Gastric outlet obstruction: Difference between revisions

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===Other differentials===
Gastric outlet obstruction should also be differentiated from other diseases that cause chronic [[nausea and vomiting]]. The differentials include the following:<ref name="pmid25667023">{{cite journal |vauthors=Parkman HP |title=Idiopathic gastroparesis |journal=Gastroenterol. Clin. North Am. |volume=44 |issue=1 |pages=59–68 |year=2015 |pmid=25667023 |pmc=4324534 |doi=10.1016/j.gtc.2014.11.015 |url=}}</ref><ref name="pmid17015559">{{cite journal |vauthors=Werlin SL, Fish DL |title=The spectrum of valproic acid-associated pancreatitis |journal=Pediatrics |volume=118 |issue=4 |pages=1660–3 |year=2006 |pmid=17015559 |doi=10.1542/peds.2006-1182 |url=}}</ref><ref name="pmid16369243">{{cite journal |vauthors=Noddin L, Callahan M, Lacy BE |title=Irritable bowel syndrome and functional dyspepsia: different diseases or a single disorder with different manifestations? |journal=MedGenMed |volume=7 |issue=3 |pages=17 |year=2005 |pmid=16369243 |pmc=1681633 |doi= |url=}}</ref><ref name="pmid23226859">{{cite journal |vauthors=Gupta R, Kalla M, Gupta JB |title=Adult rumination syndrome: Differentiation from psychogenic intractable vomiting |journal=Indian J Psychiatry |volume=54 |issue=3 |pages=283–5 |year=2012 |pmid=23226859 |pmc=3512372 |doi=10.4103/0019-5545.102434 |url=}}</ref><ref name="urlBody weight in bulimia nervosa | SpringerLink">{{cite web |url=https://link.springer.com/article/10.1007/BF03339730 |title=Body weight in bulimia nervosa &#124; SpringerLink |format= |work= |accessdate=}}</ref><ref name="pmid25904280">{{cite journal |vauthors=Sağlam F, Sivrikoz E, Alemdar A, Kamalı S, Arslan U, Güven H |title=Bouveret syndrome: A fatal diagnostic dilemma of gastric outlet obstruction |journal=Ulus Travma Acil Cerrahi Derg |volume=21 |issue=2 |pages=157–9 |year=2015 |pmid=25904280 |doi= |url=}}</ref><ref name="pmid21475419">{{cite journal |vauthors=Talley NJ |title=Rumination syndrome |journal=Gastroenterol Hepatol (N Y) |volume=7 |issue=2 |pages=117–8 |year=2011 |pmid=21475419 |pmc=3061016 |doi= |url=}}</ref><ref name="pmid15067630">{{cite journal |vauthors=Tutuian R, Castell DO |title=Rumination documented by using combined multichannel intraluminal impedance and manometry |journal=Clin. Gastroenterol. Hepatol. |volume=2 |issue=4 |pages=340–3 |year=2004 |pmid=15067630 |doi= |url=}}</ref><ref name="pmid24921208">{{cite journal |vauthors=Kessing BF, Smout AJ, Bredenoord AJ |title=Current diagnosis and management of the rumination syndrome |journal=J. Clin. Gastroenterol. |volume=48 |issue=6 |pages=478–83 |year=2014 |pmid=24921208 |doi=10.1097/MCG.0000000000000142 |url=}}</ref><ref name="pmid19232280">{{cite journal |vauthors=Parkman HP |title=Assessment of gastric emptying and small-bowel motility: scintigraphy, breath tests, manometry, and SmartPill |journal=Gastrointest. Endosc. Clin. N. Am. |volume=19 |issue=1 |pages=49–55, vi |year=2009 |pmid=19232280 |doi=10.1016/j.giec.2008.12.003 |url=}}</ref><ref name="pmid19115465">{{cite journal |vauthors=Waseem S, Moshiree B, Draganov PV |title=Gastroparesis: current diagnostic challenges and management considerations |journal=World J. Gastroenterol. |volume=15 |issue=1 |pages=25–37 |year=2009 |pmid=19115465 |pmc=2653292 |doi= |url=}}</ref><ref name="pmid3699409">{{cite journal |vauthors=Mearin F, Camilleri M, Malagelada JR |title=Pyloric dysfunction in diabetics with recurrent nausea and