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expanded signs and symptoms as well as complications. I moved the complications section to signs and symptoms to stay consistent with the Wikipedia format for medical conditions.
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Diagnosis is via one or more of the following: [[barium swallow]] X-ray, barium beefsteak meal, [[radioisotope]] gastric-emptying scan, gastric [[Pressure measurement|manometry]], [[esophagogastroduodenoscopy]] (EGD), and a [[Breath test|stable isotope breath test]]. Complications include [[malnutrition]], fatigue, weight loss, vitamin deficiencies, [[intestinal obstruction]] due to [[bezoar]]s, and [[small intestine bacterial overgrowth]]. Patient nutritional state should be managed by oral dietary modification, or if oral intake is not adequate through a [[Jejunostomy feeding tube|jejunostomy]] feeding tube.<ref name=":4">{{cite journal | vauthors = Camilleri M, Kuo B, Nguyen L, Vaughn VM, Petrey J, Greer K, Yadlapati R, Abell TL | display-authors = 6 | title = ACG Clinical Guideline: Gastroparesis | journal = The American Journal of Gastroenterology | volume = 117 | issue = 8 | pages = 1197–1220 | date = August 2022 | pmid = 35926490 | pmc = 9373497 | doi = 10.14309/ajg.0000000000001874 }}</ref>
Diagnosis is via one or more of the following: [[barium swallow]] X-ray, barium beefsteak meal, [[radioisotope]] gastric-emptying scan, gastric [[Pressure measurement|manometry]], [[esophagogastroduodenoscopy]] (EGD), and a [[Breath test|stable isotope breath test]]. Complications include [[malnutrition]], fatigue, weight loss, vitamin deficiencies, [[intestinal obstruction]] due to [[bezoar]]s, and [[small intestine bacterial overgrowth]]. Patient nutritional state should be managed by oral dietary modification, or if oral intake is not adequate through a [[Jejunostomy feeding tube|jejunostomy]] feeding tube.<ref name=":4">{{cite journal | vauthors = Camilleri M, Kuo B, Nguyen L, Vaughn VM, Petrey J, Greer K, Yadlapati R, Abell TL | display-authors = 6 | title = ACG Clinical Guideline: Gastroparesis | journal = The American Journal of Gastroenterology | volume = 117 | issue = 8 | pages = 1197–1220 | date = August 2022 | pmid = 35926490 | pmc = 9373497 | doi = 10.14309/ajg.0000000000001874 }}</ref>


⚫
Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches.<ref name=Thorn2010/> Additionally, [[gastric electrical stimulation]] (GES; approved on a humanitarian device exemption) can be used as treatment.<ref name=":4" /> Overall survival in gastroparesis patients is significantly lower than survival in the general population.<ref name="Jung Choung Locke Schleck 2009">{{cite journal | vauthors = Jung HK, Choung RS, Locke GR, Schleck CD, Zinsmeister AR, Szarka LA, Mullan B, Talley NJ | display-authors = 6 | title = The incidence, prevalence, and outcomes of patients with gastroparesis in Olmsted County, Minnesota, from 1996 to 2006 | journal = Gastroenterology | volume = 136 | issue = 4 | pages = 1225–1233 | date = April 2009 | pmid = 19249393 | doi = 10.1053/j.gastro.2008.12.047 | publisher = Elsevier BV | pmc = 2705939 }}</ref> It is associated with poor outcomes.<ref name="Jung Choung Locke Schleck 2009" />
Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches.<ref name=Thorn2010/>


⚫
== Signs and symptoms ==
Additionally, gastric electrical stimulation (GES; approved on a humanitarian device exemption) can be used as treatment.<ref name=":4" />
Gastroparesis has been linked to [[vomiting]], [[bloating]], early [[satiety]], and [[epigastric pain]]. Symptoms of delayed gastric emptying tend to be exacerbated by eating, particularly after fatty foods and indigestible solids like salads and leafy vegetables.<ref name="Clinical Presentations of Gastroparesis">{{cite book |last1=Reddy |first1=Shilpa C. |last2=Wo |first2=John M. |editor1-last=Parkman |editor1-first=Henry P. |editor2-last=McCallum |editor2-first=Richard W. |title=Gastroparesis |date=August 24, 2011 |publisher=Humana Press |location=Totowa, NJ |isbn=978-1-60761-551-4 |pages=25–35 |url=https://link.springer.com/book/10.1007/978-1-60761-552-1 |access-date=20 November 2023 |chapter=Clinical Presentations of Gastroparesis|doi=10.1007/978-1-60761-552-1_3}}</ref> In general, [[nausea]] is the most commonly reported symptom, affecting up to 96% of gastroparesis patients. However, depending on the etiology, the predominant symptom reported can differ.<ref name="Bharadwaj Meka Tandon Rathur 2016 pp. 285–294">{{cite journal | last=Bharadwaj | first=Shishira | last2=Meka | first2=Krishna | last3=Tandon | first3=Parul | last4=Rathur | first4=Abdullah | last5=Rivas | first5=John M. | last6=Vallabh | first6=Hiren | last7=Jevenn | first7=Andrea | last8=Guirguis | first8=John | last9=Sunesara | first9=Imran | last10=Nischnick | first10=Amy | last11=Ukleja | first11=Andrew | title=Management of gastroparesis‐associated malnutrition | journal=Journal of Digestive Diseases | publisher=Wiley | volume=17 | issue=5 | year=2016 | issn=1751-2972 | doi=10.1111/1751-2980.12344 | pages=285–294|url=https://onlinelibrary.wiley.com/doi/10.1111/1751-2980.12344|access-date=20 November 2023 }}</ref> The severity of gastric emptying dysfunction does not correspond to the severity of symptoms.<ref name="Clinical Presentations of Gastroparesis"/> [[Heartburn]] and poor glycemic control may be the only symptoms of delayed gastric emptying in [[Diabetes|diabetic]] patients. Physical examination in patients with gastroparesis may be completely normal, or in its more severe forms, [[dehydration]], [[malnutrition]], as well as a [[succussion splash]] can be present.<ref name="Pace 2019 pp. 21–31">{{cite book | last=Pace | first=Laura A. | title=Gastroparesis | chapter=Etiology and Clinical Presentation of Gastroparesis | publisher=Springer International Publishing | publication-place=Cham | date=November 9, 2019 | isbn=978-3-030-28928-7 | doi=10.1007/978-3-030-28929-4_2 | page=21–31|url=https://link.springer.com/book/10.1007/978-3-030-28929-4|access-date=20 November 2023}}</ref>


