Gastroparesis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]; Madhu Sigdel M.B.B.S.[3]

Gastroparesis is a medical condition consisting of a paresis (partial paralysis) of the stomach (“gastro-“), resulting in food remaining in the stomach for a longer period of time than normal in absence of mecchanical obstruction. Normally, the stomach contracts to move food down into the small intestine for digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not work normally. Food then moves slowly or stops moving through the digestive tract.

In 1958, Paul Kassander, a US physician, was the first to discover the association between diabetes and the development of asymptomatic gastric retention. He coined the term ‘gastroparesis diabeticorum’

Gastroparesis may be classified according to etiology into 4 subtypes/groups which include, idiopathic gastroparesis, diabetic gastroparesis, postsurgical gastroparesis and gastroparesis due to other causes. It may also be classified into 3 subtypes based on the presenting symptoms, which include, vomiting-predominant, regurgitation-predominant and dyspepsia– predominant gastoparesis.

The exact pathogenesis of gastroparesis is not fully understood. However, gastric emptying process is the result of interaction of smooth muscles, extrinsic and enteric autonomic nervous system, and interstitial cells of Cajal (ICC). Loss of expression of neuronal nitric oxide synthase (nNOS) and loss of interstitial cells of Cajal (ICC) play pivotal role in the pathogenesis of gastroparesis. 

The etiology of gastroparesis can be broadly classified into idiopathic, diabetic, post-surgical and medication induced. Life threatening causes of gastroparesis include brainstem stroke and hypokalemia (which may lead to cardiac arrythmias). Surgical procedures most commonly associated with gastroparesis include distal gastrectomy, pancreatoduodenectomy, cholecystectomy and fundoplication. Common medications associated with the development of gastroparesis include narcotics, tricyclic antidepressants, octreotide, amylin analogues, dopamine analogues and phenothiazines. 

Gastroparesis should be differentiated from other diseases that cause chronic nausea and vomiting. The differentials include psychiatric illnesses, rumination syndrome, funtional dyspepsia and cyclic vomiting syndrome. 

The age adjusted incidence of gastroparesis was approximately 2.8 for men and 9.8 for women 100,000 person-years for year 1996-2006 worldwide. It’s incidence increases with age; with peak incidence of 10.5 per 100000 for age greater than 60 years.The female to male ratio is approximately 4 to 1.

Common risk factors associated with gastroparesis includal viral infection, cholecystectomy, diabetes, gastrectomy, collagen vascular diseases, neurological diseases, use of medication that inhibits certain nerve signals (anticholinergic medication).

There is insufficient evidence to recommend routine screening for gastroparesis.

The natural history of gastroparesis is largely unknown. Common complications include fluctuations in blood glucose due to unpredictable digestion times in diabetic patients, malnutrition, weight loss, malnutrition and vitamin and mineral deficiencies, Intestinal obstruction due to the formation of bezoars and bacterial infection due to overgrowth in undigested food. Postviral gastroparesis has a good prognosis while prognosis for diabetic gastroparesis is poor.

Gastric emptying scintigraphy is considered as a gold standard of gastroparesis. Delayed gastric emptying is confirmed by 10% gastric retention at 4 hours. Factors that affect the results of this test include medications, tobacco smoking, and hyperglycemia.

The hallmarks of gastroparesis are nausea and vomiting. A positive history of diabetes mellitus, parkinson’s disease, or collagen vascular disorders is suggestive of gastroparesis. Other common symptoms of gastroparesis include early satiety, abdominal pain and bloating.

Physical examination of patients with gastroparesis is usually remarkable for epigastric distension and tenderness. The presence of other findings on physical examinationdepends on the various cause of gastroparesis.

There are no diagnostic laboratory findings associated with gastroparesis. However, some laboratory findings consistent with the diagnosis of gastroparesis and its complications include elevated BUN, creatinine, ESR, or CRP. Elevated glucose or HbA1c might be seen in patients with diabetic gastroparesis.

