Stomach Paralysis – Causes, Symptoms, Treatment

Stomach Paralysis – Causes, Symptoms, Treatment

Stomach Paralysis/Gastroparesis (gastric stasis) is derived from Greek words gastro/gaster or stomach, and paresis or partial paralysis. It is a clinical condition resulting from delayed gastric emptying in the absence of mechanical obstruction and is associated with upper gastrointestinal symptoms.

The term gastroparesis literally means “stomach paralysis.” Gastroparesis could be defined as a condition of collective symptoms of nausea and vomiting associated with bloating and early satiety plus or minus upper abdominal pain, caused by delayed gastric emptying in the absence of mechanical obstruction. In the absence of mechanical obstruction, gastric stasis can occur due to abnormalities in the process of normal gastrointestinal motor function. It is a series of complex events that require coordination of the parasympathetic and sympathetic nervous systems, neurons, and pacemaker cells within the stomach and intestine, along with the smooth muscle cells of the gut.

Pathophysiology

The pathophysiology of gastroparesis is poorly understood and is not well defined, but important mechanisms associated are the loss of interstitial cells of Cajal and inability to express neuronal nitric oxide synthase. For gastric emptying to occur there needs interaction between smooth muscles, extrinsic nerves, intrinsic or enteric nerves and interstitial cells of Cajal (ICC). It has been hypothesized that there might be a poor interplay between local enteric system along with decreased local secretion of nitric oxide(NO). Nitric oxide is required for smooth muscle relaxation, as a result causing accommodation of fundus and impairment in pyloric muscle relaxation. ICC generate slow wave and transmit to the smooth muscle thus enabling contraction, which is impaired with loss of ICC. Thus both contributing to delayed gastric emptying. There are several ongoing studies to determine pathophysiology, expect to improve our understanding soon.

Causes of Stomach Paralysis

The most common etiologies for gastroparesis are Idiopathic in 64%, diabetes in 31%, and post-surgical in the remaining patients. Other less frequent etiologies include association with functional bowel disorders, dysmotility syndromes, Chagas disease, post-viral, neurological disorders, endocrine conditions, connective tissue disorders, radiation,  gastric ischemia, and medications (opioids, anticholinergics, anti-diabetic medications).

Various conditions have correlations with gastroparesis; the majority of cases are idiopathic, diabetic, medication-induced, or postsurgical. One of the studies done at a tertiary care center categorized the etiologies in 146 patients: 36% idiopathic, 29% diabetic, 13% postgastric surgery, 7.5% Parkinson disease, 4.8% collagen vascular disorders, 4.1% intestinal pseudoobstruction, and 6% miscellaneous causes. A wide variety of neurologic disorders, as mentioned below, can affect gastrointestinal motility by altering the parasympathetic or sympathetic nerve supply to the gastrointestinal (GI) tract. Etiology of gastroparesis categorizes as follows:

  • Idiopathic – most common cause present in about half of patients
  • Diabetes mellitus (DM) – most common and severe in type 1 diabetics
  • Rheumatological diseases – amyloidosis, scleroderma
  • Autoimmune – autoimmune gastrointestinal dysmotility causing delayed emptying
  • Neurological conditions – stress, Parkinson disease, multiple sclerosis, brainstem CVA and tumors, autonomic neuropathy
  • Postsurgical –  vagal nerve injury during fundoplication and partial gastric resection
  • Trauma – spinal cord injury
  • Viral infections – including Norwalk virus and rotavirus
  • Medications – narcotics, cyclosporine, phenothiazines, dopamine agonists, octreotide, alpha-2-adrenergic agonists (e.g. clonidine), tricyclic antidepressants, calcium channel blockers, GLP-1 agonists exenatide or analogs liraglutide, lithium, progesterone

