Section 2 Benign Diseases

#### **Chapter 4**

## Perspective Chapter: Update on Achalasia Treatment

*Gad Marom, Ronit Brodie and Yoav Mintz*

#### **Abstract**

Achalasia is a primary motility disorder of the esophagus characterized by failure of relaxation of the lower esophageal sphincter (LES) and aperistalsis of the esophagus. There are 3 types of achalasia, diagnosed and differentiated according to the Chicago classification using high resolution manometry (HRM). The classic symptoms of achalasia as described by the Eckardt score are dysphagia, retrosternal pain, regurgitation and weight loss. This chapter will discuss the interesting evolution of achalasia in the modern era, the ways to diagnose achalasia, different sub-groups within achalasia patients population, treat it with either endoscopic or surgical manner, pre-operative and post-operative considerations and routine follow-up.

**Keywords:** achalasia, Eckardt score, per-Oral endoscopic Myotomy, high resolution manometry, Endo-FLIP

#### **1. Introduction**

Achalasia is a primary motility disorder of the esophagus characterized by failure of relaxation of the lower esophageal sphincter (LES) and aperistalsis of the esophagus. There are 3 types of achalasia, diagnosed and differentiated according to the Chicago classification 4.0 using high resolution manometry (HRM) [1]. These types are differentiated by the functionality of the esophageal motility and do not reflect a progression of the disease from one to the other. The classic symptoms of achalasia include progressive dysphagia, retrosternal pain, regurgitation or vomiting of undigested food and weight loss [2].

Over the last few years, the incidence of achalasia has increased. Once thought to be a rare disease with an incidence of 0.03–1.63 per 100,000 persons per year, a higher incidence of 2.3–2.93 cases per 100,000 persons per year was recently reported [3, 4]. The upsurge in incidence may be attributed to the increased use of high-resolution manometry (HRM). This test has become more sensitive and easier to interpret due to better sensors and intuitive visualization of results. Additionally, the emergence of Per-Oral Endoscopic Myotomy (POEM) has also largely contributed to the increased of awareness of the disease.

The textbook presentation of patients with achalasia is outdated. Patients are no longer appearing as malnourished or cachectic as classically described [5, 6]. Counterintuitively, in recent years, due to the variety of calorie-rich, high fat soft and liquid foods, some achalasia patients have begun to present as overweight and even obese. These patients suffer from dysphagia and retrosternal pain but manage their symptoms via dietary changes and constant eating due to lack of satiety, which may further contribute to increased weight gain despite dysphagia. Additionally, the complaints of chest pain are often mistakenly contributed to a reflux disease that is more common among obese patients than achalasia, thereby delaying their diagnoses. It is quite common to find achalasia patients treated with antacid medications such as proton pump inhibitors, unsuccessfully, as the pathophysiology of achalasia is not rooted in acid reflux but regurgitation of undigested food.

Young achalasia patients often are misdiagnosed as suffering from eating disorders, specifically among adolescents and female gender [7, 8]. It is not uncommon for patients to be admitted to inpatient care for eating disorder, further delaying time to correct diagnosis.

Delays in treatment either due to delay in diagnosis, or secondary to fear of treatment may significantly impact outcomes. Delaying treatment can aggravate symptoms, exacerbate dysphagia and cause severe weight loss and secondary pulmonary complications such as recurrent pneumonias secondary to micro-aspirations. Untreated longstanding achalasia may result in end-stage achalasia, expressed as sigmoid esophagus on barium swallow studies and endoscopy. This entity limits the treatment options that are available for other achalasia patients who are treated earlier in the disease process. Another sequela from untreated achalasia is the increased risk for esophageal cancer. This is thought to be caused by long-standing stasis of food, liquid and debris in the esophagus resulting in bacterial overgrowth and subsequently squamous cell cancer [9].

#### **2. Diagnosis and work up**

The diagnosis of achalasia is determined based on findings from three studies: high-resolution esophageal manometry, contrast enhanced swallow study (CESS), and esophagogastroduodenoscopy (EGD) [10]. The clinical severity is determined based on the Eckardt score scaling system.

#### **2.1 Contrast enhanced swallow study (CESS)**

A key portion of diagnosis includes the evaluation of the anatomical image of the esophagus. Contrast enhanced swallow study, also known as barium swallow or upper GI swallow, allows for the visualization of the esophagus and elimination of alternative diagnosis such as carcinoma, strictures or diverticula [11]. CESS is non-invasive, widely available, and relatively inexpensive [12, 13]. As CESS has only 60% sensitivity for identifying achalasia [14], it cannot be solely relied upon for the diagnosis. The classic sign of tapering of the esophagus at the distal end giving a "bird's beak" appearance at the esophagogastric junction is pathognomonic for a diagnosis of achalasia (**Figure 1A**). Additional findings include dilation of the esophagus, retention of barium in the esophagus and an air-fluid level. In long standing disease a sigmoid shape esophagus may be evident. The absence of gastric air bubble is also suggestive of achalasia. A torturous twisting appearance of the esophagus in a "corkscrew" fashion (**Figure 1B**) may also be suggestive of esophageal dysmotility [15].

#### **2.2 Esophagogastrodoudenoscopy (EGD)**

EGD is important in the diagnosis of achalasia as it is necessary to rule out other possible causes of dysphagia including gastroesophageal reflux, strictures due to

*Perspective Chapter: Update on Achalasia Treatment DOI: http://dx.doi.org/10.5772/intechopen.108194*

#### **Figure 1.**

*Contrast enhanced swallow study images that correlate with achalasia. A: Pathognomonic appearance of bird's beak on CESS. B: Corkscrew esophagus from esophageal dysmotility.*

#### **Figure 2.**

*Endoscopic images of different endoscopic pathologies that can mimic achalasia symptoms. A: Esophageal diverticula- on the left fluoroscopic image, on the right endoscopic image (green asterisk marks the diverticula). B: Esophageal candidiasis.*

erosive esophagitis, esophageal diverticula (**Figure 2A**), tumors and obtaining biopsies to rule out eosinophilic esophagitis. Careful attention should be made to the ease of passage through the esophago-gastric junction (EGJ) into the stomach, any signs of esophagitis or strictures, as well as a detailed retroflexion view to rule out any tumor. Additional findings may include candidiasis infection (**Figure 2B**) as demonstrated by white plaques on the esophageal walls, not uncommon in patients with achalasia, most likely secondary to the change in pH due to food stasis [16].

#### **2.3 High resolution manometry (HRM)**

In order to understand the motility and function of the esophagus, the highresolution manometry in conjunction with the new Chicago Classification 4.0 has allowed for better understanding, earlier diagnosis and improved classification of esophageal motility disorders [1, 17]. The HRM is able to provide images detailing the information regarding vigor of each swallow, peristalsis, relaxation and pressure of the upper and lower esophageal sphincters, thereby improving diagnostic accuracy [18]. Furthermore, the ability of testing to differentiate between the pressures of

**Figure 3.**

*High resolution manometry demonstrating different types of achalasia (left to right)- all 3 types have mean IRP pressure higher than the upper limit of normal. Type 1 with 100% failed peristalsis, type 2 with panesophageal pressurization and type 3 with distal spastic contractions.*

the lower esophageal sphincter and the diaphragmatic pressure, which with previous standard manometry was not as clearly differentiated, has been beneficial. The identification of hiatal hernia versus increased esophageal pressure is one of the keys to proper diagnosis and treatment.