There are no ECG findings associated with gastroparesis. In case of malnutrition and electrolyte imbalance, an ECG may be helpful. Hypokalemia might present with arrhythmia, ST segment depression, low T wave, prominent U waves and QRS prolongation. Hypocalcemia might present with QT interval prolongation.

An upper gastrointestinal series may be helpful in the diagnosis of gastroparesis. Findings on an x-ray suggestive of gastroparesis include presence of food in the stomach for more than 12 hours.

Both 2D and 3D transabdominal ultrasound is helpful in the diagnosis of gastroparesis. Findings on ultrasound suggestive of gastroparesis include prolonged distal and proximal gastric emptying, larger antral area, lower gastric emptying rate, fewer antral contractions.

Abdominal CT scan may be helpful in the diagnosis of gastroparesis. Abdominal CT scan is used to rule out underlying causes and complications such as obstruction, malignancy, inflammation, infections, and other causes of abdominal pain.

Gastric real time high resolution MRI may be helpful in the diagnosis of gastroparesis and other motility disorders of gastrointestinal tract. Findings on MRI suggestive of gastroparesis include reduced antral peristaltic wave propagation and reduced gastric motility index. The advantages of MRI include being noninvasive, operaotor independence with no ionising radiation exposure.

Gastric emptying scintigraphy is considered as a gold standard of gastroparesis. Delayed gastric emptying is confirmed by 10% gastric retention at 4 hours. Factors that affect the results of this test include medications, tobacco smoking, and hyperglycemia.

Other diagnostic studies for diagnosis of gastroparesis include 13C-octanoic acid breath test, the SmartPill wireless motility capsule (WMC) system, and electrogastrography. All of them could measure the gastric motility and recognize delayed gastric emptying. Electrogastrography is useful for differentiating gastroparesis from functional dyspepsia by identifying underlying myoelectrical activity.

The medical management of gastroparesis consists of dietary modification, hydration and nutrition, optimization of glycemic control and pharmacotherapy. 

Surgical treatment is rarely indicated for the treatment of gastroparesis, however it can be useful in patients with persistent symptoms despite medical management and in diabetics.

Effective measures for the primary prevention of gastroparesis include strict glycemic control, nutritional therapies, having frequent, small meals that are low in fat and fiber, alcohol and smoking cessation, regular exercise and avoidance of medications that impair gastric motility.

Secondary preventive measures of gastroparesis to primary preventive measures.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]

In 1958, Paul Kassander, a US physician, was the first to discover the association between diabetes and the development of asymptomatic gastric retention. He coined the term ‘gastroparesis diabeticorum’.

• In 1958, Paul Kassander, a US physician, was the first to discover the association between diabetes and the development of asymptomatic gastric retention. He coined the term ‘gastroparesis diabeticorum’.^[1]
• In 1911, Ramon Y. Cajal discovered interstitial cell (of Cajal).^[2]
• In 1947, Ambache showed that slow electrical waves control gastrointestinal smooth muscle contraction and related them to interstitial cells of Cajal.^[2]
  

The following are a few famous cases of gastroparesis:

• Lisa Brown, an American model from Wisconsin died at the age of 34 years on January 21, 2017. She was diagnosed with superior mesenteric artery (SMA) syndrome and gastroparesis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]

Gastroparesis may be classified according to etiology into 4 subtypes/groups which include idiopathic gastroparesis, diabetic gastroparesis, post-surgical gastroparesis and gastroparesis due to other causes. It may also be classified into 3 subtypes based on the presenting symptoms, which include vomiting-predominant, regurgitation-predominant, and dyspepsia– predominant gastoparesis.

