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Git j club gastropariesis contraversies21
1. Gastroparesis is a condition characterized by delayed gastric emptying without mechanical obstruction, often accompanied by nausea, vomiting, early satiety, and abdominal pain. 2. It can be diagnosed by demonstrating delayed gastric emptying on scintigraphy using a standardized meal, as well as evaluating symptoms. 3. The diagnosis requires ruling out other potential causes and confirming that symptoms are consistent with delayed gastric emptying. Interpreting mild delays cautiously is important to avoid misdiagnosing functional dyspepsia as gastroparesis.
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Git j club gastropariesis contraversies21
- 1. AJ Gastro 21 KurdistanBoard GEH/GIT Surgery J Club 2021 Supervised by Professor Dr. Mohamed Alshekhani.
- 2. CV1:DM is mostcommon cause Gastroparesis’ described the fact that barium did not leave the stomach of patients with diabetes for over 24 hs,called ‘gastroparesis diabeticorum’. Nowadays refers to a delay in gastric emptying associated with symptoms primarily nausea,vomiting without mechanical obstruction. The incidence of hospital admissions for patients labelled as having gastroparesis is rapidly rising, increasing at a much faster rate than admissions for patients with nausea & vomiting, GERD, gastritis or GU, Gastroparesis is a major healthcare burden. Gastroparesis can be idiopathic or most frequently caused by diabetes (type 1 >type 2) or surgical procedures that can disrupt the vagus nerve (e.g. Billroth gastrectomy, oesophagectomy,GBS& fundoplication).
- 3. CV1:DM is mostcommon cause Gastroparesis (GP) is one of the 2 most common sensorimotor disorders of the stomach, the other being functional dyspepsia (FD). An estimated prevalence of GP; 37.8/100,000 for women& 9.6 for men. The etiology of GP is complex& multiple recognized causes. DM accounts for 25%–30% of known cases. Idiopathic (predominantly)women, possibly representing a previous infectious process) represents the largest category (up to 50%). Medications &bariatric surgery, cholecystectomy&antireflux surgery are frequent causes of postsurgical GP.
- 5. CV2:GP is mostcommon cause of dyspepsia The DD for chronic nausea & vomiting (N & V) is quite broad. GP is just 1 important etiology. Important causes not characterized by persistent delays in GE include chronic nausea& vomiting syndrome (CNVS), cyclic vomiting syndrome (CVS)& cannabinoid hyperemesis syndrome (CHS);1%, 2%, 0.1% respectively. A history can help distinguish CVS(stereotypical episodes of N & V with interval weeks of minimal or symptom-free periods), CHS (prolonged cannabis use; compulsivebathing), CNVS (abdominal pain is not common) from GP (prolonged periods without symptoms is not characteristic; no history of compulsive bathing; abdominal pain is common). A GE study can distinguish GP from other causes of chronic N & V unrelated to delayed GE (e.g., CNVS& CVS). Lab/ imaging can usually identify other causes of chronic N & V that mimic GP (e.g., pancreatitis, hepatitis, celiac artery compression syndrome).
- 9. CV3:Abd painis uncommon in GP Abdominal pain as a cardinal symptom of GP is often overlooked&may reflect the fact that clinicians frequently consider nausea/ vomiting the key symptoms of GP. Abdominal pain is nearly universally present in patients with GP of all subtypes,more common in idiopathic GP without a preceding infection. Pain is more commonly reported in the epigastric area, although it can occur anywhere in the abdomen. Pain can be intermittent or chronic. Many patients report that eating worsens abdominal pain. The cause of abdominal pain in GP patients in incompletely understood& likely differs based on the underlying etiology. Pain may develop because of changes in sensory afferent function, coding& /or signaling abnormalities in gastric accommodation or distension& central sensitization, among other causes.
- 11. CV4:Symptom severity predictsGP extent The relationship between the degree of GE delay & severity of symptoms is controversial. The degree of GE delay does not reliably predict symptom severity for patients with GP & FD, a common functional GI disorder characterized by similar symptoms. There is relationship between delayed GE& symptoms (e.g., nausea, vomiting, abdominal pain& early satiety) in some patients. The lack of a consistent, clear association between symptoms and the extent of delayed GE suggests that the pathophysiology of GP is more heterogeneous& diverse than previously considered.
