Diseases of the stomach and the intestine

Gastritis

Gastritis is an inflammatory disease of the stomach. Main symptoms are pain in the upper abdominal region, either sticky or crampy, abdominal fullness, bloating and nausea. Frequently, there are no specific symptoms. The most frequent cause of gastritis is infection of the mucosa with the bacterium helicobacter pylori (B-gastritis). The presence of helicobacter pylori leads to a long-lasting inflammatory disease of the stomach and might be the cause of complications such as ulcer disease or carcinoma of the stomach. The diagnosis of bacterial gastritis is usually done by direct inspection of the stomach during a gastroscopic procedure; mucosal biopsies might be taken out with a small forceps. Non-invasive tests such as 13-C-breath-tests or fecal tests for helicobacter pylori infection are available and might be used for confirming treatment success. Therapy of bacterial gastritis is done with a combination of at least two antibiotic drugs together with a so-called proton-pump-inhibitor which decreases acid production in the stomach. The very generous global use of antibiotics has led to the appearance of antibiotics-resistant helicobacter pylori strains. In case of resistant infection a repeat gastroscopy and culture and determination of resistance is useful to select an effective combination of antibiotic drugs. An other inflammatory disease of the stomach, C-gastritis (`chemical`-gastritis), is caused by various substances such as alcohol or medical drugs (e.g. pain killers) or the backflow of gall fluid into the stomach. An effective treatment consists of blockade of the acid production in the stomach by medical drugs. A third form of gastritis is autoimmune gastritis (A-gastritis). That disease is characterized by an inappropriate reaction of the immune system against cells in the mucosa of the stomach which results in chronic gastritis characterized by the loss of resorption of vitamin B 12. This might lead to complications such as pernicious anemia and vitamin B 12 deficiency-related neurologic diseases.

Esophagitis

The inner layer of the esophagus might be damaged by acids, chemical substances or hot dishes. The most frequent health problem of the esophagus is reflux esophagitis. Content of the stomach is regurgitated into a lower part of the esophagus and damages the mucosal layer due to its high acid content. Symptoms are heartburn, acid reflux, burning pain behind the chest, but sometimes even hoarseness or sore throat. Sometimes symptoms are only minimal although chronic inflammation of the lower esophagus is present. The main reason for reflux is weakness of the lower esophageal sphincter, a muscle which normally insures tight closure of the esophagus against the stomach. In addition, a so called hiatal hernia might be present and contribute to reflux disease. Sometimes, increased pressure in the abdominal region due to overweight or pregnancy might aggravate the reflux symptoms. Fatty or sweet dishes lead to relaxation of the muscles of the lower esophageal sphincter and might trigger reflux symptoms. Chronic esophagitis due to reflux might lead to narrowing of the esophagus (stenosis, strictures) and difficulties in swallowing. Reflux esophagitis is also a risk factor for certain changes in the epithelium in the lower esophagus (Barrett’s esophagus) which might be a precursor of cancer of the esophagus (esophageal carcinoma).

Therapeutic measures include weight loss, changes in life style (smoking) and medical treatment. Therapy with high dose proton pump inhibitors (PPI) usually leads to quick improvement of the symptoms. For selective cases laparoscopic surgery (fundoplicatio) or endoscopic treatments are available.

Chronic inflammatory bowel disease

Both Crohn‘s disease and ulcerative colitis are two forms of chronic inflammatory bowel disease and belong to autoimmune diseases in a wider sense. The hallmark of inflammatory bowel diseases are chronic inflammation in the mucus layer or the deeper bowel structures, mainly in the large intestine (colon), but also in the last region of the small intestine (ileum). Sometimes chronic inflammatory bowel disease might also involve other regions of the small intestine or the stomach, sometimes also other organs such as the skin. The most prominent clinical symptoms are mucous discharge and watery or bloody diarrhea, abdominal crampy pain, fever and weight loss. Complications of the disease might be fistulae - narrow connections of the intestine to other intestinal segments or towards the fatty tissue of the abdomen, to the skin or connections towards the urinary bladder. Other typical complications are stenosis (narrowing) of the intestine with subsequent crampy pain as main symptoms. The disease is characterized by inflammatory flare-ups often followed by longer phases without much disease activity. Treatment during acute flare-up of the disease is done by antiinflammatory drugs including corticosteroids and immunosuppressive drugs, treatment during the remission of the disease aims at the prevention of new inflammatory flares. Sometimes local treatments are necessary such as endoscopic dilatation of stenotic intestinal regions or surgical resection of affected intestinal segments.