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General causes of gastroparesis Etiology
Surgical causes Vagotomy and gastric resection/drainage
Fundoplication, oesophagectomy
Gastric bypass surgery
Whipple procedure
Heart/lung transplant
Infections Viruses: Epstein–Barr virus, varicella, parvovirus-like
Chagas disease
Clostridium botulinum
Central nervous system disorders Cerebrovascular accidents/trauma
Tumors
Labyrinthine disorders
Seizures
Peripheral nervous system disorders Parkinson’s disease
Guillain–Barre
Multiple sclerosis
Dysautonomias
Neuropsychiatric disorders Anorexia nervosa/bulimia
Rumination syndrome
Rheumatologic disease Scleroderma
Systemic lupus erythematosus
Polymyositis/dermatomyositis
Endocrine and metabolism diseases Diabetes
Hypothyroidism
Electrolyte disorders
Renal failure
Pregnancy
Neoplastic(para)-breast, small cell lung, pancreas
Miscellaneous neuromuscular diseases Amyloidosis
Chronic intestinal pseudo-obstruction
Myotonic dystrophy

 

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Symptoms of Stomach Paralysis

The symptoms of gastroparesis include:

  • Heartburn or gastroesophageal reflux (backup of stomach contents into the esophagus)
  • Nausea
  • Vomiting undigested food
  • Early satiety (feeling full quickly when eating)
  • Abdominal bloating (enlargement)
  • Poor appetite and weight loss
  • Poor blood sugar control
  • A feeling of fullness after eating just a few bites
  • Vomiting undigested food eaten a few hours earlier
  • Acid reflux
  • Abdominal bloating
  • Abdominal pain
  • Changes in blood sugar levels
  • Lack of appetite
  • Weight loss and malnutrition

Other symptoms include the following

  • Abdominal bloating
  • Body aches (myalgia)
  • Erratic blood glucose levels
  • Acid reflux (GERD)
  • Heartburn
  • Lack of appetite
  • Morning nausea
  • Muscle weakness
  • Night sweats
  • Palpitations
  • Spasms of the stomach wall
  • Constipation or infrequent bowel movements
  • Weight loss, malnutrition

Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.[4]

Diagnosis of Stomach Paralysis

Histopathologic studies from tissues of diabetic and idiopathic gastroparesis patients showed several changes like loss of ICC, decreased nerve fibers, increased smooth muscle fibrosis, and abnormal macrophage-containing immune infiltrates. On electron microscopy, there is abnormal connective tissue stroma, thick basal lamina around ICCs and myocytes, and large empty nerve endings suggest more profound conduction defects, which supports the above discussion.

History and Physical

Patients present commonly with cardinal symptoms like nausea, vomiting, early satiety, postprandial fullness, upper abdominal pain, bloating and weight loss. The gastroparesis cardinal symptom index (GCSI) is a validated clinical instrument that be can be used to assess symptoms in patients suffering from gastroparesis. This instrument has three subscales: (fullness/early satiety, nausea/vomiting, and bloating) and rates of symptom intensities from zero (none) to five (very severe) and the total is used for severity of the disease. The GCSI is used to assess response to therapy and not primarily as a diagnostic tool. In addition to gastric symptoms, the slow and unpredictable gastric emptying can cause wide fluctuations in blood sugar levels especially so in diabetic patients. In addition, this may cause weight loss, fatigue, calorie deficit, gastric bezoar formation.