vomiting |journal=Gastroenterology |volume=90 |issue=6 |pages=1919–25 |year=1986 |pmid=3699409 |doi= |url=}}</ref><ref name="pmid18028513">{{cite journal |vauthors=Abell TL, Camilleri M, Donohoe K, Hasler WL, Lin HC, Maurer AH, McCallum RW, Nowak T, Nusynowitz ML, Parkman HP, Shreve P, Szarka LA, Snape WJ, Ziessman HA |title=Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine |journal=Am. J. Gastroenterol. |volume=103 |issue=3 |pages=753–63 |year=2008 |pmid=18028513 |doi=10.1111/j.1572-0241.2007.01636.x |url=}}</ref><ref name="pmid12014357">{{cite journal |vauthors=Jiang CF, Ng KW, Tan SW, Wu CS, Chen HC, Liang CT, Chen YH |title=Serum level of amylase and lipase in various stages of chronic renal insufficiency |journal=Zhonghua Yi Xue Za Zhi (Taipei) |volume=65 |issue=2 |pages=49–54 |year=2002 |pmid=12014357 |doi= |url=}}</ref><ref name="SzmuklerYoung1990">{{cite journal|last1=Szmukler|first1=G. I.|last2=Young|first2=G. P.|last3=Lichtenstein|first3=M.|last4=Andrews|first4=J. T.|title=A serial study of gastric emptying in anorexia nervosa and bulimia|journal=Australian and New Zealand Journal of Medicine|volume=20|issue=3|year=1990|pages=220–225|issn=00048291|doi=10.1111/j.1445-5994.1990.tb01023.x}}</ref><ref name="pmid12827003">{{cite journal |vauthors=Diamanti A, Bracci F, Gambarara M, Ciofetta GC, Sabbi T, Ponticelli A, Montecchi F, Marinucci S, Bianco G, Castro M |title=Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders |journal=J. Pediatr. Gastroenterol. Nutr. |volume=37 |issue=1 |pages=35–41 |year=2003 |pmid=12827003 |doi= |url=}}</ref><ref name="pmid981449">{{cite journal |vauthors=Ferholt J, Provence S |title=Diagnosis and treatment of an infant with psychophysiological vomiting |journal=Psychoanal Study Child |volume=31 |issue= |pages=439–59 |year=1976 |pmid=981449 |doi= |url=}}</ref><ref name="pmid17914944">{{cite journal |vauthors=Lee H, Rhee PL, Park EH, Kim JH, Son HJ, Kim JJ, Rhee JC |title=Clinical outcome of rumination syndrome in adults without psychiatric illness: a prospective study |journal=J. Gastroenterol. Hepatol. |volume=22 |issue=11 |pages=1741–7 |year=2007 |pmid=17914944 |doi=10.1111/j.1440-1746.2006.04617.x |url=}}</ref><ref name="pmid9635600">{{cite journal |vauthors=Koskenpato J, Kairemo K, Korppi-Tommola T, Färkkilä M |title=Role of gastric emptying in functional dyspepsia: a scintigraphic study of 94 subjects |journal=Dig. Dis. Sci. |volume=43 |issue=6 |pages=1154–8 |year=1998 |pmid=9635600 |doi= |url=}}</ref><ref name="pmid7658213">{{cite journal |vauthors=Urbain JL, Vekemans MC, Parkman H, Van Cauteren J, Mayeur SM, Van den Maegdenbergh V, Charkes ND, Fisher RS, Malmud LS, De Roo M |title=Dynamic antral scintigraphy to characterize gastric antral motility in functional dyspepsia |journal=J. Nucl. Med. |volume=36 |issue=9 |pages=1579–86 |year=1995 |pmid=7658213 |doi= |url=}}</ref><ref name="pmid20723071">{{cite journal |vauthors=Hejazi RA, Lavenbarg TH, McCallum RW |title=Spectrum of gastric emptying patterns in adult patients with cyclic vomiting syndrome |journal=Neurogastroenterol. Motil. |volume=22 |issue=12 |pages=1298–302, e338 |year=2010 |pmid=20723071 |doi=10.1111/j.1365-2982.2010.01584.x |url=}}</ref><ref name="urlGastric outlet obstruction - an overview | ScienceDirect Topics">{{cite web |url=https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/gastric-outlet-obstruction |title=Gastric outlet obstruction - an overview &#124; ScienceDirect Topics |format= |work= |accessdate=}}</ref><ref name="pmid6370777">{{cite