HRM in which a catheter containing pressure sensors approximately 1 to 2 cm apart is positioned from the hypopharynx to the stomach (via nasal introduction) with the patient being asked to swallow mouthfuls of water at several intervals. The sensors combined with computer analytic software can build an image of higher and lower pressures, peristalsis and relaxation of the esophageal sphincters. The inclusion of impedance which allows for the visualization of bolus clearance, also aides in the differentiation of esophageal from oro-pharyngeal motility dysfunctions [19].

In achalasia findings on HRM will be dependent on what type of achalasia is present, with all types demonstrating both aperistalsis and elevated Lower esophageal sphincter residual pressures (>15). Determination of which type of achalasia will be dependent on the remaining findings on HRM (**Figure 3**).

Hallmark findings according to the Chicago classification 4.0 for Type 1 achalasia will demonstrate 100% failed peristalsis, while type 2 will demonstrate panesophageal pressurization in 20% or more swallows, and type 3 will present with 20% or more premature spastic appearing contractions.

#### **2.4 Eckardt score**

Eckardt score (**Table 1**) is a scoring panel used to assess the severity of achalasia symptoms and is based on four major symptoms: dysphagia, regurgitation, chest pain, and weight loss [10]. Symptoms of dysphagia in patients with achalasia are usually described as progressing from solids and to liquids. Regurgitation, bringing up undigested food following meals – even hours later, is also common. Retrosternal chest pain is usually described as burning pressure often radiating to the upper back and neck. Weight loss varies, according to the dietary changes made by each patient to accommodate their symptoms.

To score, each symptom is given a value between 0 and 3 depending on its frequency (**Table 1**). It is important to note that while the Eckardt score is utilized for the determination of severity and for determining success of treatment, it holds limitations, and the severity may not correlate with manometric or CESS findings. The occurrence of concomitant obesity and achalasia has been previously reported, and as the obesity endemic grows, the possibility of achalasia in obese patients presenting with dysphagia should not be discounted [20]. As such, determination of severity based on the Eckardt scale may not accurately reflect certain populations with achalasia.

*Perspective Chapter: Update on Achalasia Treatment DOI: http://dx.doi.org/10.5772/intechopen.108194*


#### **Table 1.**

*Eckardt score: Each symptom is given a value between 0 and 3 depending on frequency while weight loss is scored based on how many kilogram in weight have been lost. A summary of this score is done and a total between 0 and 12 is given.*

#### **2.5 EndoFLIP™−**

Functional luminal imaging probe (FLIP) quantifies the relationship between luminal geometry and pressure when assessing the esophageal wall and area around the lower esophageal sphincter (LES) at the esophago-gastric junction (EGJ). EndoFLIP™ (Medtronic Inc., Minneapolis, Minn, USA) provides information on both distensibility and lumen diameter of the esophagus. The technology consists of a multielectrode probe and proprietary software that measures the dynamic geometrical changes of the EGJ and esophageal body. It uses high-resolution impedance planimetry during volume-controlled distension of the probe once it passes the EGJ. Specifically, EndoFLIP analyzes the relationship between luminal cross-sectional area (CSA) and pressure, providing a measurement of the luminal distensibility (CSA/ pressure) [21, 22]. The EndoFLIP can be used intraoperatively to assess treatment results following completion of myotomy (**Figure 4**). As opposed to HRM which requires patient cooperation and swallowing, the EndoFLIP can be performed on anesthetized patients and determine the post-op distensibility and lumen diameter.

In addition, there are several reports in the literature that use FLIP to evaluate contractility in the esophageal body of patients to complement HRM results. However, in

#### **Figure 4.**

*EndoFLIP- on the left is the pre-myotomy image showing low distensibility at the EGJ with narrow passage. On the right is the post-myotomy image showing improvement in the distensibility and a wider passage at the EGJ.*

order to do so, the probe is placed more proximal along the esophagus and a special software is used to assess peristalsis [23, 24].

#### **3. Treatment options**

The mainstay of treatment for achalasia is directed toward lowering the LES pressure to allow food passage to the stomach. The non-surgical treatment options include pneumatic balloon dilatation and Botulinum toxin injection while surgical treatments include Heller myotomy and per-oral endoscopic myotomy (POEM) [25, 26]. Offering the appropriate treatment option to a specific patient is done when taking into consideration all the pre-operative work up, comorbidities, and nutritional status of each individual patient.

#### **3.1 Non-surgical treatment**

Generally, the non-surgical treatment options are preferred for patients who are considered high risk for surgical intervention secondary to their comorbidities.

#### *3.1.1 Botiluim toxin injection*

Botilium toxin A (Allergan Inc., Irvine, California, USA), a muscle paralytic which acts via inhibiting the release of acetylcholine locally at the neuromuscular junction thereby reducing the tone of the lower esophageal sphincter resulting in its relaxation [27]. Endoscopically guided injections of 25 units are placed in each of four quadrants circumferentially around the lower esophageal sphincter just above the Z line using a sclerotherapy needle, for a total of 100 units. However, its rather limited short acting results with 78.7% patients having relief of symptoms at one month post injection and declining to 40.6% at 12 months post injection [28], and approximately 50% of patients requiring repeated injections [29]. Botilium toxin injection may be used as a bridging procedure in severely malnourished patients until surgery to allow some relief of symptoms and weight gain [30]. Botilium toxin injection may be a good option for elderly high-risk surgical patients, even if repeated injections are necessary.

#### *3.1.2 Pneumatic dilation*

Under endoscopic and radiological guidance an achalasia balloon commonly the Rigiflex Balloon system (Boston Scientific Corp, Boston, Massachusetts, USA) is used to tear the musculature of the lower esophageal sphincter thereby reducing the outflow obstruction and alleviating symptoms. The balloon should be approximately 150% of the diameter of normal EG junction. It is placed under endoscopic and fluoroscopic guidance and slowly inflated to 30 to 35 or 40 mm using 7–15 psi of air. The balloon is held inflated for 15–60 seconds effectively tearing the lower esophageal sphincter muscles thereby leaving the area open [31]. A risk of pneumatic dilation (PD) is the possibility of esophageal perforation, carrying a risk of 1.9% when done by experienced clinicians (range 0–16), and if occurs requires emergent surgical intervention. With 62% of patients reporting alleviation of symptoms at 6 months post dilation, this is a good option for poor surgical candidates [32].

It should be noted that a PD post-surgical intervention either lap heller or POEM may be useful tool for treating recurrence of symptoms (see below recurrent symptoms) [33]. Typically, a one-time treatment to 30 mm is sufficient.

#### **3.2 Surgical intervention**

Laparoscopic Heller myotomy (LHM) with fundoplication is the surgical gold standard treatment of achalasia. Since 2007 with the introduction of Per-Oral Endoscopic Myotomy (POEM), has become more widely used. LHM has excellent efficacy, with an improvement in symptom scores and high satisfaction in more than 90% of patients for up to 5 years after the procedure [34]. Due to the high rate of malnutrition in patients with achalasia, it is imperative to evaluate the patient's metabolic status and consider pre-operative enteral nutrition. By providing enteral or parenteral nutrition for a short time prior to surgical intervention, the catabolic status may be reversed, thereby reducing chances of complications.