[[Nausea]] in gastroparesis is usually [[postprandial]], however, morning or persistent [[nausea]] may occur. [[Emesis]] is characterized by [[retching]] and forceful evacuation of gastric contents from the [[stomach]] up to and out of the mouth. Some patients may experience [[retching]] without gastric contents being expelled.<ref name="Clinical Presentations of Gastroparesis"/>
⚫
Overall survival in gastroparesis patients is significantly lower than survival in the general population.<ref name="Jung Choung Locke Schleck 2009">{{cite journal | vauthors = Jung HK, Choung RS, Locke GR, Schleck CD, Zinsmeister AR, Szarka LA, Mullan B, Talley NJ | display-authors = 6 | title = The incidence, prevalence, and outcomes of patients with gastroparesis in Olmsted County, Minnesota, from 1996 to 2006 | journal = Gastroenterology | volume = 136 | issue = 4 | pages = 1225–1233 | date = April 2009 | pmid = 19249393 | doi = 10.1053/j.gastro.2008.12.047 | publisher = Elsevier BV | pmc = 2705939 }}</ref> It is associated with poor outcomes.<ref name="Jung Choung Locke Schleck 2009" />


Postprandial fullness is an unpleasant feeling of stomach fullness that occurs after eating. Patients might characterize postprandial fullness as a feeling of food remaining in the stomach for an extended period of time. [[Satiety|Satiation]] is a lack of [[hunger]] after eating. It's the inverse of hunger and [[appetite]]. Early satiety is the disappearance of appetite before nutrient absorption during food ingestion. Early satiation may be described by patients with gastroparesis as a [[Anorexia (symptom)|loss of appetite]] or disappearance of appetite while eating. Early satiety is the sensation of stomach fullness that occurs shortly after beginning to eat and is out of proportion to the meal.<ref name="Clinical Presentations of Gastroparesis"/>
⚫
==Signs and symptoms==
The most common symptoms of gastroparesis are the following:<ref>{{cite web |url=http://www.mayoclinic.com/health/gastroparesis/DS00612/DSECTION=symptoms |title=Gastroparesis: Symptoms |publisher=MayoClinic.com |date=2012-01-04 |access-date=2012-10-09}}</ref>
* Chronic [[nausea]]
* [[Vomiting]] (especially of undigested food)
* [[Abdominal pain]]
* [[Satiety|A feeling of fullness]] after eating just a few bites


[[Bloating]] is a highly subjective feeling of increased abdominal pressure. [[Bloating]] without eating should be distinguished from postprandial fullness. It is sometimes, but not always, associated with food consumption.<ref name="Clinical Presentations of Gastroparesis"/>
Other symptoms include the following:
* Abdominal [[bloating]]
* Body aches ([[myalgia]])
* Erratic [[blood glucose]] levels
* [[Gastroesophageal reflux disease|Acid reflux]] (GERD)
* [[Heartburn]]
* [[Anorexia (symptom)|Lack of appetite]]
* Morning nausea
* [[Muscle weakness]]
* [[Night sweats]]
* [[Palpitation]]s
* [[Spasm]]s of the stomach wall
* [[Constipation]] or infrequent bowel movements
* [[Weight loss]], [[malnutrition]]
* [[Difficulty swallowing]]


[[Abdominal discomfort]] or pain is common, affecting 90% of gastroparesis patients. Idiopathic gastroparesis patients may experience more [[abdominal pain]] than [[Diabetes|diabetic]] gastroparesis patients.<ref name="Cherian Sachdeva Fisher Parkman 2010 pp. 676–681">{{cite journal | last=Cherian | first=Dinu | last2=Sachdeva | first2=Priyanka | last3=Fisher | first3=Robert S. | last4=Parkman | first4=Henry P. | title=Abdominal Pain Is a Frequent Symptom of Gastroparesis | journal=Clinical Gastroenterology and Hepatology | publisher=Elsevier BV | volume=8 | issue=8 | year=2010 | issn=1542-3565 | doi=10.1016/j.cgh.2010.04.027 | pages=676–681|url=https://pubmed.ncbi.nlm.nih.gov/20472097/|access-date=20 November 2023}}</ref> Physicians believe that postprandial [[epigastric pain]] is the most common symptom of gastroparesis.<ref name="Briley Harrell Woosley Eversmann 2011 pp. 412–417">{{cite journal | last=Briley | first=Lauren Carney | last2=Harrell | first2=Steven P. | last3=Woosley | first3=Allison | last4=Eversmann | first4=Jennifer | last5=Wo | first5=John M. | title=National Survey of Physicians' Perception of the Cause, Complications, and Management of Gastroparesis | journal=Southern Medical Journal | publisher=Southern Medical Association | volume=104 | issue=6 | year=2011 | issn=0038-4348 | doi=10.1097/smj.0b013e318215fa5a | pages=412–417|url=https://journals.lww.com/ajg/fulltext/2008/09001/national_survey_of_physician_s_perception_on_the.115.aspx|access-date=20 November 2023}}</ref> Abdominal pain has a wide range of symptoms. Around 40% of patients have localized epigastric pain, but it can be diffuse in some cases. Pain is usually classified as [[postprandial]], but it can also occur at night and interfere with sleep. The severity of [[abdominal pain]] is unrelated to the impairment of gastric emptying.<ref name="Cherian Sachdeva Fisher Parkman 2010 pp. 676–681"/>
Vomiting may not occur in all cases, as those affected may adjust their diets to include only small amounts of food.<ref name="autogenerated1"/>

