Diabetic gastroparesis is a complication of diabetes that results from dysfunction of the autonomic nervous system and stomach muscles. It causes delayed emptying of food from the stomach. The presentation includes nausea, vomiting, early fullness and weight changes. Diagnosis involves testing for delayed gastric emptying. Treatment focuses on diet, glycemic control, prokinetic medications, and in severe cases, procedures like gastric stimulation. Education is important for managing the chronic nature of the condition and preventing complications like malnutrition.

1. Diabetic gastroparesis
Presented by
DR. Priyank kumar sah
JR1 General medicine
Moderator
DR. [Prof] Ashis Kumar saha
sir
HOD General medicine

2. Introduction
• Gastroparesis is defined by objective delaying of gastric emptying without any
evidence of mechanical obstruction.
• Diabetic gastroparesis is a potential complication that occurs in the setting of
poorly controlled diabetes, resulting from dysfunction in the coordination and
function of the autonomic nervous system, neurons, and specialized pacemaker
cells (interstitial cells of Cajal) of the stomach and intestine, and the smooth
muscle cells of the gastrointestinal tract

3. Etiology
• Hyperglycemia (blood glucose greater than 200 mg/dL) in poorly controlled
diabetes, has been associated with diabetic gastroparesis resulting from
neuropathy in the setting of chronic hyperglycemia and does not resolve with
improved glycemic control
• Acute hyperglycemia, on the other hand, though it can also result in delayed
gastric emptying, is often reversible with improved glycemic control

4. Epidemiology
• idiopathic gastroparesis is the most common form of gastroparesis,
diabetes is the most common disease associated with the condition.
• Upper gastrointestinal symptoms are reported in11% to 18% of patients
with diabetes, most of which are associated with delayed gastric
emptying.
• Gastroparesis is seen in approximately 4.8% of individuals with type 1
diabetes, 1% of those with type 2 diabetes, and 0.1% of those without
diabetes.

5. • Although there is a stronger association between type 1 diabetes and
gastroparesis, the incidence of type 2 diabetes is much greater, and
therefore, gastroparesis associated with type 2 diabetes is seen more
frequently.
• Signs and symptoms of delayed gastric emptying are seen more
frequently in individuals with type 1 versus type 2 diabetes and typically
in those who have had the disorder for at least five years.
• It has been observed that gastroparesis typically occurs in patients with
a diagnosis of diabetes of at least ten years and is therefore seen more
commonly in older individuals with type2 diabetes.

6. Pathophysiology
• Diabetic gastroparesis occurs as a result of dysfunction in the autonomic and enteric nervous
systems.
• Chronically high levels of blood glucose (or inefficient glucose uptake) lead to
1. neuronal damage resulting in abnormal myenteric neurotransmission (e.g., vagus nerve)
2. impaired inhibitory (nitric oxide) neuronal function,
3. dysfunctional smooth muscle and pacemaker(interstitial cells of Cajal) cells.
• dysfunction results in a combination of
1. fewer contractions of the antrum,
2. uncoordinated antro-duodenal contractions,
3. pyloric spasms , ultimately resulting in delayed gastric emptying (gastroparesis).

7. • Delayed gastric emptying in patients with diabetes, particularly of solids,
may also occur in the setting of abnormal small bowel motility.
• Some patients with diabetes may additionally experience changes in
gastric compliance, both increased or decreased, which may also
contribute to delayed gastric emptying.
• serum (postprandial) glucose levels have a direct relationship with gastric
emptying.
• In the setting of diabetic autonomic neuropathy, acute hyperglycemia
stimulates gastric electrical activity.

8. • In patients with diabetes (without neuropathy) and healthy controls , acute
hyperglycemia will instead relax the proximal stomach and suppress gastric
electrical activity (e.g., reduced the frequency, propagation, and contraction of
the antrum) in both fasting and post-prandial conditions, thereby slowing gastric
emptying.
• Acute hyperglycemia is associated with increased sensitivity in the
gastrointestinal tract. This may be responsible for
1. postprandial dyspepsia
2. early satiety
3. nausea
4. vomiting
5. heartburn
6. bloating

9. • Carbohydrate absorption is dependent on the speed of gastric
emptying through there lease of peptides such as glucagon-like
peptide-1 and glucose-dependent insulinotropic polypeptide, in which
slower gastric emptying results in a higher level of carbohydrate
absorption.
• A higher serum glucose level due to delayed gastric emptying can
itself lead to the worsening of gastroparesis

10. Histopathology
• Full-thickness biopsies, which are needed to diagnose changes in the deeper layers
of the stomach wall, are not practical to be used as a diagnostic tool.
• In special studies done using full-thickness gastric biopsies, the findings in
inflammatory infiltrate, a reduction in the number of nerve cell bodies and ICCs in
the myenteric plexus, and fibrosis
• Recent studies have pointed at the role of macrophages in the pathogenesis of
diabetic gastroparesis.