- 12. CV5:GP difficult todiagnose The extent of delay helps distinguish GP from FD. GP should be considered in patients with chronic symptoms of nausea, vomiting, early satiety&/or abdominal pain. A history, including a review of medications, can help distinguish GP mimics. Physical examination can exclude an organic cause (e.g., a mass, evidence of a partial bowel obstruction), identify underlying etiologies (e.g., scleroderma),detect a succussion splash& assess for signs of malnutrition. Basic laboratory tests should be performed (complete blood count, basic metabolic profile, TSH), HbA1c if the patient is diabetic. OGDto rule out a mechanical or organic cause of symptoms; biopsies can be performed if appropriate. Accurate assessment of GE is critical to the diagnosis; a 4-hour scintigraphy using a standardized test meal is considered the gold standard.
- 14. CV6:Delayed GE isdiagnostic of GP Delayed GE, based on gastric scintigraphy, is generally defined as =>10% retention (<90% emptying) at 4 hours. It is essential to identify potential secondary causes of delayed emptying, such as hyperglycemia&medications. More importantly, a mild delay in emptying (10%–20% retention at 4 hours) is most consistent with the diagnosis of FD, given that delayed GE is present in >25% of patients with FD. Although GP & FD can be considered part of the same disease spectrum of gastric sensorimotor dysfunction, patients with typical symptoms&a mild delay in emptying should be characterized as having FD, not GP.
- 15. CV7: GE scansare easy to perform & interpret A radionuclide GE scan, using a standardized egg-white meal, is the most commonly performed measure of GE&considered the gold standard test. Consensus The key parameters for an accurate test(patient preparation, meal content, procedure protocol, imaging, interpretation, reporting). Most centers do not perform the test correctly, leading to misdiagnosis& potentially incorrect treatments. Key mistakes include not stopping medications that affect GE; not measuring blood glucoselevels; using a non-standardized meal (i.e., oatmeal)& not performing a 4-hour scan. Importantly, overinterpreting a mild delay in emptying may lead to the incorrect diagnosis of GP, rather the more prevalent FD.
- 16. CV8: improving GEimproves symptoms Unfortunately, not because the pathophysiology of GP is complex, heterogeneous&more than just a motor disorder. A variety of prokinetic agents (e.g., ABT-229, erythromycin, camicinal, mitemcinal, tegaserod, velusetrag, relamorelin) to accelerate GE have consistently failed to demonstrate global GP symptom improvement, although some individual symptoms did improve. A recent placebo-controlled crossover study demonstrated that prucalopride, a 5- HT4 agonist, improved many GP symptoms, when measured by the GP Cardinal Symptom Index.
- 17. CV9: TD riskwith plasil is not so high Metoclopramide is the only FDA-approved medication for GP. Antiemetic effects occur through central inhibition of dopamine (D2) &serotonin type 3 receptors (5-HT3), while prokinetic effects occur through stimulation of 5-HT4 receptors with release of acetylcholine. Metoclopramide is available in several forms (oral, injectable, rectal, nasal spray). The efficacy of metoclopramide at treating GP symptoms is modest. Side effects occur in 30%–40%, include mild sedation, agitation, tremors,akathisia,anxiety,depression,insomnia, menstrual changes. The FDA recommends against chronic use (>12 weeks)& use in the elderly. The development of tardive dyskinesia, an extrapyramidal disorder characterized by potentially irreversible involuntary movements, a major concern to clinicians,risk has likely been overestimated, with 1 study calculating a risk of,1%, while a more recent analysis identified an even lower risk in the range of 0.1%/1,000 patient years.
- 18. CV10: Endo pylorictherapies highly effective Interventions directed at the pylorus, including pyloromyotomy& endoscopic injection of botulinum toxin A (BoTox), an alternative treatment options for GP patients, especially those refractory to dietary interventions&/or medical therapy. BoTox is theorized to treat GP by reducing pylorospasm, improving GE,but efficacy controversial. G-POEM demonstrated durable improvement in symptoms in a significant percentage of patients with refractory GP, but larger studies needed. Recognizing that there is no validated treatment algorithm for GP, clinicians should individualize therapy based on the predominant symptom &severity.
- 22. M1: Diagnosing itwith incomplete evidence. Diagnosis requires 3: 1. A delay in gastric emptying. 2.The absence of mechanical obstruction. Typical symptoms of nausea& regurgitation/vomiting, usually of undigested food, within a few hours after a meal, but can also include other dyspeptic symptoms as early satiety (feeling full very quickly after a few mouthfuls), postprandial fullness,epigastric bloating (which can be visible) & epigastric discomfort or pain. A delay in gastric emptying not accompanied by typical symptoms should not be classified as gastroparesis but simply ‘delayed gastric emptying’. If the predominant symptoms are more those of dyspepsia but there is no nausea&vomiting, the diagnosis is most likely to be functional dyspepsia, which has a different treatment algorithm. A diagnosis of delayed gastric emptying after performing a gastroscopy showing food in the stomach after a 6-hour fast can be inferred but would be DD of symps of nausea&vomiting&right predisposing factors as DM.
