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Screening methods for colon cancer depend on detecting either precancerous changes such as certain kinds of polyps or on finding early and thus more treatable cancer. The extent to which screening procedures reduce the incidence of gastrointestinal cancer or mortality depends on the rate of precancerous and cancerous disease in that population. gFOBT (guaiac fecal occult blood test) and flexible sigmoidoscopy screening have each shown benefit in randomized clinical trials. Evidence for other colon cancer screening tools such as iFOBT (immunochemical fecal occult blood test) or colonoscopy is substantial and guidelines have been issued by several advisory groups but does not include randomized studies.
In 2009 the American College of Gastroenterology (ACG) suggest that colon cancer screening modalities that are also directly preventive by removing precursor lesions should be given precedence, and prefer a colonoscopy every 10 years in average-risk individuals, beginning at age 50. The ACG suggests that cancer detection tests such as any type of FOB are an alternative that is less preferred, and if a colonoscopy is declined, the FIT (fecal immunochemical test, or iFOBT) should be offered instead. Two other recent guidelines, from the US Multisociety Task Force (MSTF) and the US Preventive Services Task Force (USPSTF), while permitting immediate colonoscopy as an option, did not categorize it as preferred. The ACG and MSTF also included CT colonography every five years, and fecal DNA testing as considerations. All three recommendation panels recommended replacing any older low-sensitivity, guaiac-based fecal occult blood testing (gFOBT) with either newer high-sensitivity guaiac-based fecal occult blood testing (hs gFOBT) or fecal immunochemical testing (FIT). MSTF looked at six studies that compared high sensitivity gFOBT (Hemoccult SENSA) to FIT, and concluded that there was no clear difference in overall performance between these methods.
The American College of Gastroenterology has recommended the abandoning of gFOBT testing as a colorectal cancer screening tool, in favor of the fecal immunochemical test. Though the FIT test is preferred, even the guaiac FOB testing of average risk populations may have been sufficient to reduce the mortality associated with colon cancer by about 25%. With this lower efficacy, it was not always cost effective to screen a large population with gFOBT.
If colon cancer is suspected in an individual (such as in someone with an unexplained anemia) fecal occult blood tests may not be clinically helpful. If a doctor suspects colon cancer, more rigorous investigation is necessary, whether or not the test is positive.
In 2006, the Australian Government introduced the National Bowel Cancer Program which has been updated several times since; targeted screening will be done of all Australians aged over 50 to 74 by 2017–2018. Cancer Council Australia recommended that FOBT should be done every two years. Gradually government fund disbursement meant that some people are not yet eligible for the national program and should pay for a FOBT by themselves.
The Canadian Cancer Society recommends that men and women age 50 and over have a FOBT at least every 2 years.
In colon cancer screening, using only one sample of feces collected by a doctor performing a digital rectal examination is discouraged.
The use of the M2-PK Test is encouraged over gFOBT for routine screening as it may pick up tumors that are both bleeding and non bleeding. It is able to pick up 80 percent of colorectal cancer and 44 percent for adenoma > 1 centimeter, while gFOBT picks up 13 to 50 percent of colorectal cancers.
An extensive literature has examined the clinical value of FOBT in iron deficiency anemia.
Diagnosis of gastric varices is often made at the time of upper endoscopy.
The Sarin classification of gastric varices identifies four different anatomical types of gastric varices, which differ in terms of treatment modalities.
Once a patient complains of dysphagia they should have an "upper endoscopy" (EGD). Commonly patients are found to have esophagitis and may have an esophageal stricture. Biopsies are usually done to look for evidence of esophagitis even if the EGD is normal. Usually no further testing is required if the diagnosis is established on EGD. Repeat endoscopy may be needed for follow up.
If there is a suspicion of a proximal lesion such as:
- history of surgery for laryngeal or esophageal cancer
- history of radiation or irritating injury
- achalasia
- Zenker's diverticulum
a "barium swallow" may be performed before endoscopy to help identify abnormalities that might increase the risk of perforation at the time of endoscopy.
