Gastroparesis is a general term to describe a condition in which a patient has delayed gastric emptying. There are multiple etiologies to gastroparesis that include neurologic disorders, metabolic disorders, medication side effects, post-surgical and infectious.
The exact mechanism of gastroparesis development is not fully understood likely because of the many often overlapping etiologies, but the primary mechanism is felt to be autonomic dysfunction, primarily within the myenteric plexus, resulting in gastric dysmotility resulting in a reduction in coordinated transit of food through the gastrointestinal system.
Some causes are believed to be reversible such as infection or hyperglycemia and others irreversible including chronic or acute nerve damage.
There are multiple ways in which to diagnose patients with gastroparesis who demonstrate the classic symptoms. The most common diagnostic test is gastric emptying scintography in which a patient consumes a radiotracer and gastric contents fail to pass into the small intestine within 4 hours of ingestion. If radiologic gastric emptying studies are not available, endoscopic evaluation may be considered with manometry or capsule endoscopy to further assess gastric motility and transit.
In the absence of testing, a clinical diagnosis of exclusion may be in patients who recurrently present with symptoms of nausea, vomiting, early satiety, abdominal pain, and unintentional weight loss. It is important to note that 90% of patients with gastroparesis complain of abdominal pain. Confirmatory testing should be considered when available in order to prompt further work-up if gastric emptying is found to be normal. Other history including medication changes, glycemic control, recent or current acute illness, and diet changes may be helpful in determining other causes for symptoms common in gastroparesis.
Diabetic gastroparesis is the most studied and most common etiology of gastroparesis with a prevalence that has been increasing steadily over time due to increasing rates of diabetes mellitus within the general population.
One study looking at hospitalization trends from 1995-2004 and found an incidence of 30-50% in type I diabetics and 16-30% in type II diabetics. The total number of patients with gastroparesis with type II diabetes outnumbered those with type I by a ratio of 10 to 1.
Young to middle-aged women are about 4 times more likely to develop gastroparesis when compared to age adjusted men.
The prevalence of gastroparesis related to many other disorders is difficult to ascertain.
Delayed gastric emptying related to connective tissue disorders is not easily identifiable given the overlap between many disorders and the difficulty in making a definitive rheumatologic diagnosis in some cases. Patients with scleroderma and significant intestinal involvement are cited the most in literature as being prone to gastroparesis.
The prevalence of medications causing delayed gastric emptying is likely quite high given the prevalence of nausea and vomiting listed among the adverse reactions for the majority of medications. Medications that are commonly related to nausea and vomiting include narcotics, GLP-1 receptor agonists, alpha-2 receptor agonists such as clonidine and methyldopa, tricyclic antidepressants, and many others.
The prevalence of primary neurologic disorders associated with gastroparesis is also very difficult to determine because many neurologic disorders can also cause delayed gastric emptying.
Trauma, surgical injury, degeneration, or other neuropathy involving the vagus nerve may lead to delayed gastric emptying due to loss of the primary extrinsic intestinal innervation that guides coordinated intestinal motility. Other neurologic disorders such as Parkinson’s disease may have pathologic deposits that affect the intrinsic innervation of the intestinal tract which may be further exacerbated by medical treatment with dopaminergic and anticholinergic medications.
Functional dyspepsia has a similar presentation to gastroparesis as it is defined as one or more of the following: postprandial fullness, early satiety, epigastric pain or burning and no evidence of structural disease. This should be considered if gastric emptying scintography is normal. Other common etiologies include chronically uncontrolled diabetes mellitus, nerve trauma often associated with gastric bypass and other abdominal surgeries, and a growing number of cases considered to be idiopathic. In one study, an underlying cause could not be found in approximately 50% of patients with gastroparesis. Psychological disorders that may also be considered related to delayed gastric emptying would include bulemia, anorexia, and rumination syndrome. Malignancy may also be considered whether via direct nervous injury or paraneoplastic syndromes, including autoimmune antibody production leading to nerve damage.
For acute gastroparesis admissions, the following exam findings may guide therapy:
General: Patients often present in mild to significant distress and can appear to be anywhere from cachectic to obese.