- 23. M1: Diagnosing itwith incomplete evidence. After excluding obstruction,cancer & drugs,gastropariesis confirmed using either breath testing or scintigraphy tests. The degree of gastric emptying is dependent on the type of meal & the pattern/rate of emptying can vary considerably between individuals. With a typical 255 kcal (2% fat/low fat) meal, delayed gastric emptying is defined as retention ≥60% at 2 hours& ≥10% at 4 hours. Normal values for gastric emptying will change if the meal is high fat, nutrient drink, or mixed solid/liquid. Scintigraphy is performed over 4 hours to ensure accuracy of the results.
- 26. M2: Not consideringmimics. Many conditions, including several functional GI disorders, can have a similar clinical presentation& associated with delays in gastric emptying. 1.Functional dyspepsia; the closest mimic to gastroparesis. FD can be divided into epiga pain syndrome& postprand distress synd. PPDS is characterised by symptoms of early satiety, postprandial fullness, epigastric bloating& epigastric discomfort or pain, symptoms almost identical to those of gastroparesis but with less nausea and vomiting. About 1/3 patients with functional dyspepsia will have mild to moderate delays in gastric emptying. The pathophysiology of FD is mainly due to a combination of ab gastric accommodation&visceral hypersensitivity. The presence of regular nausea/vomiting/regurgitation of undigested food would point towards a diagnosis of gastroparesis.
- 27. M2: Not consideringmimics. 2.Rumination syndrome, causes effortless regurgitation, mainly postprandially,a behavioural phenomenon caused by subconscious abd contractions that cause the regurgitation of food back into the oesophagus. It can be associated with dyspeptic symptoms& in some patients, the develops as a response to the dyspepsia as it often relieves this sensation. Typical symptoms of rumination syndrome include a cycle of regurgitation followed by swallowing of the regurgitant during or after meals, continuing until the regurgitant becomes acidic then expelled orally. Rumination syndrome can be diagnosed using combined high-resolution manometry–impedance monitoring, reveal a typical pattern of low- pressure gastric straining followed by regurgitation. Patients often complain that they vomit after eating; however, if a thorough history is taken, it can become clear that the vomiting is effortless (i.e. regurgitation). The treatment for this involves education & deep-breathing exercises.
- 29. M2: Not consideringmimics. 3.cyclical vomiting& cannabinoid hyperemesis syndromes, which cause episodic attacks of vomiting usually last for a few days, can be associated with dehydration& electrolyte imbalance. Between episodes, patients are completely asymptomatic, not like GP. Cyclical vomiting is very strongly associated with a personal or family history of migraines& cannabinoid hyperemesis syndrome is associated with heavy cannabis intak& the use of hot showers to relieve the nausea. Both of these syndromes can be associated with delay in gastric emptying. 4.Eating disorders,anorexia nervosa& bulimia nervosa, because low BMI index is associated with delays in gastric emptying&disturbed gastric func. 5.Stress& anxiety, centrally induced nausea&vomiting. If the anxiety is directed towards food, so-called ‘avoidant restrictive food intake disorder’,might present more like gastroparesis, with immediate postprandial nausea & vomiting&they only have to see food or put it in their mouth for vomiting to occur,with very early response to food, before the food even reaches the stomach.
- 30. M2: Not consideringmimics. 6. Narcotic bowel syndrome (opiate-induced central sensitisation syndrome), caused by the side effects of opiates on the gut. Typically, patients have worsening abdominal pain, but they can also have nausea, vomiting& epigastric bloating, which are symptoms similar to that of gastroparesis. As gastric emptying is delayed by opiates, it is useful to reassess symptoms & gastric emptying in patients once they have been weaned off them
- 32. M3: Not consideringphysiological factors. In gastroparesis, there is no correlation between the severity of symptoms & the severity of diseas&, the symptoms are not necessarily related to the delayed gastric emptying alone but arise due to a complex interplay between abnormal physiology (e.g. delayed gastric emptying or possible visceral hypersensitivity)&psychosocial factors such as poor sleep, low mood, stress& poor diet. So for the successful management of gastroparesis to use a biopsychosocial approach& ask about these factors & manage them rather than simply targeting the delayed gastric emptying with prokinetics, pyloric Botox or more invasive therapies as POEM or gastric pacing. It is also important to consider the role that visceral hypersensitivity has to play, as it will cause nutrient intolerance & pain even with post-pyloric feeding (e.g. nasojejunal feeding)&will need to be treated with neuromodulators.