#### *3.2.1 Laparoscopic or robotic Heller myotomy*

Laparoscopic Heller Myotomy (LHM) includes the division of the circular and longitudinal muscles 2 cm distal and 5–7 cm proximal to the EGJ in achalasia types 1 and 2. For achalasia type 3 a longer, esophageal myotomy is done, and can be tailored to each patient according to the HRM. In order to avoid gastro- esophageal reflux, a fundoplication, either posterior (Toupet) or anterior (Dor) is added to the procedure.

This procedure can be done robotically with enhanced visualization of the circular muscles and better control of their delicate division and several studies and metaanalysis have demonstrated a lower of esophageal perforation rate and reduction of technical complications [35, 36].

Several studies have shown excellent results with LHM, demonstrating improvement of symptoms and patient satisfaction of >90% in the 6 months post-operative period. These results were maintained in most studies for up to 5 years. However, there were some studies demonstrating a decrease with time in symptoms improvement of up to 57% in some reports [32, 34, 37]. Although LHM is done with fundoplication, some patients still suffer from GERD symptoms and have esophagitis on endoscopy.

#### *3.2.2 Per-Oral endoscopic myotomy (POEM)*

Once considered innovative novel procedure, POEM is becoming more and more accepted as a viable alternative to LHM. POEM is performed under general anesthesia using a standard gastroscope inserted into the esophagus per orally.

A small longitudinal incision is made on the esophageal mucosa approximately 10 cm proximal to the EGJ to allow the gastroscope to slide into the submucosal plane. A sub-mucosal dissection is then performed and carried all the way until 2 cm distal to the EGJ. Then the myotomy is performed including the circular muscle layer only, leaving the longitudinal layer intact. The length of the myotomy is tailored to each patient according to the HRM but usually begins from 2 cm distal to the EGJ to 5–7 cm proximal to it. This can be done in an antegrade fashion or retrograde. It can be done on the anterior or the posterior aspects of the esophagus [38]. POEM is especially recommended for patients with type 3 achalasia as a long thoracic myotomy is indicated for these patients [39], which is more difficult to perform in LHM.

POEM has excellent results as demonstrated by a reduction in Eckardt score to <3, achieving clinical success and improvement of dysphagia in 83–98% of the patients [40, 41]. However, GERD is a concern among post-operative achalasia patients. Several studies have compared LHM to POEM regarding post-operative GERD symptoms. Werner et al. [41] randomly assigned 221 patients to undergo either POEM (112 patients) or LHM plus Dor's fundoplication (109 patients). They showed that after POEM 44% of the patients had esophagitis after 24 months vs. 29% in the LHM group. However, high-grade esophagitis (Los Angeles Classification grade C or D) was similar between POEM and LHM at 24 months, suggesting 5% in the POEM group and 6% in the LHM group. They also found that 24 h pH monitoring was similar among patients who underwent POEM and LHM.

In order to reduce reflux symptoms that could potentially lead to GERD, esophagitis, strictures, Barrett's esophagus and even cancer Inoue et al. [42] described adding an endoscopic fundoplication to POEM (F-POEM), but this technique is still novel and needs to be further explored.

#### *3.2.3 Esophagectomy*

End-stage achalasia is characterized by severe dysphagia and a sigmoid, torturous esophagus seen on endoscopy and on barium swallow study. Although patients with end-stage achalasia might suffer from complications such as pulmonary complications, esophagitis and risk for cancer, they do not have many treatment options [43]. Although most studies suggest that POEM, LHM or PD might be the first step in trying to treat patients with end-stage achalasia [44, 45], others suggest that esophagectomy alone is the treatment that these patients should be offered [46].

Reconstruction after esophagectomy can be done preferably using gastric pull-up or colonic interposition. This is a high morbidity procedure that should be reserved to specific patients as it comes with the potential for significant post-operative complications, morbidity and although rare, mortality [47, 48].

#### **4. Special considerations**

#### **4.1 Pediatric population**

In recent years, the incidence of achalasia has risen rather significantly including an increase in pediatric population and may in part be due to the increased sensitivity of testing and increased awareness of the diagnosis. Children who were otherwise misdiagnosed, with anorexia, chronic pulmonary manifestations such as recurrent pneumonia and failure to thrive are now being diagnosed with achalasia. Diagnosis is made as in the adult population, via HRM, EGD and CESS. Special attention should be made to biopsies for evaluation of eosinophilic esophagitis which may mimic achalasia symptoms but requires treatment with oral steroid gel rather than surgical intervention. In general, the treatment options for the pediatric population need to take into consideration growth and long-term risk for reflux. The gold standard of treatment in pediatric patients is laparoscopic Heller myotomy Botilium toxin injection is not recommended as there is no clear dose known for pediatric population [49]. Pneumatic dilation is not a good option for children as first line therapy, due to need for recurrent dilations [50]. In recent years, POEM has gained popularity and is

often preferred over traditional surgery. With results similar to their adult counterparts, POEM is a good option for pediatric population in the hands of experienced surgeons [51, 52].

#### **4.2 Pregnancy**

Maternal nutrition has long been a subject in the medical world and similar to malnutrition from other causes, achalasia is known to cause intrauterine growth restriction, preterm labor and small for gestational age [53]. Additional considerations include the socioeconomic effects of absent mothers due to extended hospitalizations, missed work, and increased healthcare costs. The early diagnosis and treatment of achalasia prior to pregnancy is imperative to ensure healthy outcomes for both mother and fetus. As such ideally, diagnosis and treatment are made prior to pregnancy. However, in cases where the diagnosis is only made during pregnancy the clinician must take into consideration both patients, mother and fetus. Treatment options during pregnancy may include enteral nutrition supplements via feeding tube placement and delaying definitive treatment until delivery with close monitoring of fetus for IUGR and SGA.

Non-surgical treatments such as Botox injection have been reported in the literature [54, 55] however, Botox is labeled as a pregnancy category C, based on studies using significantly lower doses for cosmetic use. As such the use Botox in pregnancy and its safety is not clear [56].

Following delivery, standard surgical intervention can be scheduled either laparoscopic Heller myotomy or POEM.

#### **4.3 Follow up**

Post POEM follow up should include surveillance with Eckardt score, with a score less than three regarded as treatment success, barium swallow study, 24 hours pHmetry, manometry and EGD as needed based on patient symptomatology [57]. While follow up diagnostics and treatments vary from center to center, studies have found that surveillance EGD at 1 year post POEM may help to identify those patients with reflux [58]. The recommendation for yearly EGD examination has also been suggested by Milito et al. [59].

#### **4.4 Salvage therapy for recurrence or failed treatment**

Recurrence of symptoms can occur in some patients. These symptoms need to be investigated to understand if the symptoms are related to outflow obstruction, GERD or dysmotility of the esophagus. A barium swallow study should be performed for an accurate imaging of the esophagus with dynamic evaluation, an upper endoscopy to assess the LES, presence of esophagitis, candidiasis or other pathology and a manometry to evaluate the esophagus and the LES function. If available, EndoFLIP is a reasonable complementary test for evaluation.