Evaluation
  • Breath test – After ingestion of a meal containing a small amount of isotope, breath samples are taken to measure the presence of the isotope in carbon dioxide, which is expelled when a person exhales. The results reveal how fast the stomach is emptying.
  • SmartPill – Approved by the U.S. Food and Drug Administration (FDA) in 2006, the SmartPill is a small device in capsule form that can be swallowed.The device then moves through the digestive tract and collects information about its progress that is sent to a cell phone-sized receiver worn around your waist or neck. When the capsule is passed from the body with the stool in a couple of days, you take the receiver back to the doctor, who enters the information into a computer.
  • Gastric emptying study – This is the most important test used in making a diagnosis of gastroparesis. It involves eating a light meal, such as eggs and toast, that contains a small amount of radioactive material. A scanner that detects the movement of the radioactive material is placed over your abdomen to monitor the rate at which food leaves your stomach.
  • Gastroduodenal manometry – is a test that measures how well the smooth muscle of the stomach and small intestine contracts and relaxes. The test is performed by placing a thin tube into the stomach usually with the aid of the endoscope. The tube is advanced into the small intestine and over the next few hours the contractile responses while the subject is fasting and eating are observed and recorded. The manometry catheter provides information on how strong and how often the muscles of the stomach and intestine contract and whether the stomach contractions are coordinated with the contractions in the small bowel. Gastric duodenal manometry may be helpful but is often not needed to make a diagnosis of gastroparesis. This test is not widely available.
  • A Small Intestinal X -ray –  is a contrast radiograph used to outline the anatomy of the small bowel. This study is not generally needed to make a diagnosis of gastroparesis, but a blockage anywhere in the small intestine will result in a back up of material and could account for delayed gastric emptying. An obstruction in the small bowel may cause symptoms similar to gastroparesis, but the treatment is different. Treatment for intestinal obstruction is avoiding intake of any food or liquid until the cause of obstruction such as inflammation resolves or surgery is performed to remove the blockage.
  • Esophagogastroduodenoscopy or barium radiography – is done to rule out mechanical obstruction. The most common test used in clinical practice is the gastric scintigraphic emptying of solids. A study result of retention of solids at 4 hours is considered to be diagnostic of gastroparesis. Other alternative methods to assess gastric emptying include motility testing by a wireless capsule and 13 C breath testing using octanoate or spirulina integrated into a solid meal. Drugs that affect gastric emptying should be held at least 48 hours prior to the study. Furthermore, patients with diabetes should have plasma blood glucose less than 275 mg/dl to eliminate acute impairment of gastric emptying from hyperglycemia.
  • Delayed gastric emptying – The goal of the evaluation is to exclude a mechanical obstruction and establish the diagnosis of gastroparesis by an assessment of gastric motility. Robust patient history should point to suspicion of a possible diagnosis. Gastroparesis should be a suspicion in patients with chronic nausea, vomiting, early satiety, postprandial fullness, abdominal pain, or bloating. The next step would be ruling out mechanical obstruction, which could be done with a careful upper GI endoscopy to rule out malignancy or strictures due to peptic ulcer disease.
  • Imaging modalities like computed tomographic (CT) scan – or magnetic resonance imaging (MRI) abdomen may be needed to exclude mechanical obstruction. After ruling out mechanical causes, gastric emptying studies (GES) are performed by scintigraphy to confirm the presence of delayed gastric emptying of solids. A solid or liquid radioisotope containing meal may be used to measure gastric emptying.
  • Upon scintigraphy – based on the gastric retention of contents at the end of four hours, gastroparesis could be graded into mild (less than 15 percent), moderate (15 to 35 percent), and severe (over 35 percent). Symptoms of gastroparesis may also be quantifiable via GCSI (gastroparesis cardinal symptom index), a questionnaire based on the severity of symptoms postprandial fullness, early satiety, nausea vomiting, and bloating. As compared to the traditional method of GES (testing for 2 hours or less), the sensitivity of the test results could increase by extending the imaging of solid gastric emptying to 4 hours. In patients with normal solid gastric emptying, adding a liquid GES study could further increase its sensitivity to diagnose gastroparesis.
