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Emesis and Other Complications Post Roux-en-Y Gastric Bypass Surgery

| November 20, 2012

by Hira Ahmad, MD; Savannah Moon, MS-IV; and J. Patrick O’Leary, MD, FACS

Hira Ahmad, MD is PGY-1 Resident at Cleveland Clinic Foundation, Cleveland Clinic Florida, Weston, Florida. Savannah Moon is a fourth year medical student from Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Florida. J. Patrick O’Leary, MD, FACS, is Executive Associate Dean, Clinical Affairs and Assistant Vice President of Strategic Planning, Florida International University College of Medicine, Miami, Florida.

Bariatric Times. 2012;9(11):16–18


FUNDING: No funding was provided.

DISCLOSURES: The authors report no conflicts of interest relevant to the content of this article.

ABSTRACT
After Roux en-Y gastric bypass surgery, patients may experience nausea and vomiting. The procedure is often associated with other complications, including staple line failure, mechanical obstruction, marginal ulceration, dumping, and vitamin/mineral deficiencies. The pathophysiologic mechanisms associated with nausea and emesis are complex and involve numerous neural transmitters and neural pathways. In this article, we explore the relationship between these symptoms and discuss complications after Roux-en-Y gastric bypass and our current understanding on how vomiting occurs.

Introduction
More than one third of the United States adult population has obesity. Obesity is the second leading cause of preventative death in the United States, estimated to cause 30,000 deaths annually.[14] Surgical therapy has become the treatment of choice of the morbidly obese defined as a body mass index (BMI) of 40kg/m2 or more. The restrictive procedure Roux-en-Y gastric bypass (RYGB) is the most common procedure performed and is currently the gold standard.[14] As the incidence of surgical intervention has increased, so too has the incidence of gastrointestinal (GI) complications. The most common GI complications from bariatric surgery include the following: dumping, vitamin/mineral deficiencies, vomiting and nausea, staple line failure, infection, stenosis/obstruction, and postoperative anastomosis ulceration.1 Although postoperative nausea and vomiting can occur independent of an underlying problem, the symptom complex is most often associated with a mechanical problem. The mechanical issues that are associated with nausea and vomiting are marginal ulceration, gastro-gastric fistula, gastrojejunostomy anastomotic stricture, pouch dilation, and pouch gastritis. Furthermore, understanding the complex pathophysiology involved in vomiting has proved a challenge to surgeons.

Complications in Roux-en-Y Gastric Bypass
Marginal ulcer after RYGB. Marginal ulceration has been defined as peptic ulceration in the jejunal mucosa at the site of the gastrojejunal anastomosis. A marginal ulcer occurs in 1 to 16 percent of patients.[8,12] Although the exact etiology mechanism remains unknown, causes of marginal ulcers include poor tissue perfusion due to tension or ischemia at anastomosis, the presence of a foreign body, such as staples or sutures, excess acid exposure in the gastric pouch secondary to a gastro-gastric fistula, nonsteroidal anti-inflamatory drug (NSAID) use, Helicobacter pylori infection, and smoking.[12] The most common symptom is epigastric pain. Patients may also present with nausea, vomiting, bleeding, and perforation. Upper GI endoscopy is the diagnostic test of choice. Medical treatment includes gastric acid suppression, sucralfate, and H. pylori eradication. Surgical revision of the gastrojejunostomy with truncal vagotomy is indicated if symptoms or bleeding persist despite adequate medical therapy.

Gastro-gastric fistula after RYGB. Gastro-gastric fistula occurs between the proximal gastric pouch and distal gastric remnant with an incidence of 1.5 to 6 percent.[7,8] The compartmentalized stomach creates the potential for fistula formation.[3] Symptoms include weight gain, epigastric pain, nausea, and vomiting. Various possible etiologies involve anastomotic leak, incomplete gastric division, marginal ulcers, distal obstruction, and erosion of a foreign body. An UGI series may confirm the diagnosis.[3] Patients can be treated with proton pump inhibitors (PPIs), sucralfate, and eradication of H. pylori if present.[7,8] If symptoms persist or if weight regain is a problem, reoperation may be indicated.