After these assessments, if a diagnosis of recurrence or failed treatment is established, a salvage therapy may be offered. The salvage therapy depends on the type of initial treatment. Studies trying to evaluate what kind of salvage therapy is more appropriate, failed to demonstrated superiority of one over the other [60–63]. After failed LHM or POEM either posterior POEM or PD can be offered. If a patient suffers from GERD after POEM a treatment with either medical management or laparoscopic fundoplication are viable options. In patients with candida which can mimic recurrence of symptoms, the recommended treatment is oral antifungals.

#### **5. Summary**

While achalasia was once thought to be a rare disorder, recent years has seen a significant increase in the incidence, perhaps attributable to the increased use of HRM and general recognition of the disease. Contrary to classic textbook descriptions, achalasia patients may present in normal weight or even obese due to the availability of high calorie and protein soft and liquid food. Diagnosis should be made based on three exams, HRM, CESS and EGD. The Eckardt score can aid in understanding the severity of symptoms, but may not adequately reflect actual disease status, and may not be correlated with exam findings. Early treatment is key especially in younger populations, in order to prevent disease progression and complications. Treatment options should be tailored to each patient based on age, nutrition status and comorbidities. The gold standard of treatment is Laparoscopic Heller Myotomy with fundoplication; however, POEM has been accepted as a comparable surgical treatment if performed in experienced centers. Follow-up is mandatory to assist patients with coping with this chronic disease and screen for early or late complications as well as offering salvage treatment when needed.

Achalasia is a chronic and irreversible condition. Early treatment may slow down the progression of the disease. Opening the LES may facilitate passage of food into the stomach and alleviate symptoms, however aperistalsis of the esophagus persists.

#### **Author details**

Gad Marom1,2\*, Ronit Brodie1 and Yoav Mintz1,2

1 Department of General Surgery, Hadassah Hebrew University Medical Center, Jerusalem, Israel

2 Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel

\*Address all correspondence to: gadimarom@gmail.com

© 2023 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Perspective Chapter: Update on Achalasia Treatment DOI: http://dx.doi.org/10.5772/intechopen.108194*

#### **References**

[1] Yadlapati R et al. Esophageal motility disorders on high-resolution manometry: Chicago classification version 4.0(©). Neurogastroenterology and Motility. 2021;**33**(1):e14058

[2] Eckardt VF, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation. Gastroenterology. 1992;**103**(6):1732-1738

[3] Samo S et al. Incidence and prevalence of achalasia in Central Chicago, 2004- 2014, since the widespread use of high-resolution manometry. Clinical Gastroenterology and Hepatology. 2017;**15**(3):366-373

[4] Duffield JA et al. Incidence of achalasia in South Australia based on esophageal manometry findings. Clinical Gastroenterology and Hepatology. 2017;**15**(3):360-365

[5] Annese V, Bassotti G. Non-surgical treatment of esophageal achalasia. World Journal of Gastroenterology. 2006;**12**(36):5763-5766

[6] Howard PJ et al. Five year prospective study of the incidence, clinical features, and diagnosis of achalasia in Edinburgh. Gut. 1992;**33**(8):1011-1015

[7] Goldacre M, Benians R, Goldacre R. Esophageal achalasia diagnosed in people previously diagnosed with an eating disorder: Epidemiological study using record-linkage. The International Journal of Eating Disorders. 2021;**54**(11): 2015-2018

[8] Letranchant A et al. Eating disorder or oesophageal achalasia during adolescence: Diagnostic difficulties. Eating and Weight Disorders. 2020;**25**(1): 87-90

[9] Chino O et al. Clinicopathological studies of esophageal carcinoma in achalasia: Analyses of carcinogenesis using histological and immunohistochemical procedures. Anticancer Research. 2000;**20**(5c):3717-3722

[10] Eckardt AJ, Eckardt VF. Current clinical approach to achalasia. World Journal of Gastroenterology. 2009;**15**(32):3969-3975

[11] Schlottmann F, Patti MG. Esophageal achalasia: Current diagnosis and treatment. Expert Review of Gastroenterology & Hepatology. 2018;**12**(7):711-721

[12] Aviv JE et al. Cost-effectiveness of two types of dysphagia care in head and neck cancer: A preliminary report. Ear, Nose, & Throat Journal. 2001;**80**(8):553- 556 558

[13] Administration HCF. Enrollment Package, Medicare Part B, Area 01, Manhattan. Washington DC: H.C.F. Administration; 2000

[14] El-Takli I, O'Brien P, Paterson WG. Clinical diagnosis of achalasia: How reliable is the barium x-ray? Canadian Journal of Gastroenterology. 2006;**20**(5):335-337

[15] Debi U et al. Barium esophagogram in various esophageal diseases: A pictorial essay. Indian Journal of Radiology and Imaging. 2019;**29**(2):141-154

[16] Pandolfino JE, Gawron AJ. Achalasia: A systematic review. JAMA. 2015;**313**(18):1841-1852

[17] Lafraia FM et al. A pictorial presentation of esophageal high resolution manometry current parameters. Arquivos Brasileiros de Cirurgia Digestiva. 2017;**30**(1):69-71

[18] Pandolfino JE et al. High-resolution manometry in clinical practice: Utilizing pressure topography to classify oesophageal motility abnormalities. Neurogastroenterology and Motility. 2009;**21**(8):796-806

[19] Carlson DA, Pandolfino JE. Highresolution manometry in clinical practice. Gastroenterology & Hepatology (N Y). 2015;**11**(6):374-384

[20] Almogy G, Anthone GJ, Crookes PF. Achalasia in the context of morbid obesity: A rare but important association. Obesity Surgery. 2003;**13**(6):896-900

[21] Savarino E et al. Use of the functional lumen imaging probe in clinical Esophagology. The American Journal of Gastroenterology. 2020;**115**(11):1786-1796

[22] Pannala R et al. Devices for esophageal function testing. VideoGIE. 2022;**7**(1):1-20

[23] Carlson DA et al. Classifying esophageal motility by FLIP Panometry: A study of 722 subjects with manometry. The American Journal of Gastroenterology. 2021;**116**(12):2357-2366

[24] Carlson DA et al. The functional lumen imaging probe detects esophageal contractility not observed with manometry in patients with achalasia. Gastroenterology. 2015;**149**(7):1742-1751

[25] Khashab MA et al. ASGE guideline on the management of achalasia. Gastrointestinal Endoscopy. 2020;**91**(2):213-227.e6

[26] Tolone S et al. Recent trends in endoscopic management of achalasia. World Journal of Gastrointestinal Endoscopy. 2014;**6**(9):407-414

[27] Brisinda G et al. Treatment of gastrointestinal sphincters spasms with botulinum toxin a. Toxins (Basel). 2015;**7**(6):1882-1916

[28] Campos GM et al. Endoscopic and surgical treatments for achalasia: A systematic review and meta-analysis. Annals of Surgery. 2009;**249**(1):45-57

[29] Pasricha PJ et al. Intrasphincteric botulinum toxin for the treatment of achalasia. The New England Journal of Medicine. 1995;**332**(12):774-778