  • Radiopaque Markers – Indigestible markers, i.e. ten small pieces of nasogastric tubing, are ingested with a meal. None of the markers should remain in the stomach on an X-ray taken 6 h after their ingestion. This simple test correlates with clinical gastroparesis and is readily available and inexpensive. The drawbacks of the test include lack of standardization of the meal and size of markers and difficulty in determining if the markers are located in the stomach or in other regions that overlap with the stomach, such as the proximal small bowel and transverse colon [].
  • Ultrasonography – Transabdominal ultrasound has been used to measure emptying of a liquid meal by serially evaluating cross-sectional changes in the volume remaining in the gastric antrum over time. Emptying is considered to be complete when the antral area/volume returns to the fasting baseline. Three-dimensional ultrasound is a newly developed technique that has recently been reported to be useful in determining stomach function, and duplex sonography can quantify the transpyloric flow of liquid gastric contents. These techniques are preferred over scintigraphy in certain patients, such as pregnant women and children, to minimize radiation exposure.
  • Magnetic Resonance Imaging – Magnetic resonance imaging (MRI) using gadolinium can accurately measure semi-solid gastric emptying and accommodation using sequential transaxial abdominal scans. MRI provides excellent resolution with high sensitivity. It is also non-invasive and radiation free. Antral propagation waves can be observed and their velocity calculated. In gastroparesis, a significant reduction is seen in the velocity of these waves. MRI can also differentiate gastric meal volume and total gastric volume, thereby allowing gastric secretory rates to be calculated. New rapid techniques allow careful measurements of wall motion to be made in both the proximal and distal stomach during emptying, and solid markers now permit the measurement of solid meal emptying. The drawback of this test is its expense and lack of availability [].
  • Single-Photon Emission computed tomography – This technique uses intravenously administered 99-Tc pertechnetate that accumulates within the gastric wall rather than the lumen and provides a three-dimensional outline of the stomach. Measurement of regional gastric volumes in real time to assess fundic accommodation and intragastric distribution can be made. The drawback of this test is the need for large radiation doses and its wide unavailability [].
  • Stable-Isotope Gastric Emptying Breath Testing – The gastric emptying breath test (GEBT) using a stable isotope, i.e. 13C-labeled substrates, typically 13C-octanoic acid or 13C-Spirulina platensis (blue-green algae), is a promising alternative diagnostic modality to scintigraphy. It is a noninvasive, easy-to-perform method and does not involve radiation exposure. In the GEBT, the rate of gastric emptying of the 13C substrate incorporated in a solid meal is reflected by breath excretion of 13CO2 [].
  • Electrogastrography – Electrogastrography (EGG) can be a useful adjunctive diagnostic test. EGG measures gastric slow-wave myoelectrical activity typically via cutaneous electrodes positioned along the long axis of the stomach. A pre-prandial recording is captured for approximately 45–60 min, then the patient is given a meal, followed by a 45- to 60-min postprandial recording, although shorter recording periods can be used as well. Healthy controls produce EGG recordings that exhibit uniform waveforms of three cycles per minute, which increase in amplitude after ingestion of a meal, and both the frequency and amplitude of the EGG can be important measures, as well as the propagation between channels of EGG signal. Cutaneous electrogastrography can be amplified by the use of more direct measures, such as mucosal or serosal electrograms. Electrograms are not conducted routinely, but they may offer additional sensitivity and indications of disordered gastric function in a given patient [].
  • Wireless Motility Capsule – The wireless motility capsule using the SmartPil has been approved by the U.S. FDA for the evaluation of gastric emptying, colonic transit time in patients with suspected slow transit constipation and for measurement of pH, temperature and pressure throughout the GI tract. It is a safe and practical alternative to scintigraphy. It consists of a 2-cm-long wireless transmitting capsule that has the ability to record and transmit data on pH, pressure and temperature to a portable receiver that may be worn around the patient’s neck. Data can be acquired continuously for up to 5 days, and significant events (e.g. meal ingestion, sleep or GI symptoms) can be recorded with a button. Gastric emptying is reflected by an abrupt change in pH as the capsule moves from the acidic environment of the stomach to the alkaline environment of the duodenum. This transit typically occurs with return of the fasting state and phase III migrating motor complex (MMC) after the emptying of liquids and triturable solids [].
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Treatment of Stomach Paralysis