⚫
=== Complications ===
Gastroparesis can lead to difficult glycemic control (which exacerbates gastric dysmotility), aspiration, [[bezoar]] formation, abnormalities in fluid and [[electrolyte]] balance, and inadequate nutrition intake resulting in [[weight loss]].<ref name="Bouras Vazquez Roque Aranda‐Michel 2013 pp. 437–447">{{cite journal | last=Bouras | first=Ernest P. | last2=Vazquez Roque | first2=Maria I. | last3=Aranda‐Michel | first3=Jaime | title=Gastroparesis | journal=Nutrition in Clinical Practice | publisher=Wiley | volume=28 | issue=4 | date=June 24, 2013 | issn=0884-5336 | doi=10.1177/0884533613491982 | pages=437–447}}</ref>

Some patients may experience severe [[nausea]] and [[Vomiting|emesis]], which can lead to [[dehydration]], as evidenced by [[orthostatic hypotension]] as well as acute [[renal insufficiency]]. Some patients with severe gastroparesis lose a significant amount of weight and suffer from [[nutritional deficiencies]], necessitating [[small bowel]] feeding access to bypass the stomach.<ref name="Clinical Presentations of Gastroparesis"/>

Individuals with gastroparesis are also more likely to develop gastric [[Bezoar|bezoars]]. Bezoars are large masses of foreign substances and food that have become trapped in the [[Gastrointestinal tract|GI tract]], especially in the stomach.<ref name="Bharadwaj Meka Tandon Rathur 2016 pp. 285–294"/> The incidence of [[bezoar]] formation in gastroparesis patients has been estimated to be approximately six percent based on a barium study.<ref name="Levin Levine Rubesin Laufer 2008 pp. 407–414">{{cite journal | last=Levin | first=A.A. | last2=Levine | first2=M.S. | last3=Rubesin | first3=S.E. | last4=Laufer | first4=I. | title=An 8-year review of barium studies in the diagnosis of gastroparesis | journal=Clinical Radiology | publisher=Elsevier BV | volume=63 | issue=4 | year=2008 | issn=0009-9260 | doi=10.1016/j.crad.2007.10.007 | pages=407–414}}</ref>

There is a strong link between gastroparesis and the development of [[Small intestinal bacterial overgrowth]] (SIBO). One study examined 50 gastroparesis patients using a glucose breath test and discovered that SIBO was present in 60% of their cohort. Furthermore, longer episodes of gastroparesis symptoms increase the risk of [[Small intestinal bacterial overgrowth|SIBO]]. Poor gastrointestinal motility and [[gastric acid]] production are believed to allow [[bacteria]] to colonize the [[small intestine]]. Furthermore, many individuals with gastroparesis are treated with [[Antacid|acid-suppressive drugs]], which significantly impair the GI tract's innate bactericidal activity. SIBO causes small bowel inflammation, impairing absorption and worsening nutritional deficiencies in gastroparesis.<ref name="Reddymasu McCallum 2010 pp. e8–e13">{{cite journal | last=Reddymasu | first=Savio C. | last2=McCallum | first2=Richard W. | title=Small Intestinal Bacterial Overgrowth in Gastroparesis | journal=Journal of Clinical Gastroenterology | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=44 | issue=1 | year=2010 | issn=0192-0790 | doi=10.1097/mcg.0b013e3181aec746 | pages=e8–e13}}</ref>

Because of the debilitating symptoms, patients with gastroparesis are at risk of significant nutritional abnormalities. In one study, 305 patients with gastroparesis had their dietary intake and nutritional status evaluated, and the average caloric intake was 1168 kcal/day, which resulted in substantial [[Malnutrition|nutritional deficiencies]]. Furthermore, 64% of gastroparesis patients consumed a calorie-deficient diet. Additionally, higher symptom scores were inversely proportional to caloric intake.<ref name="Parkman Yates Hasler Nguyan 2011 pp. 486–498.e7">{{cite journal | last=Parkman | first=Henry P. | last2=Yates | first2=Katherine P. | last3=Hasler | first3=William L. | last4=Nguyan | first4=Linda | last5=Pasricha | first5=Pankaj J. | last6=Snape | first6=William J. | last7=Farrugia | first7=Gianrico | last8=Calles | first8=Jorge | last9=Koch | first9=Kenneth L. | last10=Abell | first10=Thomas L. | last11=McCallum | first11=Richard W. | last12=Petito | first12=Dorothy | last13=Parrish | first13=Carol Rees | last14=Duffy | first14=Frank | last15=Lee | first15=Linda | last16=Unalp–Arida | first16=Aynur | last17=Tonascia | first17=James | last18=Hamilton | first18=Frank | title=Dietary Intake and Nutritional Deficiencies in Patients With Diabetic or Idiopathic Gastroparesis | journal=Gastroenterology | publisher=Elsevier BV | volume=141 | issue=2 | year=2011 | issn=0016-5085 | doi=10.1053/j.gastro.2011.04.045 | pages=486–498.e7}}</ref> Another study found that the severity of nutritional deficiencies was proportional to the duration of gastric emptying.<ref>{{cite journal |last1=Ogorek |first1=C P |last2=Davidson |first2=L |last3=Fisher |first3=R S |last4=Krevsky |first4=B |title=Idiopathic gastroparesis is associated with a multiplicity of severe dietary deficiencies |journal=The American journal of gastroenterology |date=1991 |volume=86 |issue=4 |pages=423-428 |pmid=2012043 |url=https://pubmed.ncbi.nlm.nih.gov/2012043/ |access-date=20 November 2023}}</ref> Minerals like [[iron]], [[fat-soluble vitamins]], [[thiamine]], and [[folate]] are commonly reported deficiencies. [[Iron deficiency]] is common in patients with gastroparesis.<ref name="Bharadwaj Meka Tandon Rathur 2016 pp. 285–294"/>