[30] DeMeester SR. Per-oral endoscopic myotomy for achalasia. Journal of Thoracic Disease. 2017;**9**(Suppl. 2): S130-s134

[31] Richter JE. Esophageal motility disorder achalasia. Current Opinion in Otolaryngology & Head and Neck Surgery. 2013;**21**(6):535-542

[32] Vela MF et al. The long-term efficacy of pneumatic dilatation and Heller myotomy for the treatment of achalasia. Clinical Gastroenterology and Hepatology. 2006;**4**(5):580-587

[33] Patti MG, Schlottmann F, Herbella FAM. Esophageal achalasia: Evaluation and treatment of recurrent symptoms. World Journal of Surgery. 2022;**46**(7):1561-1566

[34] Ortiz A et al. Very long-term objective evaluation of heller myotomy plus posterior partial fundoplication in patients with achalasia of the cardia. Annals of Surgery. 2008;**247**(2):258-264

[35] Milone M et al. Robotic versus laparoscopic approach to treat symptomatic achalasia: Systematic *Perspective Chapter: Update on Achalasia Treatment DOI: http://dx.doi.org/10.5772/intechopen.108194*

review with meta-analysis. Diseases of the Esophagus. 2019;**32**(10):1-8

[36] Ali AB et al. Robotic and per-oral endoscopic myotomy have fewer technical complications compared to laparoscopic Heller myotomy. Surgical Endoscopy. 2020;**34**(7):3191-3196

[37] Patti MG, Tamburini A, Pellegrini CA. Cardiomyotomy. Seminars in Laparoscopic Surgery. 1999;**6**(4): 186-193

[38] Marom G et al. The POEM bottom-up technique for achalasia. Surgical Endoscopy. 2021;**35**(11):6117-6122

[39] Vaezi MF et al. ACG clinical guidelines: Diagnosis and Management of Achalasia. The American Journal of Gastroenterology. 2020;**115**(9):1393-1411

[40] Delliturri A et al. A narrative review of update in per oral endoscopic myotomy (POEM) and endoscopic esophageal surgery. Annals of Translational Medicine. 2021;**9**(10):909

[41] Werner YB et al. Endoscopic or surgical Myotomy in patients with idiopathic achalasia. The New England Journal of Medicine. 2019;**381**(23):2219-2229

[42] Inoue H et al. Peroral endoscopic myotomy and fundoplication: A novel NOTES procedure. Endoscopy. 2019;**51**(2):161-164

[43] Eckardt VF, Hoischen T, Bernhard G. Life expectancy, complications, and causes of death in patients with achalasia: Results of a 33-year follow-up investigation. European Journal of Gastroenterology & Hepatology. 2008;**20**(10):956-960

[44] Qiu S et al. Advanced achalasia: Good candidate for peroral endoscopic myotomy. Diseases of the Esophagus. 2021;**34**(3):1-7

[45] Waters J, Martin LW, Molena D. Esophagectomy for end-stage achalasia. World Journal of Surgery. 2022;**46**(7): 1567-1574

[46] Devaney EJ et al. Esophagectomy for achalasia: Patient selection and clinical experience. The Annals of Thoracic Surgery. 2001;**72**(3):854-858

[47] Glatz SM, Richardson JD. Esophagectomy for end stage achalasia. Journal of Gastrointestinal Surgery. 2007;**11**(9):1134-1137

[48] Palanivelu C et al. Laparoscopic transhiatal esophagectomy for 'sigmoid' megaesophagus following failed cardiomyotomy: Experience of 11 patients. Digestive Diseases and Sciences. 2008;**53**(6):1513-1518

[49] Franklin AL, Petrosyan M, Kane TD. Childhood achalasia: A comprehensive review of disease, diagnosis and therapeutic management. World Journal of Gastrointestinal Endoscopy. 2014;**6**(4):105-111

[50] Tashiro J, Petrosyan M, Kane TD. Current management of pediatric achalasia. Translational Gastroenterology and Hepatology. 2021;**6**:33

[51] Goneidy A et al. Surgical Management of Esophageal Achalasia in pediatrics: A systematic review. European Journal of Pediatric Surgery. 2020;**30**(1):13-20

[52] Choné A et al. Multicenter evaluation of clinical efficacy and safety of per-oral endoscopic Myotomy in children. Journal of Pediatric Gastroenterology and Nutrition. 2019;**69**(5):523-527

[53] Khudyak V, Lysy J, Mankuta D. Achalasia in pregnancy. Obstetrical & Gynecological Survey. 2006;**61**(3): 207-211

[54] Hooft N, Schmidt ES, Bremner RM. Achalasia in pregnancy: Botulinum toxin a injection of lower esophageal sphincter. Case Reports Surgery. 2015;**2015**:328970

[55] Wataganara T et al. Treatment of severe achalasia during pregnancy with esophagoscopic injection of botulinum toxin a: A case report. Journal of Perinatology. 2009;**29**(9):637-639

[56] Lowe NJ et al. Dosing, efficacy and safety plus the use of computerized photography for botulinum toxins type a for upper facial lines. Journal of Cosmetic and Laser Therapy. 2010;**12**(2):106-111

[57] Oude Nijhuis RAB et al. European guidelines on achalasia: United European gastroenterology and European Society of Neurogastroenterology and Motility recommendations. United European. Gastroenterologisches Journal. 2020;**8**(1):13-33

[58] Ponds FA et al. Effect of Peroral endoscopic Myotomy vs pneumatic dilation on symptom severity and treatment outcomes among treatmentnaive patients with achalasia: A randomized clinical trial. JAMA. 2019;**322**(2):134-144

[59] Milito P et al. Revisional therapy for recurrent symptoms after Heller Myotomy for achalasia. Journal of Gastrointestinal Surgery. 2022;**26**(1):64-69

[60] Felix VN et al. Achalasia: What to do in the face of failures of Heller myotomy. Annals of the New York Academy of Sciences. 2020;**1481**(1):236-246

[61] Legros L et al. Long-term results of pneumatic dilatation for relapsing symptoms of achalasia after Heller

myotomy. Neurogastroenterology and Motility. 2014;**26**(9):1248-1255

[62] Tang X et al. Feasibility and safety of peroral endoscopic myotomy for achalasia after failed endoscopic interventions. Diseases of the Esophagus. 2017;**30**(3):1-6

[63] van Hoeij FB et al. Management of recurrent symptoms after per-oral endoscopic myotomy in achalasia. Gastrointestinal Endoscopy. 2018;**87**(1):95-101

### **Chapter 5**

### Gastric Volvulus

*Maria Carolina Jimenez, Jose M. Martinez and Robert F. Cubas*

#### **Abstract**

Gastric volvulus is one of the most worrisome complications related to large paraesophageal hernias. It is a medical emergency that requires high index of suspicion and prompt management and operation during the index admission. Here we discuss the pathophysiology and classification of gastric volvulus, clinical and radiological presentation, and treatment options. The approaches described here include endoscopic, laparoscopic, robotic and open. We advocate for the first three approaches and usually save the open approach for certain redo operations or patients with significant adhesions from prior mediastinal or foregut surgeries.

