthy controls and 61 patients with gastroparesis, the wireless motility capsule had a sensitivity of 87 % and specificity of 92 % when compared with a 4-h scintigraphic gastric emptying test [15]. The device is a reasonable alternative to conventional scintigraphy for gastroparesis but is not widely available. Advantages of this test are the ambulatory measure of the test, lack of radiation exposure, and ability to measure motility of the entire GI tract. Disadvantages of this test are the cost and lack of availability.
3.4.3 CO2 Breath Test
Another diagnostic option is the stable isotope breath test. 13C-labeled octanoate, a medium-chain triglyceride, is bound to a solid meal. After ingestion, 13C-labeled octanoate is quickly absorbed in the small intestine and metabolized to 13CO2 which is excreted from the lungs. This test is less expensive than scintigraphy and avoids radiation exposure which can be beneficial to certain populations (i.e., pregnancy, breastfeeding, children). Disadvantages of this test are the need for normal small intestinal absorption, normal liver metabolism, and the need to assess pulmonary excretion to detect radioactivity. Furthermore, this test is currently not available for clinical use in the United States.
3.5 Initial Treatment
Treatment should be tailored for each patient based on symptoms. Disease severity is assessed by the patients’ ability to maintain adequate nutrition and by symptoms. A daily diary of symptoms and diet may be helpful to assess severity of symptoms of gastroparesis for patients with difficulty remembering symptoms. The Gastroparesis Cardinal Symptom Index (GCSI), a validated scoring system shown in Table 3.2, can assess the severity of gastroparesis as well as response to management [16]. Figure 3.1 provides a pyramid of treatment, with progression up the pyramid as severity of gastroparesis increases [17]. Patients with mild gastroparesis can be managed with dietary modifications, glucose control, and symptom management.
Table 3.2
Gastroparesis Cardinal Symptom Index (GCSI)
None | Very mild | Mild | Moderate | Severe | Very severe | |
|---|---|---|---|---|---|---|
Nausea | 0 | 1 | 2 | 3 | 4 | 5 |
Retching | 0 | 1 | 2 | 3 | 4 | 5 |
Vomiting | 0 | 1 | 2 | 3 | 4 | 5 |
Stomach fullness | 0 | 1 | 2 | 3 | 4 | 5 |
Not able to finish a normal-sized meal | 0 | 1 | 2 | 3 | 4 | 5 |
Feel excessively full after meals | 0 | 1 | 2 | 3 | 4 | 5 |
Loss of appetite | 0 | 1 | 2 | 3 | 4 | 5 |
Bloating | 0 | 1 | 2 | 3 | 4 | 5 |
Belly visible larger | 0 | 1 | 2 | 3 | 4 | 5 |
Figure 3.1
Therapeutic pyramid for diabetic gastroparesis. Starting at the base, patients with mild symptoms can be managed with glycemic control and dietary modifications. The peak of the pyramid represents the minority of patients that do not respond to therapy, and therapeutic options are limited and not necessarily evidence based (Reproduced with permission from Sellin [17] ©Nature)
Elevated glucose levels have a significant role in slowing gastric emptying. Changes in gastric emptying may affect postprandial blood glucose concentrations, because of unpredictable delivery of food. Impaired gastric emptying with continued administration of exogenous insulin can cause hypoglycemia. Therefore, in patients with established gastroparesis, short-acting insulin should be dosed after rather than prior to meals to avoid hypoglycemia. The use of regular insulin rather than rapid-acting insulin analogues may be better as it has a sustained duration of action.
3.5.1 Dietary Treatment
Initial treatment should be dietary management with a low-fat, low-fiber diet with small frequent meals. By eating meals more frequently, patients are more likely to continue to meet their nutrition needs. Large meals lead to longer gastric emptying, so by decreasing the volume of meals, patients may experience some relief in symptoms. Fat is known to slow gastric emptying and fiber can increase risk for bezoar formation. Food should be chewed thoroughly and meal replacement drinks should be considered. Patients should sit up while eating and for 1 h after finishing their meal. Multivitamin supplementation is advisable. Foods that are acidic, spicy, high in fat, and roughage based can increase overall symptoms in patients with gastroparesis. Patients should avoid alcohol and smoking as these can delay gastric emptying [18, 19]. Table 3.3 provides suggested nutrition guidelines.
Table 3.3
Nutritional interventions
1. Decrease volume of meals |
2. Improve glycemic control |
3. Limit fat |
(a) Fat in liquid form is well tolerated; maintain 20–30 % of calories from fat |
4. Limit fiber |
(a) Identify high-fiber foods that increase upper gastrointestinal symptoms |
(b) If bezoar formation is a concern, avoid foods causing bezoar such as oranges, berries, coconut, and legumes |
(c) Fiber supplements for constipation should be discontinued |
5. Meal consistency |
(a) Chew food thoroughly and take 20–30 min to finish meal |
(b) If solids are not tolerated, any food can be blended with water, low-fat milk, vegetable juice, or broth to make a puree |
(i) Liquid nutrients are better tolerated than solid food |
(ii) Can also try solid foods in the morning, switch to semiliquid and/or liquid meals over the course of the day |
6. Additional recommendations |
(a) Monitor and replace micronutrients as needed: iron, vitamin B12, vitamin D, calcium |
(b) Avoid caffeine, alcohol, and tobacco |
(c) Eat nutritious foods prior to filling-up on “empty calories” |
(d) Avoid foods that lower esophageal sphincter pressure: peppermint, chocolate, fat, caffeine |
(e) Chew well and eat slowly (30-min meals) |
(f) Do not lie down immediately after eating – sit upright or consider walking for 1–2 h after meals |
(g) If overweight, lose weight |
(h) On days when symptoms are worse, just take liquids to let the stomach rest |
(i) Check weight twice a week; if weight is decreasing, increase the amount of liquid supplements |
If solid food is not tolerated, patients can try blended foods. In many cases, normal gastric emptying of liquids is preserved despite delayed gastric emptying of solids. Prior to blending, solid foods should be thinned with some type of liquid such as water, low-fat milk, or broth. If patients are not consuming enough calories, then patients should supplement their diet with nutritional supplements. Indications for nutritional supplementation include weight loss of greater than or equal to 10 % during a period of 3–6 months, inability to maintain recommended body weight, and severe symptoms requiring hospitalization or interventions such as a nasogastric tube to relieve nausea and vomiting [20].
3.6 Pharmacologic Treatments
When dietary management and glycemic control are not sufficient to control symptoms, pharmacologic treatment should be initiated. Initial pharmacologic treatment should be with prokinetic agent and/or antiemetic agent. If there is no clinical response to these medications, then consider further investigation by a gastroenterologist. Unfortunately, there is a dearth of medications available to treat gastroparesis. Additionally, many of the medications used are based on older trials with small sample sizes. Table 3.4 provides a short summary of medications.
Table 3.4
Medications to treat diabetic gastroparesis
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