Gastroparesis may be classified based on etiology of the disease into 4 subtypes/groups, which include:^[1]

• Idiopathic (36%)
• Diabetic (29%)
• Postsurgical (13%)
• Others (22%)

Gastroparesis may be classified into 3 subtypes based on the presenting symptoms:^[2]

• Vomiting predominant gastroparesis
• Regurgitation predominant gastroparesis
• Dyspepsia predominant gastroparesis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]

The exact pathogenesis of gastroparesis is not fully understood. However, gastric emptying process is the result of interaction of smooth muscles, extrinsic and enteric autonomic nervous system, and interstitial cells of Cajal (ICC). Loss of expression of neuronal nitric oxide synthase (nNOS) and loss of interstitial cells of Cajal (ICC) play pivotal role in the pathogenesis of gastroparesis. Recent studies suggest that the loss of antioxidant gene expression (NRF2 gene) can contribute to the development of gastroparesis. NRF2 regulates expression of phase II antioxidant genes such as HO-1, SOD1, SOD2, GCLC, GCLM, CAT, and GPX1. On microscopic histopathological analysis of full thickness biopsy of the gastric body. Decreased number of interstitial cells of Cajal (also called fibroblast like cells) in circular muscle layer, immune cells infiltration of gastric tissue especially myenteric plexus predominantly consisting of lymphocytes and macrophages showing CD45 and CD68 immunoreactivity, and enteric nerve fiber loss within the circular smooth muscle layer are characteristic findings of gastroparesis.

• The exact pathogenesis of gastroparesis is not fully understood. However, it is well known that gastric emptying process is the result of interaction of smooth muscles, extrinsic and enteric autonomic nervous system, and interstitial cells of Cajal (ICC).^[1]
• The final process for the development of delayed of gastric emptying is increased tone of pylorus.
• Gastric emptying is mediated by the vagus nerve. The process of gastric emptying involves the following sequential steps:
  • Fundal accommodation
  • Antral contraction
  • Pyloric relaxation
• Interstitial cells of Cajal generate the contractile rhythm within the gut and possess a unique ability to produce slow waves in gastrointestinal smooth muscles.
• This electrical slow wave activity is the determinant of the characteristic frequency of phasic contractions of the stomach, intestine and colon as well as the direction and velocity of propagation of peristaltic activity, in coordination with the enteric nervous system.^[2]
• Interstitial cells of Cajal regulate both gastric pacemaker activity and enteric neurons, which then initiate smooth muscle cell activity.^[3] Slow wave activity in human stomach originates from a pacemaker region at the mid/upper corpus on the greater curvature. From this pacemaker region, a band of activity is formed rapidly and propagated in an organized fashion towards the distal antrum.^[4] Hence, tone of pyloric sphincter plays an important role in the regulation of gastric emptying.
• Non-adrenergic, non-cholinergic (NANC) innervation to the pylorus is predominantly inhibitory and mediates relaxation of the sphincter.^[5]
• A high density of nitric oxide synthase-immunopositive nerve cells and fibres have been been demonstrated in the pylorus.^[6]
• They are called inhibitory nitrergic neurons. Expression of neuronal nitric oxide synthase (nNOS) activity from nitrergic neurons in gastric wall secrete nitric oxide (NO).
• Major function of NO from these nitrergic enteric nerves include accommodation of the fundus and relaxation of pylorus through smooth muscle relaxation.
• These enteric nerves also control the muscle tone of the lower esophageal sphincter, the sphincter of Oddi, and the anus.^[7] The most important mechanism behind the pathogenesis of gastroparesis appears to be:^[1]
  • Loss of expression of neuronal nitric oxide synthase (nNOS)
  • Loss of interstitial cells of Cajal (ICC)

• Recent studies suggest that the loss of antioxidant gene expression (NRF2 gene) can contribute to the development of gastroparesis. NRF2 regulates expression of phase II antioxidant genes such as HO-1, SOD1, SOD2, GCLC, GCLM, CAT, and GPX1.^[8]
• Elevated expression of the enzyme heme oxygenase-1 may mitigate the development of gastroparesis.^[9]
• High oxidative stress in interstitial cells of Cajal and nitrergic enteric nerves are the potential cause of injury and decrease in their numbers.^[8]

The following conditions may be associated with gastroparesis:

• Diabetes
• Other motility disorders of gastrointestinal tract such as achalasia, irritable bowel syndrome and constipation.^[10]
• Neurological diseases eg. Parkinson’s disease
• Collagen vascular disorders

On gross pathology, no abnormalities seen on obtaining full thickness biopsy of gastric tissue.