⚫
Other complications include fluctuations in [[blood glucose]] due to unpredictable digestion times due to changes in rate and amount of food passing into the [[small bowel]], a decrease in quality of life, since it can make keeping up with work and other responsibilities more difficult, and severe [[fatigue]] due to [[Caloric deficit|calorie deficit.]]<ref name="mayoclinic.org">{{cite web |title=Gastroparesis Complications&nbsp;– Mayo Clinic |url=http://www.mayoclinic.org/diseases-conditions/gastroparesis/basics/complications/con-20023971 |website=[[Mayo Clinic]]}}</ref>


==Causes==
==Causes==
Line 84: Line 79:


In other cases or if the X-ray is inconclusive, the physician may have the patient eat a meal of toast, water, and eggs containing a radioactive isotope so they can watch as it is digested and see how slowly the digestive tract is moving. This can be helpful for diagnosing patients who are able to digest liquids but not solid foods.<ref name=":1" />
In other cases or if the X-ray is inconclusive, the physician may have the patient eat a meal of toast, water, and eggs containing a radioactive isotope so they can watch as it is digested and see how slowly the digestive tract is moving. This can be helpful for diagnosing patients who are able to digest liquids but not solid foods.<ref name=":1" />

⚫
==Complications==
Complications of gastroparesis include:
⚫
* Fluctuations in [[blood glucose]] due to unpredictable digestion times due to changes in rate and amount of food passing into the small bowel. This makes diabetes worse, but does not cause diabetes. Lack of control of blood sugar levels will make the gastroparesis worsen.<ref name="mayoclinic.org">{{cite web|url=http://www.mayoclinic.org/diseases-conditions/gastroparesis/basics/complications/con-20023971|title=Gastroparesis Complications&nbsp;– Mayo Clinic|website=[[Mayo Clinic]]}}</ref>
* General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it. This is especially true for vitamin deficiencies such as scurvy because of inability to tolerate fresh fruits.<ref>Lisa Sanders MD "Diagnosis" NY Times Magazine 3.4.18 p.16-18.</ref>
* Severe fatigue and weight loss due to calorie deficit<ref name="mayoclinic.org" />
* [[Intestinal obstruction]] due to the formation of [[bezoar]]s (solid masses of undigested food). This can cause nausea and vomiting, which can in turn be life-threatening if they prevent food from passing the small intestine.<ref name="mayoclinic.org"/>
* [[Small intestine bacterial overgrowth]] is commonly found in patients with gastroparesis.<ref name="pmid27111029">{{cite journal | vauthors = Bharadwaj S, Meka K, Tandon P, Rathur A, Rivas JM, Vallabh H, Jevenn A, Guirguis J, Sunesara I, Nischnick A, Ukleja A | display-authors = 6 | title = Management of gastroparesis-associated malnutrition | journal = Journal of Digestive Diseases | volume = 17 | issue = 5 | pages = 285–294 | date = May 2016 | pmid = 27111029 | doi = 10.1111/1751-2980.12344 | s2cid = 26992080 }}</ref>
* [[Bacterial infection]] due to overgrowth in undigested food<ref name="mayoclinic.org"/>
* A decrease in quality of life, since it can make keeping up with work and other responsibilities more difficult.<ref name="mayoclinic.org" />


==Treatment==
==Treatment==

Revision as of 04:20, 20 November 2023

Gastroparesis
Other namesdelayed gastric emptying
Pronunciation
  • (/,ɡæstroʊ,pəˈriːsɪs/)[1]
SpecialtyGastroenterology
SymptomsNausea, vomiting, abdominal pain, feeling full after eating just a few bites
ComplicationsMalnutrition, fatigue, weight loss, vitamin deficiencies, intestinal obstruction due to bezoars, and small intestine bacterial overgrowth.
CausesDamage to the vagus nerve,[2] chemotherapy-induced neuropathy,[3] and autonomic neuropathy.[4]
Risk factorsDiabetes, abdominal or esophageal surgery, infection, certain medications that slow the rate of stomach emptying, scleroderma, nervous system diseases, and hypothyroidism.[2]
Diagnostic methodBarium swallow X-ray, barium beefsteak meal, radioisotope gastric-emptying scan, gastric manometry, esophagogastroduodenoscopy (EGD), and a stable isotope breath test.
TreatmentDietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting,[5] and gastric electrical stimulation.[6]
Frequencypossibly up to 4%[citation needed]

Gastroparesis (gastro- from Ancient Greek γαστήρ – gaster, "stomach"; and -paresis, πάρεσις – "partial paralysis"), also called delayed gastric emptying, is a medical disorder consisting of weak muscular contractions (peristalsis) of the stomach, resulting in food and liquid remaining in the stomach for a prolonged period of time. Stomach contents thus exit more slowly into the duodenum of the digestive tract. This can result in irregular absorption of nutrients, inadequate nutrition, and poor glycemic control.[7][8]

Symptoms include nausea, vomiting, abdominal pain, feeling full soon after beginning to eat (early satiety), abdominal bloating, and heartburn. The most common known mechanism is autonomic neuropathy of the nerve which innervates the stomach: the vagus nerve. Uncontrolled diabetes mellitus is a major cause of this nerve damage; other causes include post-infectious and trauma to the vagus nerve.