**Keywords:** gastric volvulus, paraesophageal hernia, gastropexy, endoscopy, hernia

#### **1. Introduction**

Gastric volvulus, from the Latin volvere (meaning 'to roll'), is an uncommon clinical entity, occurring in both adult and pediatric populations and defined as the pathological rotation of the stomach beyond 180 degrees. It was first described by Berti in 1866 based on the autopsy of a woman who died of closed loop obstruction and Berg described the first operation in 1897. It is considered a life-threatening emergency due to formation of a closed loop obstruction with strangulation which can progress to gastric ischemia, necrosis and perforation [1–9].

Its true incidence is unknown because besides being a rare condition, many chronic cases are never diagnosed. The clinical presentation is variable and may range from an intermittent non-specific abdominal pain to acute abdomen requiring emergency surgery. The mortality rate for acute volvulus ranges from 30–50%, highlighting the importance of early diagnosis and treatment [2, 3, 5, 10].

#### **2. Pathophysiology**

Primary gastric volvulus refers to the absence of diaphragmatic defects or intra-abdominal abnormality causing the volvulus, accounting for approximately 30% of cases [2, 6, 10]. The stomach is fixed to the abdominal wall by the gastrocolic, gastrohepatic, gastrophrenic, and gastrosplenic ligaments. Together with the gastroesophageal junction and the pylorus, these ligaments provide anchorage and prevent malrotation. When these mechanisms fail, the patient may be at risk of primary gastric volvulus [5, 6].

Secondary gastric volvulus may arise due to disorders of gastric anatomy or gastric function or abnormalities of adjacent organs such as the diaphragm or spleen. Up to 75% are associated with a paraesophageal hernia (PEH), diaphragmatic hernia, wandering spleen, abdominal adhesions, diaphragmatic eventration, phrenic nerve paralysis, or other diaphragmatic or intraabdominal conditions [1–3, 5, 6, 10, 11].

Risk factors include age over 50, gastric ligament laxity, pyloric stenosis, gastroduodenal tumors, diaphragmatic injury and eventration, left lung resection, or pleural adhesions [2].

The fifth decade is the age group with the highest incidence with children less than one year old making up 10–20% of cases. No association with either sex or race has been reported [2, 3, 5, 6, 10].

#### **3. Classification**

Several anatomopathological classifications have been proposed, and the most complete one was proposed by Von Haberer and Singleton, modified by Carter in 1978 describing three types of gastric volvulus according to the axis of rotation: organoaxial, mesenteroaxial and combined [1, 2, 5, 11].

Organoaxial volvulus is a rotation of the stomach around a longitudinal axis passing through the cardia and the pylorus. It is the most common form, occurring in approximately 60% of cases. The most common causes of this subtype are paraesophageal hernias and diaphragmatic eventration. It causes the greater curvature of the stomach to rest superior to the lesser curvature, resulting in an 'inverted' stomach. The distinguishing feature of this variant is that it lies in the horizontal plane when viewed on plain radiography **Figure 1** [1, 2, 5, 11].

The second type of gastric volvulus is mesenteroaxial. It is a less common subtype, comprising approximately 29% of cases. Rotation occurs along a transverse axis, passing through the midpoints of the small and the great curvature. This type is more likely found in the pediatric population and is rarely described in adult individuals. Strangulation is less likely to occur due to spontaneous detorsions with recurrent acute episodes **Figure 2** [1, 2, 5, 11].

The third and rarest subtype of gastric volvulus is when the stomach rotates about both the organo-axial and mesenteroaxial axes resulting in a combined volvulus [1, 2, 5, 11].

**Figure 1.** *Organoaxial volvulus.*

**Figure 2.** *Mesenteroaxial volvulus.*

### **4. Clinical presentation**

The clinical presentation of patients with gastric volvulus depends on the speed of onset, type of volvulus and degree of obstruction [1, 5].

Given that gastric volvulus is a rare condition, it is rarely considered at the top of the differential diagnoses when a patient presents with abdominal, or chest pain associated with nausea and vomiting [5].

The classic symptoms, known as "Borchardt's triad," consist of:


However, these symptoms may not be present in as many as 25% of patients. Hematemesis may also be seen and is thought to occur due to mucosal sloughing as a result of ischemia or a mucosal tear due to retching [1, 2, 4–6, 10].

On physical exam there are a variety of possible characteristic findings such as gastric sounds audible in the chest, abdominal distention and dullness to percussion. Once the disease has progressed to peritonitis, abdominal wall rigidity and rebound tenderness may also be found [6].

In contrast, chronic or intermittent gastric volvulus may present with nonspecific symptoms which may go unnoticed. These include mild upper abdominal pain, chest pain, dysphagia, bloating, early satiety, heartburn, and occasionally symptoms of pancreatitis. Such features may be protracted and are often misattributed to other upper gastrointestinal disorders such as peptic ulcer disease [4–6, 11].

Laboratory findings include [6]:


Reported complications of gastric volvulus include ulceration, perforation, hemorrhage, pancreatic necrosis, and omental avulsion. On rare occasions, rotation of the stomach may even cause disruption of the splenic vessels resulting in hemorrhage and splenic rupture [5, 12].

#### **5. Diagnosis**

Diagnosis based on physical examination findings and symptoms alone is difficult, therefore a high index of suspicion is required, as it is a condition with a high mortality rate in acute cases [3, 4].

The gold standard is a barium swallow, which has a very high sensitivity and specificity for diagnosing gastric volvulus [10]. However, the increased availability of computed tomography has displaced barium swallow to a second place in the diagnostic armamentarium.

The diagnosis is frequently made by an abdominal radiograph and an upper gastrointestinal series, although the results may be normal during the asymptomatic period [2, 4, 11, 13].

In a typical presentation of gastric volvulus, an erect abdominal radiograph may demonstrate double air-fluid levels in the antrum and fundus, a single air bubble with no additional luminal gas or a distended fluid-filled stomach. Chest radiographs also can demonstrate a retrocardiac, air-filled mass. These features may be absent in cases of intermittent obstruction and therefore further imaging is often necessary to confirm diagnosis [5].

Upper gastrointestinal series can provide information on the rotation of the stomach and passage of ingested oral contrast material into the duodenum [4]. However, it is usually not performed routinely in mild cases due to the vagueness of symptoms and low suspicion of gastric volvulus.

Most patients, particularly those with acute abdominal pain, undergo CT scan. CT of the abdomen or chest typically demonstrates a dilated stomach, often abnormally positioned in the chest. A swirl sign may also be evident. CT also defines other anatomic abnormalities, such as diaphragmatic defects, and excludes other abdominal pathology as the source of symptoms [6]. The most frequent and sensitive CT findings of volvulus are stenosis at the hernia neck and transition point at the pylorus [4]. CT findings of ischemia including gastric wall edema, lack of contrast enhancement of the gastric wall, perigastric fluid, pneumatosis of the gastric wall, pleural effusion, and pneumoperitoneum could also be seen [2, 4, 11, 13].

Gastric volvulus can sometimes be initially diagnosed through upper endoscopy where tortuous appearance of the stomach and difficulty or inability for the endoscope to reach the pylorus may be found [2, 11]. It is also typical to see the pylorus adjacent to the esophagogastric junction on retroflexion.

#### **6. Treatment**

The treatment of acute gastric volvulus is medical, endoscopic and/or surgical.