HEENT: Mucous membranes may be dry.
Skin: Look for signs of increased skin turgor and reduced capillary refill consistent with dehydration.
Abdomen: Generalized or epigastric tenderness are common with reduced bowel sounds. There should be no signs of rebound or peritonitis.
Clinical labs are not particularly helpful in diagnosing gastroparesis, but may provide information regarding hydration, nutrition status, or underlying diseases that may predispose to gastroparesis.
Serum lipase may be useful acutely in the process of ruling out other causes for nausea, vomiting, and abdominal pain such as pancreatitis.
Comprehensive metabolic profile may be considered looking for signs of dehydration or azotemia as well as signs of malnutrition.
Hemoglobin A1c may be useful in determining glycemic control over the weeks prior to presentation.
The most useful test for diagnosis of gastroparesis is the gastric emptying study or scintography. This monitors transit of a consumed radiotracer to give a quantitative measure of gastric emptying. A diagnosis of gastroparesis is given for patients without passage of at least 90% of the radiotracer at 4 hours according to the American Neurogastroenterology and Motility Society. An upper endoscopy is also recommended to rule out any mechanical obstruction.
Other, generally less useful imaging tests for gastroparesis may include:
Abdominal x-rays: Useful in screening for signs of obstruction.
Abdominal computerized tomography (CT): Useful without contrast in ruling out other etiologies of abdominal pain including nephrolithiasis, pancreatitis, biliary disease and enteritis. Oral contrast may be used as in enterolysis if intestinal obstruction is suspected but may require a prolonged period of time for gastric transit.
Abdominal ultrasound: Ultrasound has no radiation exposure and is useful in evaluating for biliary obstruction, cholecystitis, or nephrolithiasis.
Fiberoptic or capsule endoscopy: Performed by gastroenterologists may demonstrate retained food and may be able to have associated testing including manometry.
Frequent abdominal CT scans without signs of an acute abdomen should be avoided due to radiation exposure and widespread availability of alternatives including ultrasound. Real time magnetic resonance imaging for intestinal motility disorders is generally applicable in the research setting at this time but does not carry the radiation exposure risks that computerized tomography has.
NPO status until emesis is controlled and abdominal pain improved, which may take up to several days, is prudent.
Intravenous fluids at 125-200% of maintenance fluid rates depending on degree of associated dehydration.
Ondansetron: A prophylactic antiemetic that can be useful in treating intractable nausea. Consider scheduled dosing of 4-8mg IV or PO every 6-12 hours for 1-2 days until nausea improves. The medication can then be tapered to the lowest efficacious dose if nausea improves.
Promethazine and prochlorperazine: 12.5-25mg PO and IV is useful for acute nausea. May be dosed as frequent as every 4 hours.
Benzodiazepines: IV, PO, and sublingual versions of lorazepam are available and can be effective as antiemetics; particularly for anticipatory nausea.
Metoclopramide: 5-10mg IV or PO prior to meals and at bedtime is a common first line pro-motility regimen for inpatients and outpatients. Intranasal metoclopramide has shown some promising results and may be superior to oral administration in reducing gastroparesis symptoms.
Erythromycin: Dosing recommendations range from 3mg/kg to 200mg three times daily before meals. Use may be limited by GI upset and potentially worsened nausea and vomiting (azithromycin may also be used by some reports with less frequent dosing and higher cost). Long-term clinical use is limited by diminishing clinical response secondary to tachyphylaxis.
A dedicated assessment regarding the patient’s nutrition, eating habits, and insight into the disease process can be helpful in reducing the frequency of exacerbations as well as diet compliance. Recommendations regarding nutritional and vitamin supplements may be useful in management. Continued nutrition assessments may help in determining the need for more aggressive interventions such as enteral or parenteral nutrition.
Nasogastric tube placement may be useful in patients who demonstrate persistent gastric dilatation or intractable emesis despite other therapy to provide further bowel rest. Long-term gastrostomy for decompression or percutaneous gastric or jejunal feeding tubes may be needed for patients who are unable to maintain PO intake despite maximal medical therapy.