If achalasia suspected an upper endoscopy is required to exclude a malignancy as a cause of the findings on barium swallow. Manometry is performed next to confirm. A normal endoscopy should be followed by manometry, and if manometry is also normal, the diagnosis is functional dysphagia.
After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of epithelial dysplasia (or "intraepithelial neoplasia").
Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproductibility, it is also recommended to follow international classification system as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000).
Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. Among those not expected to live more than 5 years screening is not recommended.
The patient is generally sent for a GI, pulmonary, or ENT, depending on the suspected underlying cause. Consultations with a speech therapist and registered dietitian nutritionist (RDN) are also needed, as many patients may need dietary modifications such as thickened fluids.
The diagnosis of nutcracker esophagus is typically made with an esophageal motility study, which shows characteristic features of the disorder. Esophageal motility studies involve pressure measurements of the esophagus after a patient takes a wet (fluid-containing) or dry (solid-containing) swallow. Measurements are usually taken at various points in the esophagus.
Nutcracker esophagus is characterized by a number of criteria described in the literature. The most commonly used criteria are the Castell criteria, named after American gastroenterologist D.O. Castell. The Castell criteria include one major criterion: a mean peristaltic amplitude in the distal esophagus of more than 180 mm Hg. The minor criterion is the presence of repetitive contractions (meaning two or more) that are greater than six seconds in duration. Castell also noted that the lower esophageal sphincter relaxes normally in nutcracker esophagus, but has an elevated pressure of greater than 40 mm Hg at baseline.
Three other criteria for definition of the nutcracker esophagus have been defined. The Gothenburg criterion consists of the presence of peristaltic contractions, with an amplitude of 180 mm Hg at any place in the esophagus. The Richter criterion involves the presence of peristaltic contractions with an amplitude of greater than 180 mmHg from an average of measurements taken 3 and 8 cm above the lower esophageal sphincter. It has been incorporated into a number of clinical guidelines for the evaluation of dysphagia. The Achem criteria are more stringent, and are an extension of the study of 93 patients used by Richter and Castell in the development of their criteria, and require amplitudes of greater than 199 mm Hg at 3 cm above the lower esophageal sphincter (LES), greater than 172 mm Hg at 8 cm above the LES, or greater than 102 mm Hg at 13 cm above the LES.
It can be diagnosed with an X-ray while the patient swallows barium (called a barium study of the esophagus), by a computerized tomography scan, a biopsy, or by an endoscopy.
If it is caused by esophagitis, in turn caused by an underlying infection, it is commonly treated by treating the infection (typically with antibiotics). In order to open the stricture, a surgeon can insert a bougie – a weighted tube used to dilate the constricted areas in the esophagus. It can sometimes be treated with other medications. For example, an H2 antagonist (e.g. ranitidine) or a proton-pump inhibitor (e.g. omeprazole) can treat underlying acid reflux disease.
Initial treatment of bleeding from gastric varices focuses on resuscitation, much as with esophageal varices. This includes administration of fluids, blood products, and antibiotics.
The results from the only two randomized trials comparing band ligation vs cyanoacrylate suggests that endoscopic injection of cyanoacrylate, known as gastric variceal obliteration or GVO is superior to band ligation in preventing rebleeding rates. Cyanoacrylate, a common component in 'super glue' is often mixed 1:1 with lipiodol to prevent polymerization in the endoscopy delivery optics, and to show on radiographic imaging. GVO is usually performed in specialized therapeutic endoscopy centers. Complications include sepsis, embolization of glue, and obstruction from polymerization in the lumen of the stomach.