On microscopic histopathological analysis of full thickness biopsy of the gastric body. Decreased number of interstitial cells of Cajal (also called fibroblast like cells) in circular muscle layer, immune cells infiltration of gastric tissue especially myenteric plexus predominantly consisting of lymphocytes and macrophages showing CD45 and CD68 immunoreactivity,^[3] and enteric nerve fiber loss within the circular smooth muscle layer are characteristic findings of gastroparesis.^[11]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2] Farman Khan, MD, MRCP [3]

The etiology of gastroparesis can be broadly classified into idiopathic, diabetic, post-surgical and medication induced. Life threatening causes of gastroparesis include brainstem stroke and hypokalemia (which may lead to cardiac arrythmias). Surgical procedures most commonly associated with gastroparesis include distal gastrectomy, pancreatoduodenectomy, cholecystectomy and fundoplication. Common medications associated with the development of gastroparesis include narcotics, tricyclic antidepressants, octreotide, amylin analogues, dopamine analogues and phenothiazines.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Brainstem stroke
• Hypokalemia

Gastroparesis causes developed by WikiDoc.org

• Idiopathic^[1][2]
• Diabetes mellitus (Type II is more common cause than type I DM)^[1] – second commonest cause
• Post- surgical: Distal gastrectomy for cancer of stomach, pancreatoduodenectomy, cholecystectomy, fundoplication etc^[3]
• Narcotics
• Phenothiazines
• Pregnancy
• Scleroderma
• Systemic sclerosis
• Vagotomy

Transient gastroparesis may arise in acute illness of any kind:

• Certain cancer treatments or other drugs which affect digestive action
• Anorexia
• Bulimia
• Other abnormal eating patterns
• Medications (anticholinergics and narcotics) that slow contractions in the intestine

Chronic gastroparesis is frequently due to autonomic neuropathy:

• Type 1 diabetes or type 2 diabetes:
  • The vagus nerve becomes damaged by years of high blood glucose, resulting in gastroparesis
• Fibromyalgia
• Parkinson’s disease
• Mitochondrial disorder
• Abdominal surgery^[4]
• Amyloidosis
• Scleroderma
• Abdominal migraine
• Hypothyroidism
• Gastroesophageal reflux disease

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:

• Stomach flu
• Mononucleosis, and others have been anecdotally linked to the onset of the condition, but no systematic study has proven a link

Gastroparesis causes developed by WikiDoc.org

Cardiovascular	Percutaneous catheter ablation for atrial fibrillation; prevalence of gastroparesis after radio-frequency ablation is 10% and cryoablation procedures is 6%, respectively.[5]
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Tricyclic antidepressants, phenothiazines, octreotide, narcotics, muscarinic cholinergic receptor antagonists, glucagon-like peptide (GLP)-1 agonists, amylin analogues, dopamine agonists, cholangiocarcinoma, calcium channel blockers, anticholinergics, alpha-2-adrenergic agonists
Ear Nose Throat	No underlying causes
Endocrine	Hypothyroidism, hypoparathyroidism, diabetes mellitus type 2, diabetes mellitus type 1
Environmental	No underlying causes
Gastroenterologic	Ulcers in first portion of duodenum, pyloric stenosis, pyloric channel ulcer, pancreatic pseudocyst, pancreatic cancer, gastroesophageal reflux disease, gastric polyps, gastric cancer, duodenal cancer, abdominal migraine
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Surgery on the stomach or vagus nerve, complication of stomach surgery for ulcer disease or weight loss, vagotomy
Infectious Disease	Rotavirus, postviral syndromes, Norwalk virus, AIDS, acute viral infection
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	Primary dysautonomias, Parkinson’s disease, brainstem stroke or tumor, autonomic neuropathy, autoimmune gastrointestinal dysmotility
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	Pregnancy
Oncologic	Ampullary cancer
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	Psychogenic, vomiting, depression, bulimia, anxiety, neurosis, anorexia nervosa
Pulmonary	Small cell lung cancer[6]
Renal/Electrolyte	Kidney failure, hypomagnesemia, hypokalemia
Rheumatology/Immunology/Allergy	Systemic sclerosis, scleroderma, polymyositis, lupus
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Myotonic dystrophy, idiopathic, congenital obstruction, Bouveret syndrome, amyloidosis, amyloid neuropathy

Gastroparesis causes developed by WikiDoc.org

Gastroparesis causes developed by WikiDoc.org

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Gastroparesis should be differentiated from other diseases that cause chronic nausea and vomiting. The differentials include psychiatric illnesses, rumination syndrome, functional dyspepsia and cyclic vomiting syndrome.