Gastroparesis itself is not a medical emergency but may lead to the need for emergent treatment of dehydration, electrolyte derangements, and even management of acute GI bleed if repeated emesis causes a Mallory Weiss tear. If a patient presents to the emergency department with complaints consistent with gastroparesis consider:
IV fluid resuscitation if signs of dehydration;
IV antiemetics including phenergan and compazine;
Abdominal plain film may be considered if unable to rule out obstruction by patient history;
CT of the abdomen and pelvis if concern for an acute abdomen.
Response to therapy would be indicated by improved bowel sounds and reduced tenderness to palpation.
Monitoring for resolution of dehydration with normalized skin turgor and capillary refill may be helpful in monitoring therapy efficacy. In patients at risk for refeeding syndrome, monitoring for development of edema could indicate the need for adjustment in nutritional therapy.
As the acute exacerbation resolves, PO intake should improve.
Electrolyte monitoring in significantly dehydrated patients may help in titrating resuscitation daily or more frequent if necessary.
Prealbumin monitoring once or twice weekly is useful in monitoring improvements in malnutrition.
Liver function and lipids is recommended every 4-5 days for patients requiring parenteral nutrition.
If oral intake has been affected chronically, monitoring for refeeding syndrome with serum magnesium, potassium, and phosphorus levels may be a consideration.
To minimize the risks of acute bouts of gastroparesis, patients should be advised to change their eating pattern. Instead of 3 large meals daily, eating more frequent small meals is advisable. A recent study showed a small particle diet (consistent of soft, digestible foods and lacking in peels, membranes and seeds) resulted in improvement of gastroparesis symptoms. In addition to the above management, surgical intervention is another consideration for some gastroparesis patients.
Currently the primary available interventions are surgical decompression with a gastrostomy or jejunostomy, partial gastrectomy with gastric bypass, and as a last option implantable devices for gastric pacing/stimulation. Limited data is available for gastric pacing and should be considered only as a last resort with a referral to a qualified, experienced specialist if needed.
Upper GI series is not the same as a gastric emptying study and is less helpful in diagnosis of gastroparesis. To work most effectively, it is important to take pro-kinetic agents like metoclopramide at least 30 minutes prior to meals.
Med-surg floor bed
Subcutaneous heparin for DVT prophylaxis and proton pump inhibitor or H2 blocker for GI prophylaxis.
Admit – CMP, lipase, CBC, prealbumin, and consider hemoglobin A1c;
Daily – BMP, CBC, Magnesium
NPO to advance to clear and eventually full liquids.
Normal saline with rate determined by fluid status (100-200% of maintenance).
Dietician nutritional assessment.
Promethazine – 25mg IV or PO Q4 hours as needed for nausea;
Ondansetron – 4mg IV or PO ranging from prn Q4-6 hours prn to Q6 hours schedule;
Sublingual lorazepam – 0.5-1mg sublingual every 4 hours as needed for nausea;
Sliding scale insulin as needed for diabetic patients;
Discuss boundaries and side effects of narcotics to determine role in each patient with abdominal pain complaints.
Gastric emptying study to assess for gastroparesis.
Abdominal KUB vs CT abdomen if there is concern for obstruction or other abdominal pathology.
Nursing: Out of bed to chair for meals and ambulate as tolerated.
Patients with renal insufficiency may be sensitive to reductions in fluid intake related to intractable vomiting or nausea related to gastroparesis. Monitoring renal function closely, I&O’s, renally dosing medications if needed, and monitoring output are essential to maintaining renal function in patients with acute or chronic renal insufficiency.
Hepatic insufficiency is not typically effected by gastroparesis, but cirrhotic patients or patients with poor hepatic protein synthetic capability may have significantly worsened ascites and anasarca if their intravascular oncotic pressure is further diminished by nutritional deficiencies from reduced caloric intake.
No change in standard management.
No change in standard management.
Diabetic patients need tight glycemic control to aid in reducing gastroparetic symptoms. Titration of home diabetic regimens, use of sliding scale insulin regimens, and diabetic education as needed are imperative. An endocrinology consult may be beneficial for patients with difficult to control diabetes.