Medical management includes the use of prokinetic agents such as metoclopramide, erythromycin, and anti-emetic agents. Endoscopic and surgical methods are used for refractory cases. Intrapyloric botulinum injection, gastric electrical stimulation, venting gastrostomy, feeding jejunostomy, pyloroplasty, partial gastrectomy and most recently endoscopic techniques such gastric peroral endoscopic myotomy (G-POEM) are being utilized for relieving symptoms

Lifestyle Changes
  • The initial goal of the management of gastroparesis is the restoration of fluid and electrolyte balance. Also, nutritional status and blood sugar levels should be optimized. Dietary modifications include switching to small frequent meals, low-fat diet. Drinks such as carbonated and alcoholic beverages and foods rich in insoluble fiber should be avoided entirely.
  • In addition, quitting smoking has also been reported to be helpful. Oral intake is encouraged, and if the patient does not tolerate solid foods, then a liquid diet could be attempted. In case of intolerance to oral diet, enteral feeding by post-pyloric feeding tube can be used. Parenteral nutrition is not encouraged and remains the last alternative if everything else fails.

Changes to your diet

Maintaining adequate nutrition is the most important goal in the treatment of gastroparesis. Many people can manage gastroparesis with diet changes and dietary changes are the first step in managing this condition. Your doctor may refer you to a dietitian who can work with you to find foods that are easier for you to digest so that you’re more likely to get enough calories and nutrients from the food you eat. A dietitian might suggest that you try to:

  • Eat smaller meals more frequently
  • Chew food thoroughly
  • Eat well-cooked fruits and vegetables rather than raw fruits and vegetables
  • Avoid fibrous fruits and vegetables, such as oranges and broccoli, which may cause bezoars
  • Choose mostly low-fat foods, but if you can tolerate them, add small servings of fatty foods to your diet
  • Try soups and pureed foods if liquids are easier for you to swallow
  • Drink about 34 to 51 ounces (1 to 1.5 liters) of water a day
  • Exercise gently after you eat, such as going for a walk
  • Avoid carbonated drinks, alcohol and smoking
  • Try to avoid lying down for 2 hours after a meal
  • Take a multivitamin daily
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Here’s a brief list of foods recommended for people with gastroparesis (your dietitian can give you a more comprehensive list):

Starches

  • White bread and rolls and “light” whole-wheat bread without nuts or seeds
  • Plain or egg bagels
  • English muffins
  • Flour or corn tortillas
  • Pancakes
  • Puffed wheat and rice cereals
  • Cream of wheat or rice
  • White crackers
  • Potatoes, white or sweet (no skin)
  • Baked french fries
  • Rice
  • Pasta

Protein

  • Lean beef, veal and pork (not fried)
  • Chicken or turkey (no skin and not fried)
  • Crab, lobster, shrimp, clams, scallops, oysters
  • Tuna (packed in water)
  • Cottage cheese
  • Eggs
  • Tofu
  • Strained meat baby food

Fruits and vegetables

  • Baby food vegetables and fruits
  • Tomato sauce, paste, puree, juice
  • Carrots (cooked)
  • Beets (cooked)
  • Mushrooms (cooked)
  • Vegetable juice
  • Vegetable broth
  • Fruit juices and drinks
  • Applesauce
  • Bananas
  • Peaches and pears (canned)

Dairy

  • Milk, if tolerated
  • Yogurt (without fruit pieces)
  • Custard and pudding
  • Frozen yogurt

Diet modifications

Small Meal size could limit emptying time and help symptom alleviation. Patients may need to eat 4 or 5 times per day to compensate for the small meal size. Carbonated drinks like soda and beer could release carbon dioxide, which can aggravate gastric distention. Smoking or high doses of alcohol can decrease antral contractility and impair gastric emptying. The nutritional state of the patient should be promptly assessed, utilizing ancillary service consultation. If oral intake is not adequate, then enteral nutrition via jejunostomy tube should be considered. Parenteral nutrition is rarely required.

Medical treatment

As needed antiemetics such as prochlorperazine (5 to 10 mg up to 3 times a day), diphenhydramine (12.5 mg up to 3 or 4 times a day) and ondansetron (4 or 8 mg up to 3 times a day) can provide symptomatic relief in gastroparesis.