Gastroparesis should be differentiated from other diseases that cause chronic nausea and vomiting. The differentials include the following:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]}

Disorder	Clinical features												Laboratory findings
	Chronic nausea	Vomiting	Diarrhea	Retching	Lethargy	Social withdrawal	Photophobia	Epigastric pain/burning	Lanugo hair	Hypogonadism	Russel’s sign	Body mass index (normal range: 18.5 to 24.9)	Complete blood count (CBC)	Electrolyte imabalance	Lipase and amylase levels	Gastric scintigraphy	Ambulatory esophageal pH and impedance testing
Gastroparesis	✔	✔ (within 1 hour of eating)	–	✔	✔	–	–	✔	–	–	–	↓	Anemia	✔	Normal (maybe elevated if chronic renal failure is the cause of gastroparesis- usually less than threefold)	Periodic measurement of radiolabeled solid meal:   Grade 1 (mild), 11%-20% retention at 4 h Grade 2 (moderate), 21%-35% retention at 4 h Grade 3 (severe), 36%-50% retention at 4 h Grade 4 (very severe), > 50% retention at 4 h	Impedance testing (antroduodenal manometery): Loss of normal fasting migratory motor complexes (MMCs) and reduced postprandial antral contractions and, in some cases pylorospasm
Anorexia nervosa	✔	✔	✔	–	✔	✔	–	–	✔	✔	–	↓	Leukocytosis, anemia	✔	Increased	Gastric emptying may be delayed but may become normal as feeding recommences (short lived)	Esophageal pH: May be decreased if patient develops gastroesophageal reflux disease
Bulimia nervosa	✔	✔	✔	✔	✔	✔	–	–	–	✔	✔	Normal	Leukocytosis, anemia	✔	Increased	Gastric emptying delayed for a longer duration as compared to anorexia nervosa	Esophageal pH: May be decreased if patient develops gastroesophageal reflux disease
Rumination syndrome	✔	✔ (Regurgitation more common- within minutes of meal intake)	✔	–	✔	✔	✔	✔	–	–	–	↓	Normal	✔	Normal	Delayed gastric emptying	Esophageal pH: Fall in esophageal pH immediately after reguritation (occurs while patient is awake and erect; this is in contrast to GERD, where reflux occurs diurnally and supine position) Impedance testing:Increased intra-abdominal pressure leading to regurgitation of gastric contents (Tall R waves)
Functional dyspepsia	✔	✔	✔	✔	–	–	–	–	–	–	–	Normal	Normal	✔	Increased (especially lipase)	Delayed gastric emptying	Esophageal pH: May be decreased if patient develops reflux
Cyclic vomiting syndrome	✔	✔	–	✔	✔	–	–	–	–	–	–	↓	Leukocytosis, anemia	✔	Increased (alongwith increased lactic acid – in cases of concomitant mitochondrial disease)	Rapid or normal	Esophageal pH: Decreased
Pancreatitis	✔	✔	✔	✔	✔	–	–	✔	–	–	–	Normal	Leukocytosis	✔	Increased	Not indicated	Esophageal pH: Normal
Gastric outlet obstruction	✔	✔ (within 1 hour of eating)	–	–	–	–	–	✔	–	–	–	↓	Leukocytosis	✔	Increased (in cases of pancreatic disease)	Delayed gastric emptying	Esophageal pH: Increased Esophageal manometery:   High manoraetric score

