Some research suggested that about 1/3 of patients develop post bariatric hypoglycaemia 1 to 4 years after gastric bypass surgery

Post bariatric hypoglycaemia can be profoundly disabling with symptoms ranging from fatigue, headache to severe neuroglycopenia leading to loss of consciousness and seizures

Post prandial response: *There is a rapid hyperglycaemia peak after meal ingestion (in the first 30 minutes) *Followed by a hyperinsulinaemic response in the 30-60 minutes *Followed by hypoglycaemic drop 2 hours later After gastric bypass surgery, alteration in the anatomy and rapid/intense nutrient flow causing elevation in incretin resulting in overcompensation of insulin secretion and the subsequent hypoglycaemia   Our understanding of the pathophysiology is still incomplete: The causes of post bariatric hypoglycaemia may include the combination of: *Rapid gastric emptying *Excessive post prandial insulin secretion *Elevated GIT peptides (GLP-1 and GIP) as well as other hormones (FGF-19, FGF-21) *Improved insulin sensitivity *Inappropriate B cell secretion (late dumping syndrome) from ingested nutrients entering the distal small bowel *Abnormal counter regulatory hormone (glucagon) response *The impact of other hormones such as ghrelin, peptide YY and leptin remains uncertain *Gut hypertrophy and adaptation with the increase in the numbers of enteroendocrine L cells and more incretin released *? increased levels of carnitine and acylcholines that may signal inhibition of mitochondrial fatty acid beta oxidation, inducing glycolysis and lower blood glucose *? other unknown factors involved as well     Although for all patients after gastric bypass there is elevation in GLP-1 but only 1/3 of patients develop post bariatric hypoglycaemia *Counter regulatory hormones such as glucagon fail to prevent hypoglycaemia *The negative feedback loop on the liver fail to compensate for the hypoglycaemia *Changes in the energy regulating hormones *Patients with insulin resistance or T2DM are less likely to suffer from post bariatric hypoglycaemia           Patients who is treated (with glucose) may trigger subsequent sugar spikes and a recurrent cycle of hypoglycaemia (roller coaster hypoglycaemia)   After RYGBP, the secretion of GLP-1 and GLP-2 increases proportionally with insulin secretion and glucose absorption *The ileal L cells release proglucagon, which is cleaved into GLP-1 and GLP-2 *GLP-2 may help reduce inflammation and potentially decrease hypoglycaemia episodes   Non diabetic patients after RYGBP may experience prolonged hypoglycaemia due to the improved insulin sensitivity *This is also due to increased GIT peptides, post prandial insulin and better insulin sensitivity/response

Dumping	Post prandial hypoglycaemia
Usually occurs within 30 minutes after meals	Usually occurs 1 to 3 hours after meals
GIT symptoms (rapid gastric emptying) Epigastric discomfort/cramps or fullness Borboryygmi Nausea Diarrhoea, green stools Vasomotor symptoms Headache Flushing Sweaty Syncope, faint Palpitations Need to lie down	Neuroglycopenic symptoms Weakness Fatigue Dizzy Confusion, poor concentration Blur vision Decrease conscious state, coma     Autonomic (adrenergic and cholinergic) symptoms Pale Tremor, sweaty, anxiety Tachycardia (palpitation) Hunger sensation Parasthesia

Management options   Dietary changes Small frequent meals 5 to 6 times a day is recommended Avoid high GI index fluids and food Avoid milk and dairy products Low carbohydrate intake is recommended (10-30g a day only)   Medications Alpha glycoside inhibitor (Acarbose) *to decrease carbohydrate absorption and insulin spike but may cause diarrhoea Immodium Somatostatin analogue (Octreotide) *to decrease gastric/small bowel gut transit time, inhibit gut hormone and insulin release, inhibit post prandial vasodilatation GLP-1 agonist injection *the mechanism is uncertain