#### **6.1 Initial management**

Initial treatment involves stabilization of the patient, balanced crystalloid resuscitation, correction of electrolyte abnormalities and urgent upper endoscopy with

#### *Gastric Volvulus DOI: http://dx.doi.org/10.5772/intechopen.107382*

placement of NG tube for decompression, which will assist with reduction of the gastric volvulus and evaluation of the mucosa [6, 11, 14]. Blood-based resuscitation should be considered for patients with chronic anemia from this condition or presenting with acute upper gastrointestinal bleed. In the presence of suspected perforation or ischemia, broad spectrum antibiotics should be administered early [14].

Some authors consider that chronic gastric volvulus can be managed conservatively with prokinetic agents and antisecretory therapy [2].

Immediate surgical consultation should be obtained, particularly in the case of an acute volvulus where the risk of vascular compromise and death are high [5].

Urgent surgery is mandated in the following instances [6]:


#### **6.2 Endoscopy**

An upper endoscopy may be initially attempted to manually reduce the hernia in stable patients, particularly when unable to pass an NG tube. If successful, this will allow further assessment of the extent of damage as a result of the volvulus and will allow time to resuscitate the patient prior to surgery. Many times decompression of the stomach with a nasogastric tube will result in reduction of the volvulus [3, 14].

The airway should be secured prior to endoscopic intervention to avoid aspiration during the procedure. Once the endoscope is inserted, esophageal and gastric contents can be suctioned and NG or orogastric tube can be guided under endoscopic visualization into the stomach for decompression [14].

Endoscopic derotation with endoscopic gastropexy via percutaneous endoscopic gastrostomy (PEG) tube has been described as conservative first-line management in patients with isolated gastric volvulus and high surgical risk [5, 10, 11, 14]. The rationale for placement of a PEG tube is that it helps prevent recurrent volvulus by fixing the stomach to the abdominal wall in its normal orientation. In the rare case that PEG is used as the sole therapy, a second PEG tube will be needed to prevent future rotation. In such cases, one PEG is placed in the usual position in the gastric body while the other is placed more distal in the stomach [14].

However, the risk of gastric perforation with endoscopic therapy as main treatment is significant and patients should therefore be considered carefully for conservative treatment [2, 10]. There is also a risk of recurrence due to inadequate fixation, persistence of predisposing factors such as hernias and adhesions from previous surgeries, and the potential that the fixation point will act as an axis for further rotations **Figure 3** [11].

#### **6.3 Surgery**

Surgical management is aimed at ensuring gastric viability [15]. The principles of treatment of gastric volvulus include decompression of the stomach with reduction

**Figure 3.** *Endoscopic view of devolvulized stomach.*

of the volvulus to restore the stomach to a more normal anatomic position, followed by gastropexy and correction of the intra-abdominal factors predisposing to volvulus and thus preventing future stomach rotation. Gastric resection is necessary if fullthickness necrosis is present [5–7, 11, 16].

Traditionally, open surgery has been the preferred approach, allowing broad access to the abdominal cavity [1, 2, 6, 17]. Patients demonstrating signs of metabolic derangement or necrosis might benefit from open transabdominal damage-control laparotomy for reduction and relief of ischemia or resection of necrotic tissue and planned second look for definitive repair [14].

Due to the paucity of literature comparing laparoscopic and open surgery it is difficult to compare their respective outcomes. However, laparoscopic surgery has largely demonstrated its usefulness in elective surgery for chronic gastric volvulus and increasingly in cases of acute volvulus [7, 11, 12, 16–18]. Koger and Stone in 1993 described the first successful laparoscopic treatment of acute gastric volvulus by performing reduction and gastropexy [11]. Over time, good results with laparoscopic approaches have been described for gastric volvulus in stable patients, but its use in cases of perforation remains controversial [19].

Channer et al. have reported successful reduction of organoaxial gastric volvulus using standard laparoscopic foregut port placement in a small series [12]. Yates et al. have modified the port configuration to allow for sutured gastropexy of the distal gastric body and antrum [18].

In high-operative risk patients, management of gastric volvulus with laparoscopic paraesophageal hernia (PEH) repair can result in significant perioperative morbidity and mortality, and in the presence of severe thoracoabdominal musculoskeletal deformities the repair may turn into a technically challenging one [18].

#### *Gastric Volvulus DOI: http://dx.doi.org/10.5772/intechopen.107382*

Laparoscopic gastropexy requires much shorter operative time compared with laparoscopic PEH repair, possibly resulting in less perioperative morbidity and mortality for patients [8, 18]. Many technical variations of gastropexy have been reported in the literature and include [1, 5, 12, 17]:


In the past, more definitive procedures that were performed included gastropexy with colonic displacement (Tanner's procedure), fundoantral gastrostomy (Oozler's operation), gastrojejunostomy and gastrocolic disconnection. However, these are rarely used nowadays.

Laparoscopic approach with excision of the hernia sac, re-approximation of the diaphragmatic crura, anti-reflux procedure and gastropexy, when indicated, has been tolerated, securing the stomach intra-abdominally and preventing migration of the stomach to an intrathoracic position. Complete excision of the hernia sac can also help to eliminate one of the causes of recurrence [12].

Due to the robust collateral circulation of the stomach, gastric necrosis is unusual, but the stomach should always be thoroughly examined for evidence of ischemia after reduction of the gastric volvulus. When it occurs, gastric necrosis is usually located at the fundus, which is a location amenable to partial resection with a linear stapler [6]. It is crucial to perform an intraoperative upper endoscopy to be able to evaluate the condition of the mucosa and the repair performed.

In the rare case of full thickness necrosis of the stomach with absence of perfusion after reduction of volvulus, a total gastrectomy may be required, leaving the esophagus and duodenum in discontinuity, placing a feeding jejunostomy tube and creating a diverting esophagostomy at the initial surgery for damage control. Once the patient is more stable, they can be taken back for definitive repair with esophagojejunal reconstruction or colonic interposition [6].

While there has been debate in the literature concerning the indications of an additional anti-reflux procedure when repairing a diaphragmatic defect, Fundoplication, especially if the wrap is sutured to the crura, has shown to decrease recurrence in patients with hiatal hernia [2, 10]. An anti-reflux procedure should be performed routinely in patients with PEH [12, 20].

More recently robotic-assisted surgery has been gaining popularity in General Surgery, and there are increasing reports demonstrating that robotic approach to the management of GERD and PEH repair is safe and effective with low complication rates [21, 22]. To date, there are very few case reports of robotic repair

**Figure 4.** *Robotic repair of paraesophageal hernia presenting with a gastric volvulus.*

of paraesophageal hernia with finding of gastric volvulus in children and adults **Figure 4** [21, 23–25].

#### **6.4 Postoperative considerations**

Postoperatively, patients should be admitted to an appropriate level of care based on clinical condition. Antiemetics should be scheduled to help prevent retching and vomiting. Currently there are no guidelines on postoperative use of NG tube or timing of enteral feeding.

Some authors tend to leave an NGT in situ, while others do not routinely leave one. Some surgeons perform a barium swallow within the first 2 postoperative days to interrogate the hernia repair, assess gastric emptying and evaluate for the presence of an esophageal leak [7, 14, 15]. We do not routinely follow this approach at our institution, unless there has been transmural gastric violation requiring repair or partial gastrectomy.