Celiac disease

Celiac disease (gluten-induced enteropathy) is an inflammatory disease of the small intestine caused by an altered immunologic reaction against wheat-derived gluten which leads to reduced uptake of nutrients, minerals and vitamins A, E, D and K from food. Weight loss and diarrhea are frequent symptoms. Certain autoantibodies (endomysial autoantibodies (EMA), tissue transglutaminase antibodies (TTG), antigliadin antibodies) might give first clues towards the diagnosis which is usually confirmed by taking a biopsy from the deeper regions of the duodenum during gastroscopy. The therapy consists of consequent and life-long gluten-free diet which results in weight gain and cessation of symptoms without any further medical treatment.

Food intolerances

Lactose intolerance

Lactose intolerance (milk sugar intolerance) is a frequent condition and is seen in approximately 15% of the European population. Very often symptoms start in early adulthood, sometimes also in older or even older patients. Bloating, crampy pains, soft stools or diarrhea are the main symptoms. Often, but not always, the patients recall an association with intake of milk or dairy products. Lactose intolerance is caused by a genetic mutation which leads to reduced expression of the enzyme lactase on the mucosal lining of the small intestine. The enzyme lactase splits lactose, a disaccharide molecule, into its monosugars galactose and glucose. Lactose cannot be directly absorbed by the small intestine into the bloodstream, but needs to be split by lactase. When the content of lactase in the small intestine is reduced various amounts of the ingested lactose is not digested and reaches the colon; there it is digested by bacteria which produce hydrogen gas and thus cause bloating. Lactose in the colon raises the osmotic pressure and causes water retention in the bowels resulting in soft stool or even diarrhea. The diagnosis is usually done by hydrogen breath test after ingesting a test dose of lactose. There is also a genetic test for genetic lactase deficiency. For management of lactose intolerance reduction of lactose intake is necessary. Strict dietary adherence leads to cessation of symptoms. Today, there are many lactose-free food products available. Careful reading of the food labels is essential. In addition, specific counselling by a dietician is very often helpful.

Fructose Intolerance

Fructose intolerance is the result of an impaired expression of the fructose carrier enzyme in the small intestine which facilitates absorption of fructose into blood. Thus, some of the fructose ingested reaches the colon and reduces water resorption osmotically; fructose is further metabolized by colonic bacteria producing gases such as hydrogen, carbondioxid and methan leading to diarrhea and bloating. A restricted dietary intake of fructose after dietary counselling might lead to symptom relief in most patients. Fructose intolerance is best diagnosed by hydrogen breath test after ingesting a challenging dose of fructose.

Pancreatitis (inflammation of the pancreas)

Inflammation of the pancreas results in severe upper abdominal pain radiating to both sides. Pancreatitis is diagnosed by elevated blood levels of amylase and lipase and by organ changes detected with ultrasound, CT scan or MR scan. Very often an acute pancreatitis resolves spontaneously without much permanent damage to the organ. Chronic pancreatitis might lead to organ changes such as stenosis of the pancreatic duct, cysts, calcifications and stone formation. The most frequent cause of pancreatitis are gall duct stones which clog the excretion of pancreatic fluid into the small intestine. Another prevalent cause is chronic alcohol intake. Rare causes are drugs, hypertriglyceridemia, pancreas divisum, viral infections, autoimmune pancreatitis, and hereditary pancreatitis. Most often the course of acute pancreatitis is clinically mild, in rare cases massive pancreatic necrosis and bacterial superinfections (abscess) might be life threatening. Treatment of mild pancreatitis consists of reducing food intake, intravenous administration of fluid and pain killers. Severe necrotising pancreatitis is treated with antibiotics and drainage of abscesses. Intensive care is very often necessary. For patients with chronic pancreatitis absolute alcohol abstinence is advisable. Stenosis and stones in the pancreatic duct might be treated during ERCP (endoscopic retrograde cholangio-pancreaticography) by implantation of stents or mechanical extraction of stones.

Severe chronic pancreatitis also leads to changes in the consistency of stool with bloating, diarrhea, weight loss, fatty stools due to impaired digestion of fat-containing foods. Symptoms might be improved by treatment with pancreatic enzymes taken together with meals.

Gallstones

Stones in the gallbladder are frequently observed, more often in women than in men. A high risk situation for development of gallstones is overweight, age over 40 years, and female gender. Another risk factor is rapid weight loss during phases of calorie-restricted diet.