Diagnosis is via one or more of the following: barium swallow X-ray, barium beefsteak meal, radioisotope gastric-emptying scan, gastric manometry, esophagogastroduodenoscopy (EGD), and a stable isotope breath test. Complications include malnutrition, fatigue, weight loss, vitamin deficiencies, intestinal obstruction due to bezoars, and small intestine bacterial overgrowth. Patient nutritional state should be managed by oral dietary modification, or if oral intake is not adequate through a jejunostomy feeding tube.[6]

Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches.[5] Additionally, gastric electrical stimulation (GES; approved on a humanitarian device exemption) can be used as treatment.[6] Overall survival in gastroparesis patients is significantly lower than survival in the general population.[9] It is associated with poor outcomes.[9]

Signs and symptoms

Gastroparesis has been linked to vomiting, bloating, early satiety, and epigastric pain. Symptoms of delayed gastric emptying tend to be exacerbated by eating, particularly after fatty foods and indigestible solids like salads and leafy vegetables.[10] In general, nausea is the most commonly reported symptom, affecting up to 96% of gastroparesis patients. However, depending on the etiology, the predominant symptom reported can differ.[11] The severity of gastric emptying dysfunction does not correspond to the severity of symptoms.[10] Heartburn and poor glycemic control may be the only symptoms of delayed gastric emptying in diabetic patients. Physical examination in patients with gastroparesis may be completely normal, or in its more severe forms, dehydration, malnutrition, as well as a succussion splash can be present.[12]

Nausea in gastroparesis is usually postprandial, however, morning or persistent nausea may occur. Emesis is characterized by retching and forceful evacuation of gastric contents from the stomach up to and out of the mouth. Some patients may experience retching without gastric contents being expelled.[10]

Postprandial fullness is an unpleasant feeling of stomach fullness that occurs after eating. Patients might characterize postprandial fullness as a feeling of food remaining in the stomach for an extended period of time. Satiation is a lack of hunger after eating. It's the inverse of hunger and appetite. Early satiety is the disappearance of appetite before nutrient absorption during food ingestion. Early satiation may be described by patients with gastroparesis as a loss of appetite or disappearance of appetite while eating. Early satiety is the sensation of stomach fullness that occurs shortly after beginning to eat and is out of proportion to the meal.[10]

Bloating is a highly subjective feeling of increased abdominal pressure. Bloating without eating should be distinguished from postprandial fullness. It is sometimes, but not always, associated with food consumption.[10]

Abdominal discomfort or pain is common, affecting 90% of gastroparesis patients. Idiopathic gastroparesis patients may experience more abdominal pain than diabetic gastroparesis patients.[13] Physicians believe that postprandial epigastric pain is the most common symptom of gastroparesis.[14] Abdominal pain has a wide range of symptoms. Around 40% of patients have localized epigastric pain, but it can be diffuse in some cases. Pain is usually classified as postprandial, but it can also occur at night and interfere with sleep. The severity of abdominal pain is unrelated to the impairment of gastric emptying.[13]

Complications

Gastroparesis can lead to difficult glycemic control (which exacerbates gastric dysmotility), aspiration, bezoar formation, abnormalities in fluid and electrolyte balance, and inadequate nutrition intake resulting in weight loss.[15]

Some patients may experience severe nausea and emesis, which can lead to dehydration, as evidenced by orthostatic hypotension as well as acute renal insufficiency. Some patients with severe gastroparesis lose a significant amount of weight and suffer from nutritional deficiencies, necessitating small bowel feeding access to bypass the stomach.[10]

Individuals with gastroparesis are also more likely to develop gastric bezoars. Bezoars are large masses of foreign substances and food that have become trapped in the GI tract, especially in the stomach.[11] The incidence of bezoar formation in gastroparesis patients has been estimated to be approximately six percent based on a barium study.[16]

There is a strong link between gastroparesis and the development of Small intestinal bacterial overgrowth (SIBO). One study examined 50 gastroparesis patients using a glucose breath test and discovered that SIBO was present in 60% of their cohort. Furthermore, longer episodes of gastroparesis symptoms increase the risk of SIBO. Poor gastrointestinal motility and gastric acid production are believed to allow bacteria to colonize the small intestine. Furthermore, many individuals with gastroparesis are treated with acid-suppressive drugs, which significantly impair the GI tract's innate bactericidal activity. SIBO causes small bowel inflammation, impairing absorption and worsening nutritional deficiencies in gastroparesis.[17]

Because of the debilitating symptoms, patients with gastroparesis are at risk of significant nutritional abnormalities. In one study, 305 patients with gastroparesis had their dietary intake and nutritional status evaluated, and the average caloric intake was 1168 kcal/day, which resulted in substantial nutritional deficiencies. Furthermore, 64% of gastroparesis patients consumed a calorie-deficient diet. Additionally, higher symptom scores were inversely proportional to caloric intake.[18] Another study found that the severity of nutritional deficiencies was proportional to the duration of gastric emptying.[19] Minerals like iron, fat-soluble vitamins, thiamine, and folate are commonly reported deficiencies. Iron deficiency is common in patients with gastroparesis.[11]

Other complications include fluctuations in blood glucose due to unpredictable digestion times due to changes in rate and amount of food passing into the small bowel, a decrease in quality of life, since it can make keeping up with work and other responsibilities more difficult, and severe fatigue due to calorie deficit.[20]

Causes

Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns. Patients with cancer may develop gastroparesis because of chemotherapy-induced neuropathy, immunosuppression followed by viral infections involving the GI tract, procedures such as celiac blocks, paraneoplastic neuropathy or myopathy, or after an allogeneic bone marrow transplant via graft-versus-host disease.[3]

Gastroparesis present similar symptoms to slow gastric emptying caused by certain opioid medications, antidepressants, and allergy medications, along with high blood pressure. For patients already with gastroparesis, these can make the condition worse.[21] More than 50% of all gastroparesis cases are idiopathic in nature, with unknown causes. It is, however, frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes, about 30–50% among long-standing diabetics.[4] In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves.[22] The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis.[2] Adrenal and thyroid gland problems could also be a cause.[23]

Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease and multiple system atrophy.[24] It may occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis. Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.[25] Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining. Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection.[2] Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.[26]

People with gastroparesis are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.[27] A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest.[28] Neither theory has been proven definitively.