journal |vauthors=Minami H, McCallum RW |title=The physiology and pathophysiology of gastric emptying in humans |journal=Gastroenterology |volume=86 |issue=6 |pages=1592–610 |year=1984 |pmid=6370777 |doi= |url=}}</ref><ref name="pmid2431640">{{cite journal |vauthors=Humphries LL, Adams LJ, Eckfeldt JH, Levitt MD, McClain CJ |title=Hyperamylasemia in patients with eating disorders |journal=Ann. Intern. Med. |volume=106 |issue=1 |pages=50–2 |year=1987 |pmid=2431640 |doi= |url=}}</ref><ref name="pmid2480214">{{cite journal |vauthors=Hempen I, Lehnert P, Fichter M, Teufel J |title=[Hyperamylasemia in anorexia nervosa and bulimia nervosa. Indication of a pancreatic disease?] |language=German |journal=Dtsch. Med. Wochenschr. |volume=114 |issue=49 |pages=1913–6 |year=1989 |pmid=2480214 |doi=10.1055/s-2008-1066848 |url=}}</ref><ref name="pmid19204432">{{cite journal |vauthors=Okada R, Okada A, Okada T, Okada T, Hamajima N |title=Elevated serum lipase levels in patients with dyspepsia of unknown cause in general practice |journal=Med Princ Pract |volume=18 |issue=2 |pages=130–6 |year=2009 |pmid=19204432 |doi=10.1159/000189811 |url=}}</ref><ref name="pmid23198276">{{cite journal |vauthors=Sansone RA, Sansone LA |title=Hoarseness: a sign of self-induced vomiting? |journal=Innov Clin Neurosci |volume=9 |issue=10 |pages=37–41 |year=2012 |pmid=23198276 |pmc=3508961 |doi= |url=}}</ref><ref name="pmid15972301">{{cite journal |vauthors=Tack J, Caenepeel P, Arts J, Lee KJ, Sifrim D, Janssens J |title=Prevalence of acid reflux in functional dyspepsia and its association with symptom profile |journal=Gut |volume=54 |issue=10 |pages=1370–6 |year=2005 |pmid=15972301 |pmc=1774686 |doi=10.1136/gut.2004.053355 |url=}}</ref><ref name="urlgut.bmj.com">{{cite web |url=http://gut.bmj.com/content/gutjnl/early/2005/06/21/gut.2004.053355.full.pdf |title=gut.bmj.com |format= |work= |accessdate=}}</ref><ref name="pmid10490048">{{cite journal |vauthors=Boles RG, Williams JC |title=Mitochondrial disease and cyclic vomiting syndrome |journal=Dig. Dis. Sci. |volume=44 |issue=8 Suppl |pages=103S–107S |year=1999 |pmid=10490048 |doi= |url=}}</ref><ref name="pmid24112485">{{cite journal |vauthors=Ranasinghe WK, Smith M |title=Gastric outlet obstruction with an elevated serum pancreatic lipase secondary to an infraumbilical hernia |journal=Ann R Coll Surg Engl |volume=95 |issue=7 |pages=122–4 |year=2013 |pmid=24112485 |doi=10.1308/003588413X13629960047795 |url=}}</ref><ref name="UiShibusawa2015">{{cite journal|last1=Ui|first1=Takashi|last2=Shibusawa|first2=Hiroyuki|last3=Tsukui|first3=Hidenori|last4=Sakuma|first4=Kazuya|last5=Takahashi|first5=Shuhei|last6=Lefor|first6=Alan K.|last7=Hosoya|first7=Yoshinori|last8=Sata|first8=Naohiro|last9=Yasuda|first9=Yoshikazu|title=Pretreatment of gastric outlet obstruction with pancrelipase: Report of a case|journal=International Journal of Surgery Case Reports|volume=12|year=2015|pages=87–89|issn=22102612|doi=10.1016/j.ijscr.2015.05.023}}</ref>
{| class="wikitable"
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disorder
! colspan="12" align="center" style="background:#4479BA; color: #FFFFFF;" + |Clinical features
! colspan="5" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory findings
|-
|
|'''Chronic nausea'''
|'''Vomiting'''
|'''Diarrhea'''
|'''Retching'''
|'''Lethargy'''
|'''Social withdrawal'''
|'''Photophobia'''
|'''Epigastric pain/burning'''
|'''Lanugo hair'''
|'''Hypogonadism'''
|'''Russel's sign'''
|'''Body mass index (normal range: 18.5 to 24.9)'''
