Diabetic Gastroparesis


Article Author:
Ganesh Aswath
Lisa Foris
Ashwini Ashwath


Article Editor:
Krunal Patel


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
11/13/2019 3:09:20 PM

Introduction

Gastroparesis is defined by objective delaying of gastric emptying without any evidence of mechanical obstruction. Diabetic gastroparesis is a potential complication that occurs in the setting of poorly controlled diabetes, resulting from dysfunction in the coordination and function of the autonomic nervous system, neurons and specialized pacemaker cells (interstitial cells of Cajal, ICC) of the stomach and intestine, and the smooth muscle cells of the gastrointestinal tract.[1][2][3][4]

Etiology

Hyperglycemia (blood glucose greater than 200 mg/dL), commonly seen in the setting of poorly controlled diabetes, has been associated with diabetic gastroparesis that occurs as a result of neuropathy in the setting of chronic hyperglycemia and does not resolve with improved glycemic control. Acute hyperglycemia, on the other hand, though it can also result in delayed gastric emptying, is often reversible with improved glycemic control.[5][6][7]

Gastric emptying requires coordination of fundal tone and antral phasic contraction with simultaneous inhibition of pyloric and duodenal contractions. This coordination also requires interactions between the enteric and autonomic nervous systems, smooth muscle cells, and the specialized pacemaker cells (ICC) of the stomach. The gastric motor dysfunction that is encountered in the setting of diabetes may occur as a result of autonomic neuropathy (both sympathetic and parasympathetic), enteric neuropathy (both excitatory and inhibitory neurons), ICC abnormalities (intrinsic neuropathy), acute blood glucose fluctuations, use of incretin-based medications, or psychosomatic factors.  As a result, most patients with diabetes tend to have dysfunction at multiple points in the process of gastric emptying. This includes abnormal postprandial proximal gastric accommodation and contraction, as well as abnormalities in antral motor function.

Epidemiology

Although idiopathic gastroparesis is the most common form of gastroparesis, diabetes is the most common disease associated with the condition. Upper gastrointestinal symptoms are reported in 11% to 18% of patients with diabetes, the majority of which are associated with delayed gastric emptying. Gastroparesis is seen in approximately 4.8% of individuals with type 1 diabetes, 1% of those with type 2 diabetes, and 0.1% of those without diabetes. Although there is a stronger association between type 1 diabetes and gastroparesis, the incidence of type 2 diabetes is much greater, and therefore, gastroparesis associated with type 2 diabetes is seen more frequently. Additionally, incretin mimetics are used to treat patients with type 2 diabetes, and these medications pose an additional risk factor for developing gastroparesis.[8]

Signs and symptoms of delayed gastric emptying are seen more frequently in individuals with type 1 versus type 2 diabetes, and typically in those patients who have had the disorder for at least five years. It has been observed that gastroparesis typically occurs in patients with a diagnosis of diabetes of at least ten years, and therefore seen more commonly in older individuals with type 2 diabetes.

Pathophysiology

Diabetic gastroparesis occurs as a result of dysfunction in the autonomic and enteric nervous systems. Chronically high levels of blood glucose (or inefficient glucose uptake) leads to neuronal damage resulting in abnormal myenteric neurotransmission (e.g., vagus nerve), impaired inhibitory (nitric oxide) neuronal function, and dysfunctional smooth muscle and pacemaker (interstitial cells of Cajal) cells. Altogether, this dysfunction results in a combination of fewer contractions of the antrum, uncoordinated antro-duodenal contractions, and pyloric spasms, ultimately resulting in delayed gastric emptying (gastroparesis).

Delayed gastric emptying in patients with diabetes, particularly of solids, may also occur in the setting of abnormal small bowel motility, which is thought to occur by a similar mechanism as that which is described in the stomach. Some patients with diabetes may additionally experience changes in gastric compliance, both increased or decreased, which may also contribute to delayed gastric emptying.[9]

In addition to this, serum (postprandial) glucose levels have a direct relationship with gastric emptying. In the setting of diabetic autonomic neuropathy, acute hyperglycemia stimulates gastric electrical activity.  In patients with diabetes (without neuropathy) and healthy controls, acute hyperglycemia will instead relax the proximal stomach, and suppress gastric electrical activity (e.g., reduced the frequency, propagation, and contraction of the antrum) in both fasting and post-prandial conditions, thereby slowing gastric emptying.