Other techniques for refractory bleeding include:
- Transjugular intrahepatic portosystemic shunts (TIPS)
- Balloon occluded retrograde transvenous obliteration techniques (BORTO)
- Gastric variceal ligation, although this modality is falling out of favour
- Intra-gastric balloon tamponade as a bridge to further therapy
- a caveat is that a larger balloon is required to occupy the fundus of the stomach where gastric varices commonly occur
- Liver transplantation
In patients who have dysphagia, testing may first be done to exclude an anatomical cause of dysphagia, such as distortion of the anatomy of the esophagus. This usually includes visualization of the esophagus with an endoscope, and can also include barium swallow X-rays of the esophagus. Endoscopy is typically normal in patients with nutcracker esophagus; however, abnormalities associated with gastroesophageal reflux disease, or GERD, which associates with nutcracker esophagus, may be seen. Barium swallow in nutcracker esophagus is also typically normal, but may provide a definitive diagnosis if contrast is given in tablet or granule form. Studies on endoscopic ultrasound show slight trends toward thickening of the muscularis propria of the esophagus in nutcracker esophagus, but this is not useful in making the diagnosis.
Because of its sensitivity, manometry (esophageal motility study) is considered the key test for establishing the diagnosis. A catheter (thin tube) is inserted through the nose, and the patient is instructed to swallow several times. The probe measures muscle contractions in different parts of the esophagus during the act of swallowing. Manometry reveals failure of the LES to relax with swallowing and lack of functional peristalsis in the smooth muscle esophagus.
Characteristic manometric findings are:
- Lower esophageal sphincter (LES) fails to relax upon wet swallow (<75% relaxation)
- Pressure of LES 100 is considered achalasia, > 200 is nutcracker achalasia.
- Aperistalsis in esophageal body
- Relative increase in intra-esophageal pressure as compared with intra-gastric pressure
The patient swallows a barium solution, with continuous fluoroscopy (X-ray recording) to observe the flow of the fluid through the esophagus. Normal peristaltic movement of the esophagus is not seen. There is acute tapering at the lower esophageal sphincter and narrowing at the gastro-esophageal junction, producing a "bird's beak" or "rat's tail" appearance. The esophagus above the narrowing is often dilated (enlarged) to varying degrees as the esophagus is gradually stretched over time. An air-fluid margin is often seen over the barium column due to the lack of peristalsis. A five-minutes timed barium swallow can provide a useful benchmark to measure the effectiveness of treatment.
The treatment for bile reflux is the same as the treatment for acidic reflux. In general, everything that can
reduce acidic reflux can reduce bile reflux. Examples include lifestyle modification, weight reduction, and the avoidance of eating immediately before sleep or being in the supine position immediately after meals. In addition, smoking has been found to be a factor in the development of acidic reflux. Thus, all of these factors should be applied to bile reflux as well.
Likewise, drugs that reduce the secretion of gastric acid (e.g., proton pump inhibitors)
or that reduce gastric contents or volume can be used to treat acidic bile reflux. Because prokinetic drugs increase the motility of the stomach and accelerate gastric emptying, they can also reduce bile reflux. Other drugs that reduce the relaxations of the lower esophageal sphincter, such as baclofen, have also proven to reduce bile reflux, particularly in patients who are refractory to (medically unresponsive to) proton pump inhibitor therapy.
Medications used in managing biliary reflux include bile acid sequestrants, particularly cholestyramine, which disrupt the circulation of bile in the digestive tract and sequester bile that would otherwise cause symptoms when refluxed; and prokinetic agents, to move material from the stomach to the small bowel more rapidly and prevent reflux.
Biliary reflux may also be treated surgically, if medications are ineffective or if precancerous tissue is present in the esophagus.
The diagnosis of GERD is usually made when typical symptoms are present. Reflux can be present in people without symptoms and the diagnosis requires both symptoms or complications and reflux of stomach content.
Other investigations may include esophagogastroduodenoscopy (EGD). Barium swallow X-rays should not be used for diagnosis. Esophageal manometry is not recommended for use in diagnosis, being recommended only prior to surgery. Ambulatory esophageal pH monitoring may be useful in those who do not improve after PPIs and is not needed in those in whom Barrett's esophagus is seen. Investigation for H. pylori is not usually needed.