Gastrojejunostomy anastomotic stricture. It is estimated that in the postoperative period, 2.9 to 23 percent of RYGB patients will develop an anastomotic stenosis from tissue ischemia or increased tension on the gastrojejunal anastomosis.[8] This narrowing can create a relative gastric outlet obstruction.Patients present several weeks to months after the procedure with progressive dysphagia and vomiting. Nausea may or may not be present. The diagnosed can be established by endoscopy or upper GI series. Treatment involves endoscopic balloon dilation or surgical revision of the anastomosis.

Physiology of Vomiting
Vomiting is the mechanism by which the UGI tract expels is contents when it becomes irritated, over-distended, or over-stimulated.[17] The act of vomiting occurs at the end of a series of three events. Nausea, awareness of the urge to vomit, occurs with decreased gastric motility and increased small intestine tone. Retching results from spasmodic respiratory movements on a closed glottis. Once the vomiting center is stimulated, the sequence is as follows:
1.    Inhalation
2.    Raising of the of the hyoid and larynx to pull upper esophageal sphincter open
3.    Closing of glottis to prevent aspiration
4.    Lifting of soft palate to close the posterior nares
5.    Diaphragmatic contraction, squeezing the cardiac stomach, building intragastric pressure
6.    Relaxation the lower esophageal sphincter, allowing expulsion of the gastric contents.[16]

Pathophysiology of vomiting
The brainstem vomiting center is composed of a group of neuronal areas (area postrema, nucleus tractus solitaries, and the central pattern generator) within the medulla of brainstem that coordinates emesis. Various neurotransmitters and receptors are involved in regulation, including dopamine-2 (dopamine or D2 receptor), serotonin (serotonin or 5HT3 receptor), acetylcholine (Ach or muscarinic receptor), histamine (histamine or H1 receptor), and substance P (neurokinin-1 or NK1 receptor).

Stimulating the brainstem vomiting center. The brainstem vomiting center may be stimulated by both peripheral and central mechanisms. There are three central inputs and one peripheral input (Figure 1). Peripheral stimulation of chemo- and mechanoreceptors in the stomach, gut, liver and peritoneum activate the vomiting center via the vagus nerve.[9] The three central inputs are as follows:
1.    Activation of fibers of vestibular system. Fibers of the vestibular system have high concentrations of histamine H1 and muscarinic cholinergic receptors. Vestibular and psychogenic factors affect the vomiting center by means of the afferent routes from the labyrinth and the higher cortical centers, respectively.
2.    Stimulation of the amygdala. Stimulation can occur from certain sights, smells, and/or emotional experiences.
3.    Stimulation of the chemoreceptor trigger zone. The chemoreceptor trigger zone is located outside the blood brain barrier in the area postrema of the medulla. This area is rich in opioid, serotonin 5-HT3, neurokinin 1 (NK1), and dopamine D2 receptors. Stimulation of the vomiting center is induced by activation of receptors in the chemoreceptor trigger zone by some medications and metabolic disorders (e.g., hypercalcaemia, acute renal failure).

The vomiting center stimulates the diaphragm (via the phrenic nerve); the striated muscles of the abdominal wall and thorax (via the spinal nerves); and the muscles of the stomach, esophagus, larynx, and pharynx (via the vagus nerve). This stimulation leads to the retching sensation and/or vomiting with the accompanying symptoms.

Prokinetic drugs, such as metoclopramide or domperidone, promote gastric emptying by blocking D2 receptors in the gastric wall. Additionally, metoclopramide activates 5HT4 receptors in the gastric wall. This leads to release of acetylcholine, which in turn further promotes gastric emptying.9

Conclusions
One of the most common complications post foregut surgery is nausea/vomiting. The post RYGB complications discussed in this article can present with nausea or vomiting. The pathophysiology of emesis is a complex multifaceted phenomenon that involves both central and peripheral mechanisms. Mechanical complication for the RYGB should be investigated in postoperative patients with these symptoms.

Acknowledgment
This article is based on a presentation from the 11th Surgery of the Foregut Symposium, February 19–22, 2012, Coral Gables, Florida.

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