Acute hyperglycemia has also been associated with increased sensitivity in the gastrointestinal tract. This may be responsible for the postprandial dyspepsia (e.g., early satiety, nausea, vomiting, heartburn, bloating, and pain) frequently experienced by patients with diabetic gastroparesis.

Carbohydrate absorption is highly dependent on the speed of gastric emptying through the release of peptides such as glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in which slower gastric emptying results in a higher level of carbohydrate absorption. Therefore, a higher serum glucose level as a result of delayed gastric emptying can itself lead to the worsening of gastroparesis.

Histopathology

Histopathology does not routinely help in diagnosing a patient with diabetic gastroparesis. However, the findings seen on animal models, as well as in studies involving human pathology specimens, have helped us understand the disease process better. Full-thickness biopsies, which are needed to diagnose changes in the deeper layers of the stomach wall, are not practical to be used as a diagnostic tool. In special studies done using full-thickness gastric biopsies, the findings included an inflammatory infiltrate, reduction in nerve cell bodies, number of ICCs in the myenteric plexus, and fibrosis [10], [11], [12]. Recent studies have pointed at the role of macrophages in the pathogenesis of diabetic gastroparesis [13]

History and Physical

Nausea is the most common symptom in gastroparesis. Other common symptoms include vomiting, early satiety, postprandial fullness, and bloating. Vomitus often contains undigested chewed food. Weight loss and weight gain can be seen. Wide glycemic fluctuations can also happen in gastroparesis [14][15]. The timing of the symptoms in relation to meals is important. Physical examination is usually nonspecific. However, the presence of neuropathy, abdominal distension, halitosis can be seen in patients with diabetic gastroparesis.

Factors that may trigger an exacerbation of diabetic gastroparesis include uncontrolled blood glucose levels, medication noncompliance or intolerance, adrenal insufficiency, and infection.

Evaluation

The first step in the evaluation of patients who present with the symptoms above would be to exclude mechanical obstruction and peptic ulcer disease. All patients should undergo an upper gastrointestinal endoscopy. This should be followed by either a CT scan with oral and intravenous contrast or other imaging such as a small bowel follow-through to exclude obstruction beyond the duodenum. Retained food is seen on endoscopy without mechanical obstruction, and in rare cases, bezoars suggest gastroparesis.

The conventional test that is cost-effective and widely used for the diagnosis of gastroparesis is the measurement of gastric emptying by scintigraphy, which is considered the gold standard by many [16]. Solid-phase emptying is usually used to evaluate for gastroparesis. Liquid-phase emptying is not well demonstrated for diagnosing gastroparesis and is more widely used to assess for dumping syndrome after gastric surgery. Most centers use a 99 mTc sulfur colloid labeled egg white sandwich as the test meal [17]. Standard imaging is performed at 0,1,2,4 hours postprandially. A four-hour study is more sensitive and accurate in the diagnosis of gastroparesis, and a shortened 2- and 3-hour study should be avoided [18][19][16]. Medications such as opiates and anticholinergics can slow gastric motility, whereas prokinetics and other medications can hasten gastric emptying. Hyperglycemia is known to slow gastric motility, and it is worthwhile to try and achieve euglycemia prior to performing the test if that is an option [16]

Breath testing is another validated study for gastroparesis. Most commonly, 13C-labelled octanoate, a medium-chain triglyceride, is bound to a solid meal and ingested. After emptying from the stomach, it is absorbed by the small intestine and metabolized to 13CO2, which is expelled from the lungs during respiration. Currently, it has limited penetrance into the clinical practice and is performed for clinical research and pharmaceutical studies[16].

Electrogastrography and gastroduodenal manometry are other tests based on the myoelectrical activity that are potentially helpful tests but are not yet available for widespread clinical use.

Treatment / Management

The first step in the treatment of symptomatic gastroparesis is often lifestyle modifications. Optimal glycemic control in patients with diabetes will minimize the effects of hyperglycemia, causing delayed gastric emptying. Smaller, more frequent meals with minimizing carbonated beverages, increasing the liquid content, reducing fats, and fiber content are some of the common recommendations[20]. Alcohol and smoking should be discouraged, as they can worsen the symptoms [21][22].

Antiemetics are often the first step in patients with gastroparesis as they help with the common symptoms of nausea and vomiting. Serotonin (5-HT3) receptor antagonists like ondansetron, phenothiazines (dopamine receptor antagonists) like prochlorperazine and promethazine are commonly used. Side effects include sedation and extrapyramidal effects, and therefore, these are usually used on an 'as-needed' basis [16].