|'''Complete blood count (CBC)'''
|'''Electrolyte imabalance'''
|'''Lipase and amylase levels'''
|'''Gastric scintigraphy'''
|'''Ambulatory esophageal pH and impedance testing'''
|-
|'''Gastroparesis'''
|✔
|✔ (within 1 hour of eating)
|<nowiki>-</nowiki>
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|↓
|
* [[Anemia]]
|✔
|
* Normal (maybe elevated if chronic renal failure is the cause of gastroparesis- usually less than threefold)
|
* '''Periodic measurement of radiolabeled solid meal:'''           
** Grade 1 (mild), 11%-20% retention at 4 h
** Grade 2 (moderate), 21%-35% retention at 4 h
** Grade 3 (severe), 36%-50% retention at 4 h
** Grade 4 (very severe), > 50% retention at 4 h
|
* '''Impedance testing (antroduodenal manometery):''' Loss of normal fasting migratory motor complexes (MMCs) and reduced postprandial [[Antrum|antral]] contractions and, in some cases pylorospasm
|-
|'''[[Anorexia nervosa]]'''
|✔
|✔
|✔
|<nowiki>-</nowiki>
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|✔
|✔
|<nowiki>-</nowiki>
|↓
|
* [[Leukocytosis]], [[anemia]]
|✔
|
*Increased
|
* [[Delayed gastric emptying|Gastric emptying may be delayed]] but may become normal as feeding recommences (short lived)
|
* '''Esophageal pH:''' May be decreased if patient develops [[gastroesophageal reflux disease]]
|-
|'''[[Bulimia nervosa]]'''
|✔
|✔
|✔
|✔
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|✔
|✔
|Normal
|
* [[Leukocytosis]], [[anemia]]
|✔
|
* Increased
|
* [[Delayed gastric emptying|Gastric emptying delayed]] for a longer duration as compared to [[anorexia nervosa]]
|
* '''Esophageal pH:''' May be decreased if patient develops [[gastroesophageal reflux disease]]
|-
|'''[[Rumination syndrome]]'''
|✔
|✔ ([[Regurgitation]] more common- within minutes of meal intake)
|✔
|<nowiki>-</nowiki>
|✔
|✔
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|↓
|
* Normal
|✔
|
* Normal
|
* [[Delayed gastric emptying]]
|
* '''Esophageal pH:''' Fall in [[esophageal]] pH immediately after reguritation (occurs while patient is awake and erect; this is in contrast to [[Gastroesophageal reflux disease|GERD]], where [[Gastroesophageal reflux disease|reflux]] occurs diurnally and [[supine]] position)
* '''Impedance testing:'''Increased intra-[[abdominal]] pressure leading to [[regurgitation]] of [[gastric]] contents (Tall R waves)
|-
|'''[[Functional dyspepsia]]'''
|✔
|✔
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|Normal
|
* Normal
|✔
|
* Increased (especially [[lipase]])
|
* [[Delayed gastric emptying]]
|
* '''Esophageal pH:''' May be decreased if patient develops [[Reflux esophagitis|reflux]]
|-
|'''[[Cyclic vomiting syndrome]]'''
|✔
|✔
|<nowiki>-</nowiki>
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|↓
|
* [[Leukocytosis]], [[anemia]]
|✔
|
* Increased (alongwith increased [[lactic acid]] - in cases of concomitant [[mitochondrial disease]])
|
* Rapid or normal
|
* '''Esophageal pH:''' Decreased
|-
|'''[[Pancreatitis]]'''
|✔
|✔
|✔
|✔
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|Normal
|
* [[Leukocytosis]]
|✔
|
* Increased
|
* Not indicated
|
* '''Esophageal pH:''' Normal
|-
|'''[[Gastric outlet obstruction]]'''
|✔
|✔ (within 1 hour of eating)
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|✔
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|↓
|
* [[Leukocytosis]]
|✔
|
* Increased (in cases of [[pancreatic]] disease)
|
* [[Delayed gastric emptying]]
|
* '''Esophageal pH:''' Increased
* '''Esophageal manometery:'''    High manoraetric score
|}