- 33. M4: Not consideringnutrition. Foods that are high in fibre & fat are emptied from the stomach more slowly, so patients with gastroparesis should be advised to stick to a low- fibre, low-fat diet& to eat little&often. Liquids are easier to tolerate, so patients who continue to have difficulty consuming solids can be moved onto a liquid diet or a small-particle diet (i.e. foods that can be mashed with a fork),associated with an improvement in the symptoms of nausea, vomiting, early satiety, postprandial fullness, heartburn & regurgitation compared with a low glycaemic index diet,but neither the small-particle diet nor the low glycaemic index diet had any effect on upper abdominal pain. Gastroparesis causes dehydration &electrolyte/ nutritional deficiencies, secondary to the vomiting. Wt loss is rare but in8%, usually those with a severe delay in emptying. Enteral nutrition may be needed if nutritional deficiencies &weight loss, assessed by a dietician.
- 34. M4: Not consideringnutrition. Nutritional treatment can start with oral liquid supplements, but if patients continue to vomit& have associated weight loss, despite optimising the use of prokinetics, they may need post-pyloric feeding. If patients do not tolerate post-pyloric feeding (i.e. ongoing vomiting), this would suggest that it is not the delay in gastric emptying that is the problem but, instead, that they may have a problem with visceral hypersensitivity. Pain is not a clear indication of a requirement for jejunal feeding& if patients are overweight or do not have significant weight loss or nutritional deficiencies, then jejunal feeding may not be needed. As weight loss is rare, usually associated with severe delays in gastric emptying, it is important to consider other factors that may be contributing to vomiting in patients with weight loss& only mild-moderate delay(as in eating disorders)
- 35. M5: Not optimizingtrt. Prokinetics to work most effectively, they need to be taken half an hour before meals to induce gastric motility. Erythromycin is a motilin-receptor agonist & an effective prokinetic, but it should not be used for too long from tachyphylaxis& QT issues. It can be used as an add-on to existing treatments, as metochlorpromide. Serotonergic agents (e.g. prucalopride) should also be considered. Prucalopride is an agonist of the 5-HT4 (5-hydroxytryptamine 4) receptor &improve gastrointestinal transit,typically used to treat slow-transit constipation in females but also helps to speed up gastric emptying. The usual dose is 2 mg once a day and it can be increased to 4 mg once a day, although higher doses are associated with more side effects (e.g. headaches & diarrhoea). It can be helpful to trial prucalopride in patients who do not respond to first-line treatment, particularly if they also suffer with constipation (e.g. in patients with scleroderma or other CT disorders who have upper & lower GI hypomotility with slow-transit constipation& delayed emptying).
- 36. M5: Not optimizingtrt. Metoclopromide is associated with extrapyramidal side effects, such as dystonia & akathisia after a single dose or tardive dyskinesia/ Parkinsonism after prolonged doses,SO should not be prescribed in the long term. If patients respond symptomatically to metoclopramide, it is helpful to convert them to another prokinetic to be used more long term. Domperidone not associated with extrapyramidal side effects but do with a prolonged QT interval, so it is imperative that patients have an ECG to check for a normal QT interval before initiation of treatment — the ECG should be repeated once patients have been started on domperidone to ensure that the QT interval remains in the normal range.
- 37. M6: Not consideringopiates. Opiates cause delayed gastric emptying & symptoms. In patients with suspected gastroparesis & opiate, to repeat the gastric emptying testing to get a more accurate assessment of their symptoms& physiology in the absence of the confounding effects of the opiates. Other medications that are associated with delayed gastric emptying include anticholinergics (e.g. hyoscine), antipsychotics& incretins (e.g. liraglutide). It is therefore imperative to take a thorough medication history in the assessment of gastroparesis&to consider the withdrawal of certain drugs in the management plan, especially opiates.
- 38. M7: Overlooking GERDtrts. In patients with gastroparesis, failure to empty the stomach results in the regurgitation of acids& non-acids& it is not uncommon for patients with gastroparesis to have coexistent GERD. Over time, pathological acid reflux can lead to oesophagitis, peptic structuring,rarely, Barrett’s oesophagus. It is important that these patients take high-dose PPIs twice a day to prevent the progression of acid-induced damage to the oesophagus. In the presence of uncertainty about medication absorption (because of the recurrent vomiting of tablets), it can be helpful to use oro dispersible tablets of PPIs (e.g. or dispersible lansoprazole or omeprazole).
