Gastroparesis overview

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]

Overview[edit | edit source]

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.

Historical Perspective[edit | edit source]

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'

Classification[edit | edit source]

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.

Pathophysiology[edit | edit source]

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. 

Causes[edit | edit source]

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. 

Differentiating Gastroparesis from other Diseases[edit | edit source]

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. 

Epidemiology and Demographics[edit | edit source]

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.

Risk Factors[edit | edit source]

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).

Screening[edit | edit source]

There is insufficient evidence to recommend routine screening for gastroparesis.

Natural History, Complications and Prognosis[edit | edit source]

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.

Diagnosis[edit | edit source]

Diagnostic Study of Choice[edit | edit source]

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.

History and Symptoms[edit | edit source]

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[edit | edit source]

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.

Laboratory Findings[edit | edit source]

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.

Electrocardiogram[edit | edit source]

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.

X-ray[edit | edit source]

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.

Echocardiography and Ultrasound[edit | edit source]

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.

CT scan[edit | edit source]

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.

MRI[edit | edit source]

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.

Other Imaging Findings[edit | edit source]

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[edit | edit source]

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.

Treatment[edit | edit source]

Medical Therapy[edit | edit source]

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

Surgery[edit | edit source]

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.

Primary Prevention[edit | edit source]

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 Prevention[edit | edit source]

Secondary preventive measures of gastroparesis to primary preventive measures.

References[edit | edit source]