Physiology and Mechanism

The symptoms of gastroparesis are best understood in the context of the physiology of gastric emptying (GE). The stomach functions as a reservoir for food and nutritional content, which are broken down to produce chyme. Chyme is then released into the duodenum at a controlled rate to allow for maximum nutrient absorption. The controlled rate of chyme released is regulated by feedback mechanisms from the stomach and small intestines, which activate the vagus nerve and other hormones. The delay of any of the factors in gastric emptying causes disorganization or reduced frequency of antral contractions and thus delayed GE.[29]

On the molecular level, it is thought that gastroparesis can be caused by the loss of neuronal nitric oxide expression since the cells in the GI tract secrete nitric oxide. This important signaling molecule has various responsibilities in the GI tract and in muscles throughout the body. When nitric oxide levels are low, the smooth muscle and other organs may not be able to function properly.[30] Other important components of the stomach are the interstitial cells of Cajal (ICC) which act as a pacemaker since they transduce signals from motor neurons to produce an electrical rhythm in the smooth muscle cells.[31] Lower nitric oxide levels also correlate with loss of ICC cells, which can ultimately lead to the loss of function in the smooth muscle in the stomach, as well as in other areas of the gastrointestinal tract.[30]

Pathogenesis of symptoms in diabetic gastroparesis include:

  • Loss of gastric neurons containing nitric oxide synthase (NOS) is responsible for defective accommodation reflex, which leads to early satiety and postprandial fullness.[4]
  • Impaired electromechanical activity in the myenteric plexus is responsible for delayed gastric emptying, resulting in nausea and vomiting.[4]
  • Sensory neuropathy in the gastric wall may be responsible for epigastric pain.[4]
  • Abnormal pacemaker activity (tachybradyarrhythmia) may generate a noxious signal transmitted to the CNS to evoke nausea and vomiting.[4]

Diagnosis

Gastroparesis can be diagnosed with tests such as barium swallow X-rays, manometry, and gastric emptying studies.[32] For the X-ray, the patient drinks a liquid containing barium after fasting which will show up in the X-ray and the physician is able to see if there is still food in the stomach as well. This can be an easy way to identify whether the patient has delayed emptying of the stomach.[33] The clinical definition for gastroparesis is based solely on the emptying time of the stomach (and not on other symptoms), and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.[citation needed]

In other cases or if the X-ray is inconclusive, the physician may have the patient eat a meal of toast, water, and eggs containing a radioactive isotope so they can watch as it is digested and see how slowly the digestive tract is moving. This can be helpful for diagnosing patients who are able to digest liquids but not solid foods.[33]

Treatment

Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches.[5]

Dietary treatment involves low fiber diets and, in some cases, restrictions on fat or solids. Eating smaller meals, spaced two to three hours apart has proved helpful. Avoiding foods like rice or beef that cause the individual problems such as pain in the abdomen or constipation will help avoid symptoms.[34]

Metoclopramide, a dopamine D2 receptor antagonist, increases contractility and resting tone within the GI tract to improve gastric emptying.[35] In addition, dopamine antagonist action in the central nervous system prevents nausea and vomiting.[36] Similarly, the dopamine receptor antagonist domperidone is used to treat gastroparesis. Erythromycin is known to improve emptying of the stomach but its effects are temporary due to tachyphylaxis and wane after a few weeks of consistent use. Sildenafil citrate, which increases blood flow to the genital area in men, is being used by some practitioners to stimulate the gastrointestinal tract in cases of diabetic gastroparesis.[37] The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment.[38] This is due to its antiemetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as does the popular anti-emetic ondansetron.[39] Camicinal is a motilin agonist for the treatment of gastroparesis.

In specific cases where treatment of chronic nausea and vomiting proves resistant to drugs, implantable gastric stimulation may be used. A medical device is implanted that applies neurostimulation to the muscles of the lower stomach to reduce the symptoms. This is only done in refractory cases that have failed all medical management (usually at least two years of treatment).[34] Medically refractory gastroparesis may also be treated with a pyloromyotomy, which widens the gastric outlet by cutting the circular pylorus muscle. This can be done laparoscopically or endoscopically (called G-POEM). Vertical sleeve gastrectomy, a procedure in which a part or all of the affected portion of the stomach is removed, has been shown to have some success in the treatment of gastroparesis in obese patients, even curing it in some instances. Further studies have been recommended due to the limited sample size of previous studies.[40][41]

In cases of postinfectious gastroparesis, patients have symptoms and go undiagnosed for an average of 3 weeks to 6 months before their illness is identified correctly and treatment begins.[citation needed]

Prognosis

Post-infectious

Cases of post-infectious gastroparesis are self‐limiting, with recovery within 12 months of initial symptoms, although some cases last well over 2 years. In children, the duration tends to be shorter and the disease course milder than in adolescent and adults.[5]

Diabetic gastropathy

Diabetic gastropathy is usually slowly progressive, and can become severe and lethal.[42]

Prevalence

Post-infectious gastroparesis, which constitutes the majority of idiopathic gastroparesis cases, affects up to 4% of the American population.[citation needed] Women in their 20s and 30s seem to be susceptible. One study of 146 American gastroparesis patients found the mean age of patients was 34 years with 82% affected being women, while another study found the patients were young or middle aged and up to 90% were women.[5]

There has only been one true epidemiological study of idiopathic gastroparesis which was completed by the Rochester Epidemiology Project.[9] They looked at patients from 1996 to 2006 who were seeking medical attention instead of a random population sample and found that the prevalence of delayed gastric emptying was fourfold higher in women. It is difficult for medical professionals and researchers to collect enough data and provide accurate numbers since studying gastroparesis requires specialized laboratories and equipment.[43]