==Epidemiology and Demographics==
==Epidemiology and Demographics==

Revision as of 17:25, 9 February 2018

Gastric outlet obstruction Microchapters

Home

Overview

Classification

Pathophysiology

Causes

Differentiating Gastric outlet obstruction from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Diagnosis

Treatment

Medical Therapy
Surgery

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Synonyms and keywords: GOO

Overview

Gastric outlet obstruction occurs due to pathologies that cause intrinsic or extrinsic obstruction of the pylorus and antrum. Infiltration, scar formation or inflammation of the gastric outlet leads to intrinsic obstruction, while malignancy of neighboring structures such as the pancreas, gallbladder, liver and duodenum may lead to extrinsic obstruction of the gastric outlet. Common causes of GOO include PUD, gastric polyps, caustic ingestion, duodenal stricture, systemic amyloidosis of the gastrointestinal tract, eosinophillic gastroenteritis and obstruction by gallstones. Five percent of all cases of peptic ulcer disease (which is the most common benign cause of GOO) worldwide, develop gastric outlet obstruction. GOO presents as nausea, vomiting, dehydration, electrolyte abnormalities, weight loss, malnutrition, fullness of epigastrium, early satiety and bloating. Laboratory studies of patients may show hypokalemic hypochloremic metabolic alkalosis which is a characteristic feature due to vomiting. In case of of GOO due to suspected PUD, tests for H pylori should also be performed in patients. Barium upper GI studies help in the determination of site of obstruction, visualization of the gastric silhouette, presence of gastric dilation, pylorus narrowing, presence of ulcers, tumors and differentiation from gastroparesis. Upper endoscopy performed in patients may help with visualization of the gastric outlet, biopsy sampling in case of intraluminal pathology and thereby helps rule out the presence of malignancy in patients with symptoms of Peptic Ulcer Disease (PUD). Surgery is the primary modality of treatment for patients with GOO. It is required for more than 75 percent of patients, with scarring, fibrosis and tumors. The aims of surgery in case of GOO include relief of obstruction, relief in patients with failure to respond to medical therapy or failure to improve even after 72 hours of therapy and correction of PUD symptoms. Various types of surgical procedures performed in cases of GOO are vagotomy and antrectomy, gastrojejunostomy (vagotomy and antrectomy with Billroth II reconstruction), balloon dilatation, pylorotomy, pyloroplasty and laparoscopic techniques. Care must be taken to look out for various complications arising after surgery such as perforation, anastomotic leak, dilation and dysmotility of stomach, edema of the gastric wall and postgastrectomy syndromes.