An important point is the place of stone formation. There is cholecystolithiasis where the gall bladder is filled with stones, and choledocholithiasis, where the gall duct contains stones. Frequently stones are found in the gallbladder, but the patients are without symptoms. Sometimes, unspecific complains, such as fullness or pressure in the right upper abdominal region after fatty meals are reported. Stones in the gallbladder might be the cause of complications: colicky pain, acute or chronic inflammation of the gallbladder (cholecystitis). Stones in the gall duct (choledocholithiasis) are less frequently seen, but usually accompanied with severe symptoms. Massive colicky pain is caused when the gallstone moves down the gall duct; when it is expelled into the duodenum pain subsides very quickly. If it got stuck in the duct further complications might develop such as inflammation of the gall duct (cholangitis) or jaundice. Diagnosis of gallstones is made by ultrasound examination, sometimes magnetic resonance tomography (MRCP) or endoscopic ultrasound examination is used. Stones in the gall duct should be removed non-operatively via an endoscopic procedure called ERCP (endoscopic retrograde cholangio-pancreaticography). A special endoscope will be inserted via the stomach into the duodenum where the gall duct ends in the duodenal papilla. A small catheter is pushed through the endoscope and guided through the papillary opening, the papilla might be cut open by special instruments, and the stone can be extracted with endoscopic tools.

Liver diseases

Liver diseases are a group of diseases which show an elevation of liver enzymes, enlargement of the liver and sometimes diffuse pain in the right upper abdominal region. Liver enzymes are called liver function probes (LFP) and consist of aminotransferases such as AST (GOT) and ALT (GPT), indicators of liver cell damage, and alkaline phosphatase (AP) and gamma-glutamyl-transferase (GT), which indicate impairment in the gall flux (cholestasis). Most of the liver diseases occur in an acute and chronic form. The chronic diseases are usually without symptoms for many years or even decades and are very often detected during routine check-ups. Some of the liver disease might manifest itself in a more acute way which usually leads to symptomatic jaundice. Liver diseases might be caused by viral infection (viral hepatitis), be the result of autoimmune processes (autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC)), metabolic diseases (iron storage disease (hemochromatosis), copper storage disease (Wilson’s disease), alpha1-antitrypsin-deficiency (1-AT-deficieny)), or the result of a metabolic-toxic disease (alcoholic fatty liver, alcoholic hepatitis (ASH) or non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH)).

Viral hepatitis

Viral hepatitis is cause by various viruses, called hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV) and hepatitis E virus (HEV). Hepatitis A and hepatitis E are very similar in clinical manifestation: both are contracted by virus-contaminated food and excreted via feces. Both infections occur either without clinical symptoms or result in acute jaundice (acute hepatitis). Other symptoms are tiredness, fatigue, diffuse pressure in the right upper abdominal region, yellow discoloration of the skin and eyes, sometimes a short episode of paleness of feces and dark urine. Both hepatitis A and E resolve completely and result in life-long immunity against the disease. Hepatitis A is also known as endemic hepatitis in Europe, hepatitis E is an acute hepatitis predominantly seen in epidemic outbreaks in south-east Asia, but in sporadic cases only in Europe. Severe life-threatening forms are known in hepatitis A and hepatitis E as well. Under special circumstances such as in immunosuppressed patients after organ transplantation hepatitis E might develop into a chronic infection.

Hepatitis virus B (HBV), hepatitis virus C (HCV) and hepatitis virus D (HDV) are usually transmitted via direct contact to contaminated blood, sometimes also via the sexual route. They are able to induce chronic infection in some of the patients which leads to liver cirrhosis (end-stage liver disease, stiffness of the liver) within one to three decades.

Hepatitis B

Infection with hepatitis B virus (HBV) is transmitted via direct contact with contaminated blood (blood units, blood products, surgical procedures, i.v.-drug use, sharing needles), but also via sexual contact with infected persons. Obligatory screening of blood units for viral contamination has made that route of infection extremely rare. The universal vaccination program for children and adolescents is very effective and has resulted in a sharp decrease of new infection in the younger population.