References

  1. ^ "How to pronounce gastroparesis in English". dictionary.cambridge.org.
  2. ^ a b c d "Gastroparesis Causes – Mayo Clinic". Mayo Clinic.
  3. ^ a b Davis MP, Weller R, Regel S (2018). "Gastroparesis and Cancer-Related Gastroparesis". In MacLeod RD, van den Block L (eds.). Textbook of Palliative Care. Springer International Publishing. pp. 1–15. doi:10.1007/978-3-319-31738-0_114-1. ISBN 978-3-319-31738-0.
  4. ^ a b c d e f Owyang C (October 2011). "Phenotypic switching in diabetic gastroparesis: mechanism directs therapy". Gastroenterology. 141 (4): 1134–1137. doi:10.1053/j.gastro.2011.08.014. PMID 21875587.
  5. ^ a b c d e Thorn AR (March 2010). "Not just another case of nausea and vomiting: a review of postinfectious gastroparesis". Journal of the American Academy of Nurse Practitioners. 22 (3): 125–133. doi:10.1111/j.1745-7599.2009.00485.x. PMID 20236395. S2CID 12354903.
  6. ^ a b c Camilleri M, Kuo B, Nguyen L, Vaughn VM, Petrey J, Greer K, et al. (August 2022). "ACG Clinical Guideline: Gastroparesis". The American Journal of Gastroenterology. 117 (8): 1197–1220. doi:10.14309/ajg.0000000000001874. PMC 9373497. PMID 35926490.
  7. ^ . In: Simpson, Kathleen Rice, Creehan, Patricia A. eds. AWHONN's Perinatal Nursing. 4th Edition. 530 Walnut Street, Philadelphia, PA 19106 USA:Lippincott Williams & Wilkins; 2014. Available from: Books@Ovid at [1]. Retrieved November 09, 2020.
  8. ^ Fuglsang, J., & Ovesen, P. R. (2015). Pregnancy and delivery in a woman with type 1 diabetes, gastroparesis, and a gastric neurostimulator. Diabetes Care, 38(5), e75. doi:10.2337/dc14-2959
  9. ^ a b c Jung HK, Choung RS, Locke GR, Schleck CD, Zinsmeister AR, Szarka LA, et al. (April 2009). "The incidence, prevalence, and outcomes of patients with gastroparesis in Olmsted County, Minnesota, from 1996 to 2006". Gastroenterology. 136 (4). Elsevier BV: 1225–1233. doi:10.1053/j.gastro.2008.12.047. PMC 2705939. PMID 19249393.
  10. ^ a b c d e f Reddy, Shilpa C.; Wo, John M. (August 24, 2011). "Clinical Presentations of Gastroparesis". In Parkman, Henry P.; McCallum, Richard W. (eds.). Gastroparesis. Totowa, NJ: Humana Press. pp. 25–35. doi:10.1007/978-1-60761-552-1_3. ISBN 978-1-60761-551-4. Retrieved 20 November 2023.
  11. ^ a b c Bharadwaj, Shishira; Meka, Krishna; Tandon, Parul; Rathur, Abdullah; Rivas, John M.; Vallabh, Hiren; Jevenn, Andrea; Guirguis, John; Sunesara, Imran; Nischnick, Amy; Ukleja, Andrew (2016). "Management of gastroparesis‐associated malnutrition". Journal of Digestive Diseases. 17 (5). Wiley: 285–294. doi:10.1111/1751-2980.12344. ISSN 1751-2972. Retrieved 20 November 2023.
  12. ^ Pace, Laura A. (November 9, 2019). "Etiology and Clinical Presentation of Gastroparesis". Gastroparesis. Cham: Springer International Publishing. p. 21–31. doi:10.1007/978-3-030-28929-4_2. ISBN 978-3-030-28928-7. Retrieved 20 November 2023.
  13. ^ a b Cherian, Dinu; Sachdeva, Priyanka; Fisher, Robert S.; Parkman, Henry P. (2010). "Abdominal Pain Is a Frequent Symptom of Gastroparesis". Clinical Gastroenterology and Hepatology. 8 (8). Elsevier BV: 676–681. doi:10.1016/j.cgh.2010.04.027. ISSN 1542-3565. Retrieved 20 November 2023.
  14. ^ Briley, Lauren Carney; Harrell, Steven P.; Woosley, Allison; Eversmann, Jennifer; Wo, John M. (2011). "National Survey of Physicians' Perception of the Cause, Complications, and Management of Gastroparesis". Southern Medical Journal. 104 (6). Southern Medical Association: 412–417. doi:10.1097/smj.0b013e318215fa5a. ISSN 0038-4348. Retrieved 20 November 2023.
  15. ^ Bouras, Ernest P.; Vazquez Roque, Maria I.; Aranda‐Michel, Jaime (June 24, 2013). "Gastroparesis". Nutrition in Clinical Practice. 28 (4). Wiley: 437–447. doi:10.1177/0884533613491982. ISSN 0884-5336.
  16. ^ Levin, A.A.; Levine, M.S.; Rubesin, S.E.; Laufer, I. (2008). "An 8-year review of barium studies in the diagnosis of gastroparesis". Clinical Radiology. 63 (4). Elsevier BV: 407–414. doi:10.1016/j.crad.2007.10.007. ISSN 0009-9260.
  17. ^ Reddymasu, Savio C.; McCallum, Richard W. (2010). "Small Intestinal Bacterial Overgrowth in Gastroparesis". Journal of Clinical Gastroenterology. 44 (1). Ovid Technologies (Wolters Kluwer Health): e8–e13. doi:10.1097/mcg.0b013e3181aec746. ISSN 0192-0790.