Classification

Gastric outlet obstruction (GOO) may be due to any underlying condition that results in mechanical obstruction to emptying of gastric contents. GOO is classified based on the underlying cause into benign GOO and malignant GOO. Statistically, benign GOO comprises 37 percent of cases and includes peptic ulcer disease whereas malignant GOO comprises of the remaining 53 percent of cases.

Pathophysiology

It is understood that GOO is the result of multiple intrinsic (lumen & wall) or extrinsic (involving neighbouring structures) pathologies that involve the antrum and the pylorus.

  • Intrinsic obstruction: Conditions involving infiltration, scar formation or inflammation of antrum and the pylorus may lead to intrinsic obstruction and GOO.
  • Extrinsic obstruction: Any malignancy of neighboring structures such as duodenum, liver, gallbladder and pancreas may lead to extrinsic obstruction of gastric outlet.

Causes

Causes of GOO may be classified as benign and malignant.

Benign causes

Benign causes of GOO can either be congenital or acquired. The acquired causes of GOO may further be categorized into acute or chronic. The acquired acute causes of GOO results from edema and inflammation of antrum and the pylorus. The acquired chronic causes of GOO results from intrinsic obstruction due to fibrosis and scar formation. In general, benign causes of GOO include: [1][2][3][4]

Congenital causes of gastric outlet obstruction include:[23][24]

Malignant causes

Differentiating Gastric outlet obstruction from Other Diseases

Differential Diagnosis
Disease Symptoms Diagnosis Other findings
Pain Nausea & Vomiting Heartburn Belching or Bloating Weight loss Loss of Appetite Stools Endoscopy findings
Location Aggravating Factors Alleviating Factors
Gastric outlet obstruction (GOO) Food - ✔ ✔ ✔ ✔ ✔ Black stools in case of Peptic Ulcer Disease(PUD)

Sodium chloride load test

  • Presence of >400 mL NaCl solution in stomach after half an hour, is diagnostic of GOO.

Needle-guided biopsy

Acute gastritis Food Antacids ✔ ✔ ✔ - ✔ Black stools -
Chronic gastritis Food Antacids ✔ ✔ ✔ ✔ ✔ - H. pylori gastritis

Lymphocytic gastritis

  • Enlarged folds
  • Aphthoid erosions
 -
Atrophic gastritis - - ✔ - ✔ ✔ - H. pylori

Autoimmune

Diagnosed by:
Crohn's disease - - - - - ✔ ✔
  • Thickened antral folds
  • Antral narrowing
  • Hypoperistalsis
  • Duodenal strictures
GERD
  • Spicy food
  • Tight fitting clothing
 ✔

(Suspect delayed gastric emptying)

✔ - - - - Other symptoms:
Peptic ulcer disease

Duodenal ulcer

  • Pain aggravates with empty stomach

Gastric ulcer

  • Pain aggravates with food
  • Pain alleviates with food
 ✔ ✔ - - - Gastric ulcers
  • Most ulcers are at the junction of fundus and antrum
  • 0.5-2.5cm

Duodenal ulcers

  • Found in the first part of duodenum
  • <1cm
 Other diagnostic tests
Gastrinoma - - ✔

(suspect gastric outlet obstruction)

✔ - - - Useful in collecting the tissue for biopsy

Diagnostic tests

Gastric Adenocarcinoma - - ✔ ✔ ✔ ✔ ✔ Esophagogastroduodenoscopy
  • Multiple biopsies are taken to establish the diagnosis and determine histological variant.
 Other symptoms
Primary gastric lymphoma - - - - - ✔ - - Useful in collecting the tissue for biopsy Other symptoms
  • Painless swollen lymph nodes in neck and armpit
  • Night sweats