The cornerstone of pharmacologic therapy in diabetic gastroparesis consists of prokinetic agents.

Metoclopramide, a 5-HT4 receptor activator and dopamine receptor antagonist in the stomach with weak 5-HT3 receptor antagonism in the nervous system, is a commonly used medication that increases the contraction amplitude of esophageal, fundic, and antral musculature. It is effective for the treatment of gastroparesis for several weeks, but long term dosing has shown inconsistent results [23].

Erythromycin binds to the motilin receptors, which are responsible for the initiation of the MMC in the upper gut [24][25]. Like metoclopramide, erythromycin works well in the short term, but long term loss of response is common.

Domperidone is a dopamine (D2) agonist with effects similar to metoclopramide but is much less likely to cause extrapyramidal side effects as it does not cause the blood-brain barrier. Symptomatic patients with diabetes have reported improvement with domperidone therapy, but again, the effect could be lost in about six weeks [26][27][28]. Domperidone was associated with cardiac arrhythmias in the past and is not FDA approved in the United States. Cisapride is a 5-HT4 agonist that might have effects last up to 1 year, but unfortunately, it was also associated with ventricular arrhythmias, including torsades de pointes, and has been withdrawn from the US market. Both these drugs are available through select investigators as part of clinical trials with strict patient monitoring. In patients who do not respond well to the above therapies alone, combination prokinetic therapies can be tried. Symptomatic control of nausea using antiemetics can also be tried. Several studies have evaluated pyloric botulinum toxin injection, but these studies were often unblinded and had small numbers of patients[16]

Gastric electrical stimulation has been studied, but so far, there has not been a significant reduction in symptoms that were noted consistently across various small studies. It was granted humanitarian approval from the FDA for the treatment of chronic refractory nausea, but it is not available widely and not routinely reimbursed [16][29][16]

In refractory patients with severe symptoms, a gastrostomy tube for intermittent decompression by venting or suctioning may provide relief [29]. For patients who are not able to maintain nutrition with oral intake, placement of a feeding jejunostomy can be effective for providing nutrition, fluids, electrolytes, and reduce hospitalizations [30][31]. A trial of nasojejunal feeding can predict the response to a jejunostomy [29]

The last resort in refractory gastroparesis if surgery, which can be a partial gastrectomy with Roux-en-Y gastrojejunostomy and gastric resection. There is not enough data on surgical treatment at this time, and the decision to subject a patient to this should ideally be made by a motility expert [16].

Differential Diagnosis

Gastric outlet obstruction due to mechanical causes can present with similar symptoms and must be ruled out by endoscopy or imaging studies prior to making a diagnosis of gastroparesis.

Prognosis

The outcomes of diabetic gastroparesis are not well defined. Prognosis depends on the adequate control of hyperglycemia and compliance with medications. It affects the quality of life, and education regarding the need for lifelong management of this condition is essential. 

Complications

Malnutrition is an important complication of diabetic gastroparesis that often needs management with jejunostomy, parenteral nutrition, or surgery. Wide glycemic fluctuations can occur in diabetic gastroparesis, and this can lead to complications such as hypoglycemia and diabetic ketoacidosis or hyperosmolar hyperglycemic state. Nausea and vomiting can lead to aspiration and pneumonia from aspiration. 

Deterrence and Patient Education

Patients should be educated regarding the chronic and often irreversible nature of the disease. Adherence to a "gastroparesis diet", judicious use of medications and strict control of hyperglycemia are important patient factors that can change the course of the disease and prevent complications. 

Enhancing Healthcare Team Outcomes

Management of diabetic gastroparesis is extremely challenging. It is best done with an interprofessional team that includes an internist, endocrinologist, diabetes nurse educator, primary care provider, and a gastroenterologist, gastroenterology nurses, and pharmacists. Nurses provide patient education, monitor patients, and facilitate referrals and communication among the team. Pharmacists review prescribed medications, educate patients, and evaluated compliance. [Level 5]

Treatment of diabetic gastroparesis is aimed at alleviating the associated symptoms and replenishing electrolytes, nutrition, and hydration.

Frequently used medications include erythromycin (macrolide antibiotic-associated with increased gastrointestinal motility) and metoclopramide (antiemetic and prokinetic) and polyethylene glycol 3350 may additionally be used to provide relief from severe constipation.

Patients who continue to experience symptoms of gastroparesis despite medical therapy may be candidates for gastric electrical stimulation (GES) wherein an electrical device is implanted into the abdomen.