  18. ^ Parkman, Henry P.; Yates, Katherine P.; Hasler, William L.; Nguyan, Linda; Pasricha, Pankaj J.; Snape, William J.; Farrugia, Gianrico; Calles, Jorge; Koch, Kenneth L.; Abell, Thomas L.; McCallum, Richard W.; Petito, Dorothy; Parrish, Carol Rees; Duffy, Frank; Lee, Linda; Unalp–Arida, Aynur; Tonascia, James; Hamilton, Frank (2011). "Dietary Intake and Nutritional Deficiencies in Patients With Diabetic or Idiopathic Gastroparesis". Gastroenterology. 141 (2). Elsevier BV: 486–498.e7. doi:10.1053/j.gastro.2011.04.045. ISSN 0016-5085.
  19. ^ Ogorek, C P; Davidson, L; Fisher, R S; Krevsky, B (1991). "Idiopathic gastroparesis is associated with a multiplicity of severe dietary deficiencies". The American journal of gastroenterology. 86 (4): 423–428. PMID 2012043. Retrieved 20 November 2023.
  20. ^ "Gastroparesis Complications – Mayo Clinic". Mayo Clinic.
  21. ^ "Overview". Mayo Clinic.
  22. ^ "Spotlight on gastroparesis," unauthored article, Balance (magazine of Diabetes UK, no. 246, May–June 2012, p. 43.
  23. ^ "Gastroparesis". Jackson Siegelbaum Gastroenterology. 2011-11-08. Retrieved 2019-11-06.
  24. ^ "Gastroparesis – Your Guide to Gastroparesis – Causes of Gastroparesis". Heartburn.about.com. Retrieved 2012-02-10.
  25. ^ "Gastroparesis: Causes". MayoClinic.com. 2012-01-04. Retrieved 2012-10-09.
  26. ^ Naftali, Timna; Yishai, Ron; Zangen, Tsili; Levine, Arie (August 15, 2007). "Post‐infectious gastroparesis: Clinical and electerogastrographic aspects". Journal of Gastroenterology and Hepatology. 22 (9). Wiley: 1423–1428. doi:10.1111/j.1440-1746.2006.04738.x. ISSN 0815-9319. PMID 17716347. S2CID 26506859.
  27. ^ "Epocrates article, registration required". Online.epocrates.com. Retrieved 2012-10-09.
  28. ^ "Summary for Oley Foundation by R. W. McCallum, MD". Oley.org. Archived from the original on 2005-12-12. Retrieved 2012-10-09.[unreliable medical source?]
  29. ^ Sullivan, A.; Temperley, L.; Ruban, A. (30 April 2020). "Pathophysiology, Aetiology and Treatment of Gastroparesis". Digestive Diseases and Sciences. 65 (6): 1615–1631. doi:10.1007/s10620-020-06287-2. hdl:10044/1/79544. PMID 32350720. S2CID 216649955.
  30. ^ a b Oh JH, Pasricha PJ (January 2013). "Recent advances in the pathophysiology and treatment of gastroparesis". Journal of Neurogastroenterology and Motility. 19 (1): 18–24. doi:10.5056/jnm.2013.19.1.18. PMC 3548121. PMID 23350043.
  31. ^ Al-Shboul OA (2013). "The importance of interstitial cells of cajal in the gastrointestinal tract". Saudi Journal of Gastroenterology. 19 (1): 3–15. doi:10.4103/1319-3767.105909. PMC 3603487. PMID 23319032.
  32. ^ "Gastroparesis Tests and diagnosis – Mayo Clinic". Mayo Clinic.
  33. ^ a b "Gastroparesis". American Diabetes Association. Retrieved 2018-09-08.
  34. ^ a b "Treatment Options for Gastroparesis". Medtronic.com. Medtronic. 29 September 2014. Retrieved 9 March 2016.
  35. ^ "Metochlopramide Hydrochloride". Monograph. The American Society of Health-System Pharmacists. Retrieved 23 March 2016.
  36. ^ Rang HP, Dale MM, Ritter JM, Moore PK (2003). Pharmacology (5th ed.). Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.[page needed]
  37. ^ Gottlieb S (August 2000). "Sildenafil may help diabetic patients". BMJ. 321 (7258): 401A. PMC 1127789. PMID 10938040.
  38. ^ Kundu S, Rogal S, Alam A, Levinthal DJ (June 2014). "Rapid improvement in post-infectious gastroparesis symptoms with mirtazapine". World Journal of Gastroenterology. 20 (21): 6671–6674. doi:10.3748/wjg.v20.i21.6671. PMC 4047357. PMID 24914393.
  39. ^ Kim SW, Shin IS, Kim JM, Kang HC, Mun JU, Yang SJ, Yoon JS (2006). "Mirtazapine for severe gastroparesis unresponsive to conventional prokinetic treatment". Psychosomatics. 47 (5): 440–442. doi:10.1176/appi.psy.47.5.440. PMID 16959934.
  40. ^ Samuel B, Atiemo K, Cohen P, Czerniach D, Kelly J, Perugini R (2016). "The Effect of Sleeve Gastrectomy on Gastroparesis: A Short Clinical Review". Bariatric Surgical Practice and Patient Care. 11 (2): 84–9. doi:10.1089/bari.2015.0052.
  41. ^ Bagloo M, Besseler M, Ude A (April 2010). Sleeve gastrectomy for the treatment of diabetic gastroparesis. Proceedings 12th world congress of endoscopic surgery. pp. 14–17).
  42. ^ Buddam, Avanija; Hoilat, Gilles J.; Dacha, Sunil (July 31, 2023). "Gastric Stasis". StatPearls Publishing. PMID 29489278. Retrieved November 19, 2023.
  43. ^ Bharucha AE (March 2015). "Epidemiology and natural history of gastroparesis". Gastroenterology Clinics of North America. 44 (1): 9–19. doi:10.1016/j.gtc.2014.11.002. PMC 4323583. PMID 25667019.

Further reading

  • Overview from NIDDK National Institute of Diabetes, Digestive, and Kidney Diseases at NIH
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