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PostPosted: 30 Aug 2015 14:39 
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We all know hypoglycemia occurring before food in a diabetic patient who is on OHA or insulin or both. But hypoglycemia occurring after food is an entity which does not get the attention which it deserves. This is a complication of diabetes resulting in a condition known as diabetic gastro paresis. There is an increased gastric emptying time in this condition. Early satiety, nausea, vomiting, postprandial abdominal fullness and abdominal pain are some of the features. Diabetes more profoundly affect gastric motor functions than the small bowel transit. This results prolonged food retention in the stomach. As required the patient would have taken insulin or OHA prior to food. The medication and the delayed food transit result in hypoglycemia. When we manage diabetes this paradoxical condition must be kept in the mind. To overcome this complication patient must be advised to take small frequent meal along with plenty of fluid. Larger volume of the food taken at one time will also delay gastric emptying. Fat content must be reduced. They must be instructed to chew the food well. Alfa glycosidase inhibitors such as acarbose and voglibose before food may facilitate gastric emptying.

UA Mohammed


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PostPosted: 16 Nov 2015 01:56 
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Mohammed,

I did not know much about this subject that you wrote recently. I therefore did a little bit of reading. What a fascinating topic.

The vagus nerve appears to play a major role here. We all know that vagus carries both the sympathetic and parasympathetic fibres. It is the longest nerve in the body, innervating the throat, thorax, abdominal muscles, Heart, Lung and Stomach. I am not sure if the scientists know everything about the vagus nerve and its function as it appears to wander over a wide are of thorax and abdomen. Some of the main functions that are known include its involvement in Breathing, Speech, Sweating, Helping to keep the larynx open during breathing, Monitoring and Regulating the Heartbeat and Informing the brain of the food that is ingested and food that has been digested. It is said to perform the major function of emptying the gastric region of food.

Diabetes we know can affect nerves. Peripheral neuropathy is the most common form of diabetic neuropathy. However nerves innervating any organ can be affected. Any damage to the vagus nerve innervating the digestive system causes constipation and it can also cause Gastroparesis when the stomach empties very slowly. Severe gastroparesis can lead to persistent nausea and vomiting, bloating, and loss of appetite. Gastroparesis can also make blood glucose levels to fluctuate widely, due to abnormal food digestion.

Some of the articles indicate that gastroparesis is a frequent and severe complication of diabetes!

There is so much more on the topic. I would love to hear your views as you are actively involved with treating these patients.

Badri.


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PostPosted: 20 Nov 2015 03:29 
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Welcome back Mohammed.

Most useful and not so uncommon condition. A regular teaching topic in UK diabetic clinics.

Differential diagnosis is also worth noting.

The following are the American recommendations which cover the whole topic .

The diagnosis of gastroparesis is based on the combination of symptoms of gastroparesis, absence of gastric outlet obstruction or ulceration, and delay in gastric emptying.

Accelerated gastric emptying and functional dyspepsia can present with symptoms similar to those of gastroparesis; therefore, documentation of delayed gastric emptying is recommended before selecting therapy with prokinetics agents or GES.

Patients with gastroparesis should be screened for the presence of diabetes mellitus, thyroid dysfunction, neuro logical disease, [color=#BF00FF]prior gastric or bariatric surgery, and autoimmune disorders. Patients should undergo biochemical screen for diabetes and hypothyroidism; other tests are as indicated clinically. [/color]

A prodrome suggesting a viral illness may lead to gastroparesis (postviral gastroparesis). This condition may improve over time in some patients. Clinicians should inquire about the presence of a prior acute illness suggestive of a viral infection.

Markedly uncontrolled ( > 200 mg/dl) glucose levels may aggravate symptoms of gastroparesis and delay gastric emptying.
Optimization of glycemic control should be a target for therapy; this may improve symptoms and the delayed gastric emptying.

Medication-induced delay in gastric emptying, particularly from narcotic and anticholinergic agents and GLP-1 and amylin analogs among diabetics, should be considered in patients before assigning an etiological diagnosis.
Narcotics and other medications that can delay gastric emptying should be stopped to establish the diagnosis with a gastric emptying test.

Gastroparesis can be associated with and may aggravate GERD.
Evaluation for the presence of gastroparesis should be considered in patients with GERD that is refractory to acid-suppressive treatment.

Shall follow with Diagnosis and Management modalities


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