Unfortunately, no treatment works reliably or consistently. Once the condition has been diagnosed, it is progressive and imparts a very poor quality of life.[32][33]


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Diabetic Gastroparesis - Questions

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A patient with diabetes mellitus complains of gastric reflux, postprandial fullness, and occasional vomiting. A nuclear medicine study shows delayed gastric emptying. Which of the following medications should be prescribed?



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A 64-year-old diabetic with gastroparesis is started on a dopamine antagonist to relieve her condition. She most likely is given which of the following drugs?



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A 65-year-old female with a history of diabetes mellitus type 2, hypertension, and back pain presents complaining of episodic vomiting, nausea, and abdominal pain. Her medications include metformin, metoprolol, and aspirin. She has lost 5 pounds in the past month and an exam reveals abdominal distension. An abdominal CT and upper gastrointestinal series are negative. CBC, electrolytes, creatinine, and liver function tests are normal. What is the next step in the workup of this patient?



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A 60-year-old male with a history of type 2 diabetes mellitus, hypertension, and back pain on metformin, metoprolol, and aspirin presents with episodic vomiting, nausea, and abdominal pain. He has lost 6 pounds and all the radiological studies and blood work appear to be normal. What is the next best step?



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Which medication can be used to treat the symptoms of diabetic gastropathy?



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A person with diabetes mellitus has been diagnosed with gastroparesis. Which of the following medications may be of benefit in this disorder? Select all that apply.



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A 23-year-old woman with a history of type 1 diabetes mellitus, on insulin, since she was four years old presents with trouble controlling her blood sugars. She is on an insulin pump and is compliant with it. She has made no changes in diet and is taking the right doses of insulin as she has always done. However, lately, she has had episodes of hypoglycemia and hyperglycemia needing her to change her insulin doses. She also reports that she has lost about 8 lbs of weight in the last six weeks unintentionally. She feels full with smaller quantities of food and has nausea, mainly when she eats burgers or pizza, often leading to vomiting. Which of the following is a mediator of her symptoms in response to the fat content in her ileum?



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A 56-year-old woman with uncontrolled type 2 diabetes mellitus presents for management of gastroparesis. She has seen two other health care providers for the same problem before this. Her chief complaint is nausea, which she reports is constant and prevents her from being able to eat foods that she likes. She vomits about 2-3 times a day. She has had three admissions for diabetic ketoacidosis over the last year. Her medical history includes hypertension, hyperlipidemia, chronic kidney disease stage 3, and chronic migraines. Because of her chronic kidney disease, her nephrologist recommended against the use of NSAIDs, and therefore, she is on oxycodone for her headaches as needed, which she uses about 7-10 days a month. She has failed therapy with erythromycin. She is hesitant to try metoclopramide given the risks of tardive dyskinesia and is inquiring about gastric pacemakers. Which of the following is a predictor for optimal response to gastric pacing?



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A 28-year-old woman presents with epigastric pain and vomiting for the last eight months, which is progressively getting worse. She has a history of type 1 diabetes mellitus and is on an insulin pump. Though her diabetes has been hard to control, she is a compliant patient who works as an executive in a multinational company. An upper gastrointestinal endoscopy done after 12 hours of fasting shows mild gastritis and biopsies were negative for H. pylori and celiac disease. Which of the following statements regarding the disease process is correct?



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A 38-year-old man with diabetic gastroparesis comes in for a second opinion after failing various dietary modifications and intermittent treatments with antiemetics and prokinetic agents. He has tried eating small meals with low fat and fiber content. He takes high doses of ondansetron every day without adequate symptom relief. He responded well to erythromycin initially but soon lost that response. He had mild symptom relief with metoclopramide, but he is worried about the side effects and wants to avoid it. He has a family history of sudden cardiac death and does not wish to be referred to be evaluated for a clinical trial involving cisapride. He continues to have significant symptoms that are now leading to weight loss, and the nausea is affecting his job performance. Which of the following statements is true regarding the management of refractory gastroparesis?



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A 43-year-old man developed type 1 diabetes after having a pancreatic injury from a motorcycle accident when he was 25. He is on insulin, and his blood sugars are usually well controlled. He comes in for nausea, occasional vomiting, and early satiety that started over one year ago. He has not lost weight but is having problems maintaining his blood sugars due to the vomiting. He also complains of occasional abdominal pain after a meal, mainly when he eats out at his favorite burger joint. Which of the following factors will help improve the patient's symptoms?



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Diabetic Gastroparesis - References

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