  • 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 – a prokinetic medication, is the only FDA approved drug for gastroparesis. It is usually started with 5 mg three times a day, fifteen minutes before meals. It can be titrated up to 40 mg per day but need very close monitoring for adverse effects. Also, the duration of treatment approved by the FDA is 12 weeks due to the possibility of severe side effects. Common side effects include anxiety, restlessness, hyperprolactinemia, and QT prolongation. Metoclopramide has a black box warning for extrapyramidal symptoms like dystonia and tardive dyskinesia in about 1 percent of patients.
  • Domperidone with erythromycin (short term) – tegaserod (5-HT4 partial agonist), and centrally acting antidepressants. Domperidone is a dopamine 2 antagonist, works more like metoclopramide to improve gastric emptying and decrease nausea and vomiting. The FDA restricts domperidone use in the United States, and it is currently under review as an investigational drug. Domperidone is usually started at 10mg three a day, and dosing could potentially increase to 20mg per dose. Significant adverse effects are cardiac arrhythmias and hyperprolactinemia. It is a recommendation to monitor the QT interval while being on domperidone, avoid use for QT over 450 ms. But erythromycin is prone to tachyphylaxis (decrease in response quickly due to desensitization), and so its use is restricted to a maximum of four weeks at a time. Common side effects of erythromycin include GI toxicity, ototoxicity, bacterial resistance, QT prolongation.
  • Domperidone – is a dopamine (D2) agonist with effects similar to metoclopramide but is much less likely to cause extrapyramidal side effects as it does not cause the blood-brain barrier. Symptomatic patients with diabetes have reported improvement with domperidone therapy, but again, the effect could be lost in about six weeks .
  • Antiemetics – are often the first step in patients with gastroparesis as they help with the common symptoms of nausea and vomiting. Serotonin (5-HT3) receptor antagonists like ondansetron, phenothiazines (dopamine receptor antagonists) like prochlorperazine and promethazine are commonly used.
  • Erythromycin – binds to the motilin receptors, which are responsible for the initiation of the MMC in the upper gut . Like metoclopramide, erythromycin works well in the short term, but long term loss of response is common.
  • Cisapride – binds to serotonin receptors located in the wall of the stomach that leads to contraction of stomach smooth muscle and improved gastric emptying. In the late 1990’s cisapride was taken off the market due to complications of cardiac arrhythmias in patients who were using this drug. It is once again available but its use is restricted. Individuals with underlying kidney or heart disease should not use cisapride.
  • Gastric electrical stimulation – has been studied, but so far, there has not been a significant reduction in symptoms that were noted consistently across various small studies. It was granted humanitarian approval from the FDA for the treatment of chronic refractory nausea, but it is not available widely and not routinely reimbursed .
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Non-medical approaches

Gastric electrical stimulation (GES)-  has shown to relieve symptoms, mainly vomiting frequency and the need for nutrition supplementation. In patients with refractory symptoms even after trial of the medications mentioned above, GES is considered as compassionate treatment approved for diabetic and idiopathic gastroparesis patients as a humanitarian exemption device. Diabetic patients respond more effectively than other groups of gastroparesis patients. Implantation of GES stimulator needs surgical procedure either via laparotomy or laparoscopic approach. The device consists of a pair of leads, implanted in the muscular propria about 10 cm proximal to the pylorus, and then connected to a pulse generator. Risks of GES include infection of the device, lead migration, and perforation, necessitating repeat surgical procedures. Also may need battery replacement about every ten years or so. Other available interventions, with no substantial evidence, that are under consideration are venting gastrostomy or feeding jejunostomy, intra-pyloric botulinum toxin injection (not shown to be effective in randomized controlled trials), partial gastrectomy and pyloroplasty (used rarely, only in carefully selected patients).