The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and allows monitoring GERD patients in their response to medical or surgical treatment. One practice for diagnosis of GERD is a short-term treatment with proton-pump inhibitors, with improvement in symptoms suggesting a positive diagnosis. Short-term treatment with proton-pump inhibitors may help predict abnormal 24-hr pH monitoring results among patients with symptoms suggestive of GERD.
On chest radiography, a retrocardiac, gas-filled viscus may be seen in cases of intrathoracic stomach, which confirms the diagnosis. Plain abdominal radiography reveals a massively distended viscus in the upper abdomen. In organoaxial volvulus, plain films may show a horizontally oriented stomach with a single air-fluid level and a paucity of distal gas. In mesenteroaxial volvulus, plain abdominal radiographic findings include a spherical stomach on supine images and 2 air-fluid levels on erect images, with the antrum positioned superior to the fundus.
- Upper GI contrast studies:
The diagnosis of gastric volvulus is usually based on barium studies; however, some authors recommend computed tomography (CT) scanning as the imaging modality of choice.
Upper gastrointestinal (GI) contrast radiographic studies (using barium or Gastrografin) are sensitive and specific if performed with the stomach in the "twisted" state and may show an upside-down stomach. Contrast studies have been reported to have a diagnostic yield in 81–84% of patients.
Often performed for an evaluation of acute abdominal pain, a computed tomography (CT) scan can offer immediate diagnosis by showing two bubbles with a transition line. Proponents of CT scanning in the diagnosis of gastric volvulus report several benefits, including:
1. the ability to rapidly diagnose the condition based on a few coronal reconstructed images,
2. the ability to detect the presence or absence of gastric pneumatosis and free air,
3. the detection of predisposing factors (i.e., diaphragmatic or hiatal hernias), and
4. the exclusion of other abdominal pathology.
- Endoscopy:
Upper gastrointestinal (GI) endoscopy may be helpful in the diagnosis of gastric volvulus. When this procedure reveals distortion of the gastric anatomy with difficulty intubating the stomach or pylorus, it can be highly suggestive of gastric volvulus. In the late stage of gastric volvulus, strangulation of the blood supply can result in progressive ischemic ulceration or mucosal fissuring.
The nonoperative mortality rate for gastric volvulus is reportedly as high as 80%. Historically, mortality rates of 30–50% have been reported for acute gastric volvulus, with the major cause of death being strangulation, which can lead to necrosis and perforation. With advances in diagnosis and management, the mortality rate from acute gastric volvulus is 15–20% and that for chronic gastric volvulus is 0–13%.
Esophageal webs and rings can be treated with endoscopic dilation.
Endoscopy, the looking down into the stomach with a fibre-optic scope, is not routinely needed if the case is typical and responds to treatment. It is recommended when people either do not respond well to treatment or have alarm symptoms, including dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate either once-in-a-lifetime or 5- to 10-yearly endoscopy for people with longstanding GERD, to evaluate the possible presence of dysplasia or Barrett's esophagus.
Biopsies performed during gastroscopy may show:
- Edema and basal hyperplasia (nonspecific inflammatory changes)
- Lymphocytic inflammation (nonspecific)
- Neutrophilic inflammation (usually due to reflux or "Helicobacter" gastritis)
- Eosinophilic inflammation (usually due to reflux): The presence of intraepithelial eosinophils may suggest a diagnosis of eosinophilic esophagitis (EE) if eosinophils are present in high enough numbers. Less than 20 eosinophils per high-power microscopic field in the distal esophagus, in the presence of other histologic features of GERD, is more consistent with GERD than EE.
- Goblet cell intestinal metaplasia or Barrett's esophagus
- Elongation of the papillae
- Thinning of the squamous cell layer
- Dysplasia
- Carcinoma
Reflux changes may not be erosive in nature, leading to "nonerosive reflux disease".