Malignancy may have a direct relation to delayed gastric emptying related to the production of paraneoplastic autoantibodies that result in damage to the intrinsic or extrinsic intestinal innervation. Small cell lung cancer is the most cited malignancy; however, other malignancies may also cause a similar syndrome.
Patients with chronic immunosuppression are often on multiple medications that either treat their disease such as HAART are immunosuppressed because of their medications such as with steroids. Some immunosuppressed patients may also be on prophylactic medications to prevent opportunistic infections.
If the patient was previously stable on their medications, efforts must be made to continue administration of vital medications via an alternative form or route. Certain medications may have adverse side effects that can lead delayed gastric emptying secondary to neuropathy and may need to be changed to an alternative medication with guidance of the subspecialty that manages that medication for the patient in the outpatient setting.
No change in standard management.
Gastroparesis patients, particularly those with diabetic gastroparesis, tend to do better with better glycemic control and avoidance of high fat foods.
Consideration of multiple smaller meals and avoidance of foods with high fat content are commonly recommended. Some patients are only able to be controlled on a liquid diet to allow for easier gastric emptying.
No change in standard management
These patients may have significant difficulty complying with medication regimens and can have difficulty relating poor medication compliance or glycemic control to gastroparesis symptoms. Making arrangements for close follow-up and in some cases home health to ensure medication compliance for symptom control and appropriate treatment of contributing comorbitities.
Patients with significant anxiety may have pronounced anticipatory nausea that is often best addressed early in the hospital stay allowing for patients to identify strategies for reducing anxiety related to nausea and eating with the assistance of antiemetics and anxiety medications while in house. All such medications should be weaned to their minimal effective dose as possible prior to discharge.
If special arrangements regarding diet, antiemetics, narcotics or other medications are made with the patient during the day, it is important to convey said arrangements with the night coverage to ensure consistency. Significant changes in pain should be evaluated to rule out an obstruction or acute abdomen.
Depending on other comorbidities, dehydration, and malnutrition the typical length of stay is quite variable. One article looking at outcomes in diabetic gastroparesis admissions had 5.3 days as an average length of stay.
Discharge may be considered once patients are able to tolerate at least full liquids with the use of oral antiemetics and pro-motility agents if needed for 12-24 hours.
Gastroparesis patients often benefit from close primary care follow-up to allow for fine tuning of their therapy to prevent early readmission.
Patients that present frequently for gastroparesis or who need additional motility testing as an outpatient may be considered for referral to a gastrointestinal specialist.
Diabetic gastroparesis patients who have chronically poor glycemic control may benefit from an endocrinology referral.
Should be arranged within one week of hospital discharge, especially if the patient presents frequently with gastroparesis complaints. Close follow-up allows for potential tapering of scheduled antiemetics and pain medications as well as allowing for development of an “action plan” if the symptoms return to allow for outpatient therapy.
May be considered if already established with a provider within a month in addition to primary care follow-up. New referrals are often dependent upon the provider, but follow-up within 2-3 months is typically expected.
May be scheduled within 2-3 months of discharge or earlier if available.
Patients and their primary care providers may benefit from a log of symptoms, medications use, and blood sugar log where applicable to aid in continued outpatient symptom management.
Patients who require prolonged care and nasogastric or total parenteral nutrition can be difficult to place at almost any level of facility. Some long term acute care facilities will take such advanced methods of nutrition administration, but early consideration for gastrostomy or jejunostomy for patients with frequent hospitalizations may help in placement and allow for some patients to manage their symptoms more effectively without hospitalization.
Prognosis and symptom control are truly multifactorial in nature. Patients who are motivated to control their gastroparesis must understand how their underlying medical problems may effect their symptom control. Education from dietary, diabetic, and other ancillary specialists can be of great help. Re-enforcing small, frequent, low-fat meals along with appropriate use of antiemetics, prokinetic agents, and other medications is important in maintaining symptom control.
DVT and GI prophylaxis should be considered for all patients. GI prophylaxis may be particularly important for symptom control in gastroparesis patients with underlying ulcer disease or reflux.
The best strategy for preventing readmission is close PCP follow-up, comorbid disease control, and multidisciplinary patient education that allows patients to recognize poor symptom control early in order to seek assistance prior to needing inpatient management.
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