References

1. ↑ Parkman HP (2015). “Idiopathic gastroparesis”. Gastroenterol. Clin. North Am. 44 (1): 59–68. doi:10.1016/j.gtc.2014.11.015. PMC 4324534. PMID 25667023.
2. ↑ Werlin SL, Fish DL (2006). “The spectrum of valproic acid-associated pancreatitis”. Pediatrics. 118 (4): 1660–3. doi:10.1542/peds.2006-1182. PMID 17015559.
3. ↑ Noddin L, Callahan M, Lacy BE (2005). “Irritable bowel syndrome and functional dyspepsia: different diseases or a single disorder with different manifestations?”. MedGenMed. 7 (3): 17. PMC 1681633. PMID 16369243.
4. ↑ Gupta R, Kalla M, Gupta JB (2012). “Adult rumination syndrome: Differentiation from psychogenic intractable vomiting”. Indian J Psychiatry. 54 (3): 283–5. doi:10.4103/0019-5545.102434. PMC 3512372. PMID 23226859.
5. ↑ “Body weight in bulimia nervosa | SpringerLink”.
6. ↑ Sağlam F, Sivrikoz E, Alemdar A, Kamalı S, Arslan U, Güven H (2015). “Bouveret syndrome: A fatal diagnostic dilemma of gastric outlet obstruction”. Ulus Travma Acil Cerrahi Derg. 21 (2): 157–9. PMID 25904280.
7. ↑ Talley NJ (2011). “Rumination syndrome”. Gastroenterol Hepatol (N Y). 7 (2): 117–8. PMC 3061016. PMID 21475419.
8. ↑ Tutuian R, Castell DO (2004). “Rumination documented by using combined multichannel intraluminal impedance and manometry”. Clin. Gastroenterol. Hepatol. 2 (4): 340–3. PMID 15067630.
9. ↑ Kessing BF, Smout AJ, Bredenoord AJ (2014). “Current diagnosis and management of the rumination syndrome”. J. Clin. Gastroenterol. 48 (6): 478–83. doi:10.1097/MCG.0000000000000142. PMID 24921208.
10. ↑ Parkman HP (2009). “Assessment of gastric emptying and small-bowel motility: scintigraphy, breath tests, manometry, and SmartPill”. Gastrointest. Endosc. Clin. N. Am. 19 (1): 49–55, vi. doi:10.1016/j.giec.2008.12.003. PMID 19232280.
11. ↑ Waseem S, Moshiree B, Draganov PV (2009). “Gastroparesis: current diagnostic challenges and management considerations”. World J. Gastroenterol. 15 (1): 25–37. PMC 2653292. PMID 19115465.
12. ↑ Mearin F, Camilleri M, Malagelada JR (1986). “Pyloric dysfunction in diabetics with recurrent nausea and vomiting”. Gastroenterology. 90 (6): 1919–25. PMID 3699409.
13. ↑ Abell TL, Camilleri M, Donohoe K, Hasler WL, Lin HC, Maurer AH, McCallum RW, Nowak T, Nusynowitz ML, Parkman HP, Shreve P, Szarka LA, Snape WJ, Ziessman HA (2008). “Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine”. Am. J. Gastroenterol. 103 (3): 753–63. doi:10.1111/j.1572-0241.2007.01636.x. PMID 18028513.
14. ↑ Jiang CF, Ng KW, Tan SW, Wu CS, Chen HC, Liang CT, Chen YH (2002). “Serum level of amylase and lipase in various stages of chronic renal insufficiency”. Zhonghua Yi Xue Za Zhi (Taipei). 65 (2): 49–54. PMID 12014357.
15. ↑ Szmukler, G. I.; Young, G. P.; Lichtenstein, M.; Andrews, J. T. (1990). “A serial study of gastric emptying in anorexia nervosa and bulimia”. Australian and New Zealand Journal of Medicine. 20 (3): 220–225. doi:10.1111/j.1445-5994.1990.tb01023.x. ISSN 0004-8291.
16. ↑ Diamanti A, Bracci F, Gambarara M, Ciofetta GC, Sabbi T, Ponticelli A, Montecchi F, Marinucci S, Bianco G, Castro M (2003). “Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders”. J. Pediatr. Gastroenterol. Nutr. 37 (1): 35–41. PMID 12827003.