11. History and Physical examination
• Nausea is the most common symptom in
gastroparesis.
• Other symptoms like vomiting, early satiety,
postprandial fullness, and bloating.
• Vomitus often contains undigested chewed food.
• Both weight loss and weight gain can occur.
• Physical examination neuropathy, abdominal
distension, and halitosis can present in patients
with diabetic gastroparesis.

12. Investigations
• The first to exclude mechanical obstruction and peptic ulcer disease.
• All patients should undergo an upper gastrointestinal endoscopy.
• It is followed by either a CT scan with oral and intravenous contrast or other imaging such as a small
bowel follow-through to exclude obstruction beyond the duodenum.
• Scintigraphy, is the gold standard.
• Solid-phase emptying is usually used to evaluate for gastroparesis.
• use of a 99 mTc sulfur colloid labeled egg white sandwich as the test meal
• Standard imaging is performed at 0,1,2,4 hours postprandially. A four-hour study is more sensitive and
accurate

13. • Medications such as opiates and anticholinergics can slow gastric motility,
whereas prokinetics and other medications can hasten gastric emptying.
• Hyperglycemia is known to slow gastric motility, and it is worthwhile to
try and achieve euglycemia before performing the test.
• Breath testing -Most commonly, 13C-labelled octanoate is bound to a
solid meal and ingested. After emptying from the stomach, it is absorbed
by the small intestine and metabolized to 13CO2, which is expelled from
the lungs during respiration.
• Electrogastroraphy and gastroduodenal manometry are other tests based
on myoelectrical activity

14. Treatment
The first step is lifestyle modifications.
• Dietary modification
• Optimal glycemic control
• Smaller, more frequent meals
• minimizing carbonated beverages
• increasing the liquid content, reducing fats and fiber
• Alcohol and smoking should be discouraged,

15. Medical treatment
•Antiemetics
first step in gastroparesis patients as they help with the common symptoms
of nausea and vomiting.
1. ondansetron
2. prochlorperazine
3. Promethazine

16. Prokinetic agents
is cornerstone of pharmacologic therapy in diabetic gastroparesis
• Erythromycin -binds to the motilin receptors responsible for the initiation of the MMC in the upper gut
• Domperidone
• Cisapride
• Metoclopramide
Muscarinic cholinergic agents
Bethanechol - accelerate gastric emptying

17. NonpharmacologicTherapy
•Endoscopic treatment
pyloric botulinum toxin injection
• Gastric Electrical Stimulation
• a gastrostomy tube for intermittent decompression by venting or
suctioning may provide relief

18. • placement of a feeding jejunostomy can be effective in providing nutrition,
fluids, electrolytes and reduce hospitalizations.
• A trial of naso jejunal feeding can predict the response to a jejunostomy.
• The last resort in refractory gastroparesis is surgery, including a partial
gastrectomy with Roux-en-Y gastrojejunostomy and gastric resection.

19. Differential Diagnosis
• Gastric outlet obstruction
• Functional dyspepsia
• Chronic pancreatitis
• Biliary colic

20. Prognosis
• The outcomes of diabetic gastroparesis are not well defined. Prognosis depends on
the adequate control of hyperglycemia and compliance with medications.
• It affects the quality of life and can have significant morbidity if left uncontrolled.
• Education regarding the need for life long management of this condition is
essential to improve clinical outcomes.

21. Complications
• Malnutrition is an important complication of diabetic gastroparesis that often
needs management with jejunostomy, parenteral nutrition, or surgery.
• Wide glycaemic fluctuations can occur in diabetic gastroparesis, and this can lead
to complications such as hypoglycaemia and diabetic ketoacidosis or
hyperosmolar hyperglycaemic state.
• Nausea and vomiting can lead to aspiration pneumonia.

22. Patient Education
• Patients require education regarding the chronic and often irreversible
nature of the disease.
• Adherence to a "gastroparesis diet," judicious use of medications, and
strict control of hyperglycemia are important patient factors that can
change the course of the disease and prevent complications.
• Patient education and consultation with a doctor and dietician can
greatly improve the clinical outcomes of this disease .

23. THANK YOU