Gastropariesis CVs

1. AJ Gastro 21
Kurdistan Board GEH/GIT Surgery J Club 2021
Supervised by Professor Dr. Mohamed Alshekhani.

2. CV1:DM is most common 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 most common 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 most common 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 pain is 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 predicts GP 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 to diagnose
 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 is diagnostic 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 scans are 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 GE improves 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 risk with 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 pyloric therapies 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 it with 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 it with 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 considering mimics.
 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 considering mimics.
 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 considering mimics.
 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 considering mimics.
 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 considering physiological 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 considering nutrition.
 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 considering nutrition.
 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 optimizing trt.
 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 optimizing trt.
 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 considering opiates.
 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 GERD trts.
 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 to consider 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
&not 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 abd pain 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 selecting appropriately 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 GI motility
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).