Epidemiology and Demographics

The epidemiology of GOO is as follows:[43][44]

Diagnosis

History and Symptoms

The following history is relevant in patients with GOO:[45][46]

The clinical presentation of GOO is as follows:

Early stages:[5][26]

Late stages:[29][28][47][48]

Physical Examination

In the late stages of GOO, patients may develop signs of malnutrition and incomplete obstruction. Signs of malnutrition include weight loss and signs of dehydration. Signs of incomplete obstruction include findings such as abdominal mass, visible gastric peristalsis, fullness of epigastrium and a tympanitic mass on percussion. {{#ev:youtube|UVJYQlUm2A8}}

Laboratory Findings

Laboratory investigations suggestive of GOO include Hypokalemic hypochloremic metabolic alkalosis (due to vomiting). In order to assess the severity and etiology of GOO, other investigations such as CBC, electrolyte panel, tests for H Pylori and liver function tests may be done.[49]

Imaging Findings

Imaging studies such as plain radiographs, contrast upper gastrointestinal (GI) studies and Computed Tomography (CT) with oral contrast may be used for evaluating patients with symptoms of GOO.

X ray

An x-ray (obstruction series or barium study) may be helpful in the diagnosis of GOO. Findings on an x-ray suggestive of GOO include gastric dilatation. Findings on barium or Gastrografin study help in the determination of site of obstruction, visualization of the gastric silhouette, Gastric dilation, narrowed pylorus, presence of ulcers and tumors. GOO may also be differentiated from gastroparesis in which gastric dilation is not associated with the narrowing of the pylorus.

Computed tomography (CT) with oral contrast

CT with oral contrast or CT-guided biopsy may be done in suspected cases with equivocal findings on X Ray and Barium Upper GI studies. Findings of CT are variable and include those of the underlying condition.

Other Diagnostic Studies

Endoscopy

Upper endoscopy may be helpful in the diagnosis of GOO. An upper endoscopy aids in visualization of the gastric outlet, Biopsy sampling in case of intraluminal pathology. In addition, Endoscopic biopsy helps rule out the presence of malignancy in patients with symptoms of Peptic Ulcer Disease (PUD) :[51][52]

Sodium chloride load test

In sodium chloride test, the patient is infused with 750 mL of sodium chloride solution into the stomach via a nasogastric tube (NGT). After half an hour if > 400 mL is left in the stomach, the diagnosis of GOO is made.[53]

Needle-guided biopsy

Needle guided biopsy is used to evaluate patients for metastasis, in order to detect the primary tumor on histology.

Treatment

Medical Therapy

Surgery

Surgery is the primary modality of treatment for patients with GOO. It is required for more than 75 percent of patients, with scarring, fibrosis and tumors. The aims of surgery in case of GOO include:

  • Relief of obstruction
  • Relief in patients with failure to respond to medical therapy or failure to improve even after 72 hours of therapy
  • Correction of PUD symptoms

Preoperative evaluation

Preoperative evaluation of patients include:

Guidelines for surgery

The following points need to be considered by surgeons:

Types of surgical procedures

The types of surgical procedures performed in cases of GOO are as follows:[22][77][78][79][80][81][82]

Contraindications to surgery

Contraindications to surgery include the following conditions:

Complications of surgery

Complications arising after surgery include:[105][106]

References

  1. ↑ Bradley EL, Clements JL (1981). "Idiopathic duodenal obstruction: an unappreciated complication of pancreatitis". Ann. Surg. 193 (5): 638–48. PMC 1345138. PMID 7235767.
  2. ↑ Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK (1992). "Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history". Am. J. Gastroenterol. 87 (3): 337–41. PMID 1539568.
  3. ↑ Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, Siersema PD (2004). "Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy". Gastrointest. Endosc. 60 (3): 372–7. PMID 15332026.
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