The tests that are considered to evaluate of the passage of blood in the stool are based on the characteristics of bleeding (color, quantity) and whether or not the person passing blood has a low blood pressure with elevated heart rate, as opposed to normal vital signs. The following tests are combined to determine the causes of the source of bleeding.
- Digital rectal exam (DRE) and fecal occult blood test (FOBT)
- Colonoscopy
- Anoscopy
- Esophagogastroduodenoscopy (EGD)
- Capsule endoscopy
- CT Scan
Melena is defined as dark, tarry stools, often black in color due to partial digestion of the RBCs.
Hematochezia is defined as bright red blood seen in the toilet either inside of, or surrounding the stool.
Hematochezia is typically presumed to come from the lower portion of the GI tract, and the initial steps of diagnosis include a DRE with FOBT, which if positive, will lead to a colonoscopy. If the person has a large amount of blood in their stool, an EGD test may be necessary. If no source of active bleeding is found on these examinations, a capsule endoscopy may be performed, in order to more closely examine the small bowel, which cannot be seen with the other types of studies. With melena, a DRE with FOBT is often also performed, however the suspicion for a source from the upper GI tract is higher, leading first to the use of EGD with the other tests being required if no source is identified. The anoscopy is another type of examination, which can be used along with a colonoscopy, which exams the rectum and distal portion of the descending colon.
In an emergency room setting, someone with food bolus obstruction may be observed for a period to see if the food bolus passes spontaneously. This may be encouraged by administering fizzy drinks that release gas, which may dislodge the food.
Glucagon relaxes the lower esophageal sphincter and may be used in those with esophageal food bolus obstruction. There is little evidence for glucagon's effectiveness in this condition, and glucagon may induce nausea and vomiting, but considering the safety of glucagon this is still considered an acceptable option as long it does not lead to delays in arranging other treatments. Other medications (hyoscine butylbromide, benzodiazepines and opioids) have been studied but the evidence is limited.
Historical treatment of food bolus obstruction included administration of proteolytic enzymes (such as meat tenderizers) with the purpose of degrading the meat that was blocked; however, it is possible that these methods may increase the risk of perforation of the esophagus. Other modalities rarely used now include removal of boluses using catheters, and the use of large-bore tubes inserted into the esophagus to forcefully lavage it.
Anemia is a common complication of blood in the stool, especially when there is a large amount of blood or bleeding occurs over a long period of time. Anemia is also commonly associated with an iron deficiency, due to the importance of iron in the formation of red blood cells (RBCs). When anemia is diagnosed as a result of blood in the stool, vitamins that are important for RBC formation (folate, vitamin B12, and vitamin C) are frequently prescribed in order to ensure that all the materials are available for those cells that are made.
Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach. Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.
Transjugular intrahepatic portosystemic shunt procedures, or TIPS involve decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy. Since it treats the root cause of portal hypertension gastropathy, it has been putatively used for the condition. The literature reports suggest both regression of portal hypertensive gastropathy on endoscopic images and improvement in bleeding after TIPS.
Finally, cryotherapy involves the use of pressurized carbon dioxide administered through the endoscope to freeze and destroy tissue in a focal area. It is being studied for the treatment of portal hypertensive gastropathy.
In emergency situations, care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics such as quinolones or ceftriaxone. Blood volume resuscitation should be done promptly and with caution. The goal should be hemodynamic stability and hemoglobin of over 8 g/dl. Resuscitation of all lost blood leads to increase in portal pressure leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD guidelines)
Therapeutic endoscopy is considered the mainstay of urgent treatment. The two main therapeutic approaches are variceal ligation or banding and sclerotherapy.
In cases of refractory bleeding, balloon tamponade with a Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Esophageal devascularization operations such as the Sugiura procedure can also be used to stop complicated variceal bleeding. Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt, or a distal splenorenal shunt procedure or a liver transplantation.
Nutritional supplementation is not necessary if the patient is not eating for four days or less.
Terlipressin and octreotide for 1 to 5 days have also been used.
Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.