17. ↑ Ferholt J, Provence S (1976). “Diagnosis and treatment of an infant with psychophysiological vomiting”. Psychoanal Study Child. 31: 439–59. PMID 981449.
18. ↑ Lee H, Rhee PL, Park EH, Kim JH, Son HJ, Kim JJ, Rhee JC (2007). “Clinical outcome of rumination syndrome in adults without psychiatric illness: a prospective study”. J. Gastroenterol. Hepatol. 22 (11): 1741–7. doi:10.1111/j.1440-1746.2006.04617.x. PMID 17914944.
19. ↑ Koskenpato J, Kairemo K, Korppi-Tommola T, Färkkilä M (1998). “Role of gastric emptying in functional dyspepsia: a scintigraphic study of 94 subjects”. Dig. Dis. Sci. 43 (6): 1154–8. PMID 9635600.
20. ↑ Urbain JL, Vekemans MC, Parkman H, Van Cauteren J, Mayeur SM, Van den Maegdenbergh V, Charkes ND, Fisher RS, Malmud LS, De Roo M (1995). “Dynamic antral scintigraphy to characterize gastric antral motility in functional dyspepsia”. J. Nucl. Med. 36 (9): 1579–86. PMID 7658213.
21. ↑ Hejazi RA, Lavenbarg TH, McCallum RW (2010). “Spectrum of gastric emptying patterns in adult patients with cyclic vomiting syndrome”. Neurogastroenterol. Motil. 22 (12): 1298–302, e338. doi:10.1111/j.1365-2982.2010.01584.x. PMID 20723071.
22. ↑ “Gastric outlet obstruction – an overview | ScienceDirect Topics”.
23. ↑ Minami H, McCallum RW (1984). “The physiology and pathophysiology of gastric emptying in humans”. Gastroenterology. 86 (6): 1592–610. PMID 6370777.
24. ↑ Humphries LL, Adams LJ, Eckfeldt JH, Levitt MD, McClain CJ (1987). “Hyperamylasemia in patients with eating disorders”. Ann. Intern. Med. 106 (1): 50–2. PMID 2431640.
25. ↑ Hempen I, Lehnert P, Fichter M, Teufel J (1989). “[Hyperamylasemia in anorexia nervosa and bulimia nervosa. Indication of a pancreatic disease?]”. Dtsch. Med. Wochenschr. (in German). 114 (49): 1913–6. doi:10.1055/s-2008-1066848. PMID 2480214.CS1 maint: Unrecognized language (link)
26. ↑ Okada R, Okada A, Okada T, Okada T, Hamajima N (2009). “Elevated serum lipase levels in patients with dyspepsia of unknown cause in general practice”. Med Princ Pract. 18 (2): 130–6. doi:10.1159/000189811. PMID 19204432.
27. ↑ Sansone RA, Sansone LA (2012). “Hoarseness: a sign of self-induced vomiting?”. Innov Clin Neurosci. 9 (10): 37–41. PMC 3508961. PMID 23198276.
28. ↑ Tack J, Caenepeel P, Arts J, Lee KJ, Sifrim D, Janssens J (2005). “Prevalence of acid reflux in functional dyspepsia and its association with symptom profile”. Gut. 54 (10): 1370–6. doi:10.1136/gut.2004.053355. PMC 1774686. PMID 15972301.
29. ↑ “gut.bmj.com” (PDF).
30. ↑ Boles RG, Williams JC (1999). “Mitochondrial disease and cyclic vomiting syndrome”. Dig. Dis. Sci. 44 (8 Suppl): 103S–107S. PMID 10490048.
31. ↑ Ranasinghe WK, Smith M (2013). “Gastric outlet obstruction with an elevated serum pancreatic lipase secondary to an infraumbilical hernia”. Ann R Coll Surg Engl. 95 (7): 122–4. doi:10.1308/003588413X13629960047795. PMID 24112485.
32. ↑ Ui, Takashi; Shibusawa, Hiroyuki; Tsukui, Hidenori; Sakuma, Kazuya; Takahashi, Shuhei; Lefor, Alan K.; Hosoya, Yoshinori; Sata, Naohiro; Yasuda, Yoshikazu (2015). “Pretreatment of gastric outlet obstruction with pancrelipase: Report of a case”. International Journal of Surgery Case Reports. 12: 87–89. doi:10.1016/j.ijscr.2015.05.023. ISSN 2210-2612.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]