After an incubation period of 6 weeks to 6 months the acute phase of the disease develops. Either is the infection without symptoms and thus unnoticed by the patient, or manifests itself with unspecific and slight symptoms like a viral flu, or shows the typical symptoms of acute hepatitis with jaundice of the skin, tiredness, fatigue, loss of appetite and diffuse pain in the upper abdominal region. Liver function probes are massively elevated and bilirubin levels are high. After several weeks the symptoms disappear and hepatitis B virus infection is resolved in more than 95% of all cases; a life-long immunity results. In a small minority of infected patients ~5% the infection becomes chronic, the immune system is not able to clear the virus. The chronic infection (chronic hepatitis B) is a slow chronic inflammation of the liver running over many years or decades without symptoms. Due to the long-lasting ongoing inflammation a progressive fibrosis in the liver leads to increased stiffness and changes in the architecture of liver tissue towards cirrhosis. In that stage of the disease symptoms might occur which are complications of liver cirrhosis and include swelling of the legs and water in the belly (ascites), bleeding from esophageal varices, mental changes such as dizziness, disorientation, comatous conditions (hepatic encephalopathy), malignant tumors of the liver (hepatocellular carcinoma HCC) or progressive wasting (cachexia).

The diagnosis of acute or chronic hepatitis B is made by the detection of hepatitis B virus proteins in blood (HBsAg, HBeAg), by the direct detection of the viral genome in blood (HBV-DNA) and by detesction of antibodies against viral proteins (anti-HBs, anti-HBc, Anti-HBe).

Chronic hepatitis B can be treated effectively by direct antiviral agents (DAA) which suppress viral replication. Today the antiviral agents Entecavir (Baraclude or Tenofovir (Viread) are usually administered. It is important that those direct viral agents are taken on a regular basis without interruption to suppress viral replication, inflammation and progression of the disease towards liver cirrhosis. In some selected cases also treatment with pegylated interferon is an option. With our current therapeutics effective viral suppression is usually accomplished, but complete viral eradication is infrequently observed (1%/year); therefore, life-long treatment is indicated.

Hepatitis D (Delta Hepatitis HDV Infection)

That form of viral hepatitis is caused by the hepatitis D virus (HDV); this virus is defective and no longer able to survive and replicate on its own. For replication it needs the presence of hepatitis B virus. A chronic hepatitis D infection accelerates the course of the underlying chronic hepatitis B infection and leads towards liver cirrhosis in a shorter time.

In central Europe infection with HDV is rare, however, in mediterranean and eastern countries the infection is much more prevalent.

Diagnosis of hepatitis D is made by testing for HDV-antibodies and by detection of HDV-RNA from serum. At the moment therapy with pegylated interferon is the only treatment option.

Hepatitis C

The hepatitis C virus (HCV) is transmitted predominantly via blood, very often during i.v.drug abuse. Sexual transmission is possible, but rare. The incubation period is about six months, the acute hepatitis is in most cases without symptoms; in rare cases only, symptoms such as jaundice might occur. In the majority of patients with hepatitis C virus infection, the patients have no symptoms and the disease is diagnosed years or decades after infection. Only sometimes unspecific complaints such as tiredness, fatigue, muscle pain, joint pain or diffuse upper abdominal pain are present. Diagnosis is usually made by elevated liver function probes, by the determination of a positive anti-HCV antibody in blood and the quantification of HCV genome (HCV-RNA) in serum, and complemented by HCV genotype determination, which influences treatment decisions. Acute infection with HCV is spontaneously eliminated by the human immune system in about 20%; in 80% the virus can’t be cleared spontaneously and chronic infection ensures. The further course of the disease is highly variable. About one third of the patients with HCV infection develop severe liver fibrosis and cirrhosis within the first 15 years after infection, a second third develop liver cirrhosis within thirty years after infection, and another third have a mild course and are unlikely to develop cirrhosis.

Therapy of chronic hepatitis C has changed considerably during the last years due to the development of highly effective direct acting antiviral agents (DAA). Until recently, standard therapy consisted of pegylated interferon-alpha to be injected subcutaneously once weekly, the antiviral medication ribavirin to be taken orally, and one of two available first-generation protease inhibitors (Telapravir or Brocepravir). With that regimen a cure rate of about 75% could be reached for genotype 1 and 4. The development of new DAA (new generation protease inhibitors Simeprevir, Faldaprevir), polymerase inhibitors (Sofosbuvir, Dasabuvir) and replication-complex inhibitors (Daclatasvir, Ledipasvir, Samatasvir, Ombitasvir) promise a sustained virologic response rate in an all-oral, interferon free, side-effect free treatment over just twelve weeks. Compliance of the patient is paramount as a precise and scheduled intake of the medication and the knowledge of possible side effects are essential.