Future prospects

Multiple prospective treatments have been considered or being investigated for the management of gastroparesis. Granisetron, a 5-HT3 antagonist, administered as a transdermal patch, has improved gastroparesis symptoms of nausea and vomiting, as evident in a prospective study. Similarly, a randomized control trial involving aprepitant, a neurokinin-1 receptor antagonist, showed positive results of symptom improvement in gastroparesis patients. A scopolamine patch has undergone an evaluation with no significant effects. Also, research is ongoing studying the effects of transcutaneous acupuncture (TEA) in gastroparesis. Cannabinoids (dronabinol) have been considered in the treatment of gastroparesis symptoms, but there are no clinical trials reported. Cannabinoids are likely to be ineffective since they are known to delay gastric emptying. Attention should be given to the development of new effective therapies for symptomatic control. Relamorelin (a pentapeptide ghrelin receptor agonist) prucalopride and velusetrag (both are 5HT-4 receptor agonists) and metoclopramide nasal spray are investigational therapies undergoing evaluation in patients with gastroparesis.

Surgical Methods

  • The use of prokinetics like metoclopramide, erythromycin and anti-emetics –  can help relieve symptoms. Metoclopramide is the first-line agent; it is a dopamine D2 receptor antagonist that increases contractility, resting tone of GI tract and thereby promotes gastric emptying. It is recommended to use the lowest possible dose for the shortest duration of time given its extrapyramidal side effects unless benefits outweigh risks. Domperidone is similar to metoclopramide but with fewer central side effects and can be used when there are adverse effects with the use of metoclopramide. It is not FDA approved for use in the USA.  Domperidone can be prescribed by obtaining expanded access to investigational new drugs from the FDA. Erythromycin can be used for a short course to promote gastric emptying, but prolonged use is associated with tachyphylaxis and should be used sparingly. Other antiemetics used are prochlorperazine, promethazine, ondansetron, and tricyclic agents such as nortriptyline in the case of refractory emesis.
  • Intrapyloric botulinum injections –  have been demonstrated to improve symptoms in patients that are refractory to the above medical therapies. The effects of the botulinum injections last for about 3 to 6 months. Lack of randomized controlled trials to support the use of botulinum is the main limitation. A gastric electrical stimulator (GES) used in refractory patients as an alternative modality, it delivers high frequency and low energy stimulation to the stomach, thus enhancing gastric motility. Studies have also shown improvement in symptoms and gastric emptying from the use of GES. Surgical approaches include venting gastrostomy, feeding jejunostomy, pyloroplasty, and partial gastrectomy are performed when medical therapy fails for symptom relief. A new emerging, less invasive endoscopic technique gastric peroral endoscopic myotomy (G-POEM) is being evaluated to relieve the symptoms of gastroparesis. The initial studies are encouraging, will need further studies to evaluate efficacy and safety.
  • A feeding tube – If you have extremely severe gastroparesis that is not improved with dietary changes or medicine, a feeding tube may be recommended. Many different types of temporary and permanent feeding tube are available. A temporary feeding tube, called a nasojejunal tube, may be offered to you first. This is inserted into your digestive tract through your nose and delivers nutrients directly into your small intestine. A feeding tube can also be inserted into your bowel through a cut (incision) made in your tummy. This is known as a jejunostomy. Liquid food can be delivered through the tube, which goes straight to your bowel to be absorbed, bypassing your stomach. Speak to your doctor about the risks and benefits of each type of feeding tube. An alternative feeding method for severe gastroparesis is intravenous (parenteral) nutrition. This is where liquid nutrients are delivered into your bloodstream through a catheter inserted into a large vein.

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.[rx]
  • 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.[rx]
  • Severe fatigue and weight loss due to calorie deficit[rx]
  • Intestinal obstruction due to the formation of bezoars (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.[rx]
  • Small intestine bacterial overgrowth is commonly found in patients with gastroparesis.[rx]
  • Bacterial infection due to overgrowth in undigested food[rx]
  • A decrease in quality of life, since it can make keeping up with work and other responsibilities more difficult.[rx]

References

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