The age adjusted worldwide incidence of gastroparesis was approximately 2.8 for men and 9.8 for women per 100,000 person-years for year 1996-2006. The incidence of gastroparesis increases with age; with peak incidence of 10.5 per 100,000 for age greater than 60 years.The female to male ratio is approximately 4 to 1.

• The worldwide age adjusted incidence of gastroparesis was approximately 2.8 for men and 9.8 for women 100,000 person-years for year 1996-2006.^[1]

• The age-adjusted prevalence of gastroparesis is approximately 9.6 for men and 37.8 for women per 100,000 persons.
• Most recent studies have estimated prevalence of gastroparesis approaching nearly 2% of general population.^[1]

• The mortality rate of gastroparesis is approximately 4-38% over 2 years follow up time.^[2]

• Patients of all age groups may develop gastroparesis.^[3]
• The incidence of gastroparesis increases with age; with peak incidence of 10.5 per 100000 for age greater than 60 years.^[2]
• Mean age of women with gastroparesis is 45 years.^[4]

• There is no racial predilection to gastroparesis.

• Females are more commonly affected by gastroparesis than males.
• The female to male ratio is approximately 4 to 1.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]

Common risk factors associated with gastroparesis includal viral infection, cholecystectomy, diabetes, gastrectomy, collagen vascular diseases, neurological diseases, use of medication that inhibits certain nerve signals (anticholinergic medication).

Risk factors for gastroparesis include:^[1][2][3]

• Viral infection
• Cholecystectomy
• Diabetes
• Gastrectomy
• Collagen vascular diseases
• Neurological diseases
• Use of medication that inhibits certain nerve signals (anticholinergic medication)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]

There is insufficient evidence to recommend routine screening for gastroparesis.

There is insufficient evidence to recommend routine screening for gastroparesis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2], Shaghayegh Habibi, M.D.[3]

The natural history of gastroparesis is largely unknown. Common complications include fluctuations in blood glucose due to unpredictable digestion times in diabetic patients, malnutrition, weight loss, malnutrition and vitamin and mineral deficiencies, Intestinal obstruction due to the formation of bezoars and bacterial infection due to overgrowth in undigested food. Postviral gastroparesis has a good prognosis while prognosis for diabetic gastroparesis is poor.

• The natural history of gastroparesis is largely unknown, especially there is minimal data on the natural history of diabetic gastroparesis.^[1][2]
• In the Olmsted County epidemiology study, of all the incident cases of gastroparesis, one third patients died and another one third required medications, hospitalization or tube feeding related to gastroparesis.^[2]

Common complications of gastroparesis include:^[3][4][5]

• Fluctuations in blood glucose levels and even ketoacidosis due to unpredictable digestion times especially in diabetic patients
• Malnutrition
• Weight loss
• Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)
• Bacterial infection due to overgrowth in undigested food
• Dehydration
• Electrolyte imbalances

• Prognosis of gastroparesis is uncertain even with appropriate treatment modalities, as majority of them seem to provide only temporary benefit.
• The estimated 5-year survival for gastroparesis based on ‘Gastroparesis study in Olmsted County’, Minnesota from 1996 to 2006, was 67% with worse prognosis for diabetic gastroparesis.
• Prognosis of diabetic gastroparesis mainly depends upon blood sugar level and duration of diabetes.^[1][6]
• Postviral gastroparesis has a good prognosis. 
• The patients with autonomic dysfunction have slower resolution of their symptoms that may take several years and the prognosis is worse than in postviral gastroparesis without autonomic disorders.^[7]

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