- 39. M8: Failure toconsider DM control. Delayed gastric emptying is present in 27–65% T1D& 30% T2DM. Hyperglycaemia is independently associated with delayed gastric emptying. The presence of gastroparesis in the setting of diabetes is a consequence of autonomic neuropathy that results from a longstanding poor control of blood glucose &daily fluctuations caused by episodic hyperglycaemia. Gastroparesis makes it very difficult to control postprandial blood glucose ¬ uncommon for patients who have diabetes to struggle to accurately predict how much insulin they need,resulting in a vicious cycle in which gastroparesis leads to vomiting, diabetic ketoacidosis& high blood glucose further worsen the gastroparesis. Using a closed-loop system with a continuous glucose sensor &24-hour insulin pump can dramatically improve the stability of blood glucose &reduce gastroparesis-type symptoms.
- 40. M9: Treating abdpain by speeding up GE. Upper abdominal pain is common in gastroparesis,in almost 90% of patients &most commonly epigastrium. A third of patients will describe the pain as severe, with this being more likely if they are female& if they have any of the following — anxiety, depression, somatization& opiate use. There is no correlation between the severity of the pai& the severity of the gastric emptying delay. Therefore, medication or treatment that aims to reverse the gastroparesis by speeding up gastric emptying (e.g. prokinetics, pyloric Botox or gastric pacing) will not treat the pain. Pain is usually a marker of underlying visceral hypersensitivity, so it should be managed using a biopsychosocial approach (e.g. by addressing anxiety, depression or by managing reducing opiate use)& using medications as PPIs or neuromodulators (e.g. mirtazapine or pregabalin), as for functional dyspepsia.
- 41. M10: Not selectingappropriately for gastric pacing Gastric pacing is the delivery of electrical stimulation to stomach via an implanted pacemaker system that consists of a neurostimulator&2 leads. Implantation is done under general anaesthetic, open or laparoscopic . The rate& amplitude of stimulation can be adjusted wirelessly with a handheld external programmer. Patients may need to return to hospital for adjustment or reprogramming of the device to optimise the effect on gastric emptying. Gastric pacing is thought to work by interfering with sensory transmission to the brain, thereby improving certain symptoms. The best results seem to be in patients with nausea & vomiting, who have diabetes& who are not on opiates, so patient selection is crucial. It can be associated with multiple complications, including device migration, lead displacement, pain at site, bowel obstruction &in rare cases, erosion through the skin.
- 42. Gastropariesis: Gastroenterology 2022 Gastroparesis is characterized by symptoms suggestive of&objective evidence of, delayed gastric emptying in the absence of mechanical obst. The normal emptying of solids & liquids from the stomach has the myogenic& neuromuscular control mechanisms, including the specialized function of the pyloric sphincter, that result in normal emptying. A clear understanding of fundamental mechanisms is necessary to comprehend derangements leading to gastroparesis. Neuromuscular diseases affect non-sphincteric gastric muscle, disorders of the extrinsic neural control&pyloric dysfunction lead to gastroparesis. The potential cellular basis for gastroparesis is attributed to the effects of oxidative stress& inflammation, with incr proinflammatory&decreased resident macrophages, as observed in full-thickness biopsies from patients with gastroparesis.
- 43. Gastropariesis: Gastroenterology 2022 Predominant diagnostic tests involving measurements of gastric emptying, the use of a FLIP& high-resolution antral duodenal manometry in characterize the abnormal motor functions at the gastroduodenal junction. Management: Supporting nutrition. Dietary interventions, including the physical reduction in particle size of solid foods. Pharmacological agents, including prokinetics/anti-emetics;. Interventions such as gastric electrical stimulation & pyloromyotomy. There is potential for individualized treatments in the future, based on optimal gastric emptying measurement& objective documentation of the underlying pathophysiology causing the gastroparesis.
- 44. (A)Intrinsic excitatory cholinergic neuron.ChAT, choline acetyl trans (B) Intrinsic inhibitory nitrergic neuron (NOS). (C) Extrinsic neural control of GI motor function. Parasympathetic supply is generally excitatory to nonsphincteric muscle or excitatory to inhibitory intrinsic nerves. Sympathetic nerves are generally inhibitory to Non sphincteric muscle& stimulatory to sphincteric muscle,as pylorus
- 45. Diseases causing GImotility disorders: gastroparesis, may result from abns in PS nerves as in diabetic neuropathy or brainstem diseases affecting vagal& other autonomic nuclei; disorders affecting sympathetic nerves, including neuropathies& dysautonomias& diseases affecting primarily the enteric nerves (ENS) or smooth muscle, including myopathies, as amyloidosis&mitochon Neuro GI encephalopathy (MNGIE).