There is variety in practice with respect to feeding after surgery. We sequentially advance diet (full liquids, puree or blended diet and soft diet) for a period of 6 weeks to allow the edema at the site of the operation to resolve. Other surgeons discharge patients on a soft diet for 2 to 3 weeks after emergency repair of gastric volvulus [7, 15].

When placing a gastrostomy tube, Yates et al. typically leave it connected to a gravity bag for 12 to 24 hours postoperatively. Thereafter, the tube is selectively opened for symptoms of gastric distention (nausea, vomiting, and bloating). None of the patients in their series needed to use the gastrostomy tube for gastric decompression beyond 24 hours postoperatively [18].

#### **7. Conclusion**

The diagnosis of gastric volvulus requires familiarity with the presenting signs and symptoms. Early diagnosis is critical to timely intervention. Surgeon experience and patient physiology will drive the surgical approach.

#### **Acknowledgements**

This work was supported by the Department of Surgery at the University of Miami, Miller School of Medicine.

#### **Conflict of interest**

The authors declare no conflict of interest.

#### **Author details**

Maria Carolina Jimenez, Jose M. Martinez and Robert F. Cubas\* Department of Surgery, Miller School of Medicine, Jackson Health System, University of Miami, Miami, FL, USA

\*Address all correspondence to: rcubas@miami.edu

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **References**

[1] Morelli U, Bravetti M, Ronca P, Cirocchi R, De Sol A, Spizzirri A, et al. Laparoscopic anterior gastropexy for chronic recurrent gastric volvulus: A case report. Journal of Medical Case Reports. 2008;**2**:244

[2] El Mouhafid FYM, Bounaim A, Moujahid M. Gastric volvulus: A challenge to diagnosis and management. World Journal of Surgery and Surgical Research. 2020;**3**:1236

[3] Imperatore K, Olivieri B, Vincentelli C. Acute gastric volvulus: A deadly but commonly forgotten complication of hiatal hernia. Autopsy & Case Reports. 2016;**6**(1):21-26

[4] Mazaheri P, Ballard DH, Neal KA, Raptis DA, Shetty AS, Raptis CA, et al. CT of gastric volvulus: Interobserver reliability, Radiologists' accuracy, and imaging findings. American Journal of Roentgenology. 2019;**212**(1):103-108

[5] Rashid F, Thangarajah T, Mulvey D, Larvin M, Iftikhar SY. A review article on gastric volvulus: A challenge to diagnosis and management. International Journal of Surgery. 2010;**8**(1):18-24

[6] Pandey S, Paudel M, Parajuli A, Ghimire R, Neupane A. Mesenteroaxial Gastric Volvulus: A Case Report. JNMA; Journal of the Nepal Medical Association. 2021;**59**(237):506-509

[7] Katkhouda N, Mavor E, Achanta K, Friedlander MH, Grant SW, Essani R, et al. Laparoscopic repair of chronic intrathoracic gastric volvulus. Surgery. 2000;**128**(5):784-790

[8] Naim HJ, Smith R, Gorecki PJ. Emergent laparoscopic reduction of acute gastric volvulus with anterior

gastropexy. Surgical Laparoscopy, Endoscopy & Percutaneous Techniques. 2003;**13**(6):389-391

[9] Mistry V, Gamble EL, Chang J. Adult mesentero-axial gastric volvulus: Case report. Journal of Medical Imaging and Radiation Oncology. 2020;**64**(6):817-820

[10] Chau B, Dufel S. Gastric volvulus. Emergency Medicine Journal. 2007;**24**(6):446-447

[11] Kaoukabi AE, Menfaa M, Hasbi S, Sakit F, Choho A. Acute gastric volvulus on hiatal hernia. Case Rep Surg. 2020;**2020**:4141729

[12] Channer LT, Squires GT, Price PD. Laparoscopic repair of gastric volvulus. JSLS. 2000;**4**:225-230

[13] Light D, Links D, Griffin M. The threatened stomach: Management of the acute gastric volvulus. Surgical Endoscopy. 2016;**30**(5):1847-1852

[14] Coleman C, Musgrove K, Bardes J, Dhamija A, Buenaventura P, Abbas G, et al. Incarcerated paraesophageal hernia and gastric volvulus: Management options for the acute care surgeon, an eastern Association for the Surgery of trauma master class video presentation. Journal of Trauma and Acute Care Surgery. 2020;**88**(6):e146-e1e8

[15] Albloushi D, Quttaineh D, Alsafran S, Alyatama K, Alfawaz AA, Alsulaimy M, et al. Acute gastric volvulus: A rare case report and literature review. Ann Med Surg (Lond). 2021;**70**:102857

[16] Inaba K, Sakurai Y, Isogaki J, Komori Y, Uyama I. Laparoscopic repair of hiatal hernia with mesenterioaxial

*Gastric Volvulus DOI: http://dx.doi.org/10.5772/intechopen.107382*

volvulus of the stomach. World Journal of Gastroenterology. 2011;**17**(15): 2054-2057

[17] Teague WJ, Ackroyd R, Watson DI, Devitt PG. Changing patterns in the management of gastric volvulus over 14 years. The British Journal of Surgery. 2000;**87**(3):358-361

[18] Yates RB, Hinojosa MW, Wright AS, Pellegrini CA, Oelschlager BK. Laparoscopic gastropexy relieves symptoms of obstructed gastric volvulus in highoperative risk patients. American Journal of Surgery. 2015;**209**(5):875-880. discussion 80

[19] Martinez-Perez A, Garrigos-Ortega G, Gomez-Abril SA, Torres-Sanchez T, Uceda-Navarro D. Perforated gastric volvulus due to incarcerated paraesophageal hernia. Revista de Gastroenterología de México. 2014;**79**(3):204-206

[20] Pearson FG, Cooper JD, Ilves R, Todd TR, Jamieson WR. Massive hiatal hernia with incarceration: A report of 53 cases. The Annals of Thoracic Surgery. 1983;**35**(1):45-51

[21] Tartaglia N, Pavone G, Di Lascia A, Vovola F, Maddalena F, Fersini A, et al. Robotic voluminous paraesophageal hernia repair: A case report and review of the literature. Journal of Medical Case Reports. 2020;**14**(1):25

[22] Konstantinidis K, Konstantinidis M, Hirides SHP. Robotic hiatal hernia repair. In: Küçük S, editor. Surgical Robotics. London: IntechOpen; 2017. DOI: 10.5772/ intechopen.71164

[23] Deugarte DA, Hirschl RB, Geiger JD. Robotic repair of congenital Paraesophageal hiatal hernia. Journal of Laparoendoscopic & Advanced Surgical Techniques. 2009;**19**(s1):s187-s1s9

[24] Aslam S, Alani M, Ansari Z, Moussa J, Srinivasan I, Chuang K-Y. S3156 gastric volvulus: An underrated complication of hiatal hernia. Official journal of the American College of Gastroenterology ACG. 2021;**116**:S1301

[25] Jindal S, Hukkeri VS, Qaleem M, Tandon V, Govil D. Robotic repair of a parahiatal hernia with gastric volvulus. Apollo Medicine. 2016;**13**(4):235-238

Section 3