Autoimmune hepatitis

Autoimmune hepatitis (AIH) is caused by a deviated immune reaction towards liver tissue, leading to chronic inflammation. Similar to other chronic liver diseases autoimmune hepatitis is usually without many symptoms and is discovered incidentally during a routine check of liver function probes. Further investigations might show autoantibodies (anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (ASMA), anti-Liver-kidney-antibodies (LKM) or antibodies against liver soluble antigen (SLA) which are markers for autoimmune hepatitis. The diagnosis is usually confirmed by liver biopsy; an immunosuppressive therapy with corticosteroids or azathioprin is in most of the cases successful and results in a normal life expectancy. However, life-long medical treatment is necessary.

Primary biliary cirrhosis (PBC)

DThe primary biliary cirrhosis is another autoimmune disease of the liver in which the primary targets are cells of the gall duct. The disease is present for years without symptoms and most often detected incidentally. It is characterized by elevation of alkaline phosphatase and gamma-GT, in most patients anti-mitochondrial antibodies (AMA) are present and help in making the correct diagnosis; it is usually confirmed by liver biopsy. Treatment with ursodesoxycholic acid is successful in reducing long term complications.

Primary sclerosing cholangitis (PSC)

Another autoimmune disease in which the smaller and larger gall ducts are involved is primary sclerosing cholangitis. A chronic inflammatory process leads to severe narrowing of gall ducts, hampering the normal flux of gall out of the liver. After a chronic course of many years liver cirrhosis develops. Bacterial superinfection of the gall fluid results in episodes of infectious cholangitis. In some cases endoscopically-placed stent grafts might help to open-up narrowed gall ducts.

Haemochromatosis (iron storage disease)

Haemochromatosis is a genetically caused disease with a specific mutation in the HFE-gene, in rare cases also in other genes, which leads to increased storage of iron in the body, especially in the liver. Increased iron in the liver leads to local inflammation and, after decades, to liver cirrhosis. Screening for the disease is done by determining serum ferritin and transferrin saturation which allows identification of patients before irreversible organ damage. In those patients effective therapy of haemochromatosis might prevent severe liver damage. Treatment is done by weekly blood drawings of 500 ml blood which mobilizes iron from iron stores. After a treatment period of one to two years iron is depleted from iron storage; thereafter blood drawings are necessary one to three times a year only to maintain low body iron.

Copper storage disease (Wilson’s disease)

Copper storage disease is a genetic disease which can be identified by a specific genetic mutation. Treatment consists of chelating agents which increase urinary output of copper and reduces damage to the liver.

Alpha-1 antitrypsin deficiency

Deficiency of the blood-protein alpha-1 antitrypsin might lead to severe liver damage. It can be diagnosed by determination of blood levels of alpha-1 antitrypsin.

Alcoholic steatohepatitis (ASH)

It has been long known that chronic alcohol consumption might lead to severe damage of the liver and to liver cirrhosis. Chronic alcohol intake leads to an elevated content of fat in the liver cells which is usually completely reversible after cessation of chronic alcohol consumption. In some patients however, a chronic inflammatory disease in the fatty liver develops (fatty liver hepatitis) resulting in elevated liver function probes and changes of the liver towards liver cirrhosis. Very often diagnosis is made in a late stage when cirrhotic changes and complications of cirrhosis such as ascites, edema, variceal bleeding have occurred. It is said that 60 g alcohol (corresponding to half a liter wine) for men and 30 g alcohol (corresponding to 250 ml wine) for women is safe. However, individual variability is considerable and in some patients chronic intake of even less alcohol might lead to severe liver damage. On the other hand, less than 15 % of people who consume more than the above mentioned amount of alcohol eventually develop severe liver damage, pointing to the influence of unknown genetic risk factors. In cases of alcohol induced severe liver damage life-long abstinence from alcohol is an absolute prerequisite to avoid further clinical deterioration.

Non-alcoholic steatohepatitis (NASH)

Non-alcoholic fatty liver hepatitis (non-alcoholic steatohepatitis (NASH)) is defined as increase in fatty content and reactive inflammation in the liver in patients without daily alcohol consumption. The histologic picture is similar to that of alcoholic steatohepatitis. Non-alcoholic steatohepatitis is thought to be one of the manifestations of metabolic syndrome, together with diabetes mellitus, hypertension, overweight, hypercholesterolemia and elevated uric acid values; the syndrome is associated with insulin resistance. After decades chronic inflammatory changes in NASH might lead to liver cirrhosis. Treatment is aimed to improve the metabolic situation and weight loss is the most effective treatment. In addition, vitamin E might improve histologic changes in the liver.

Liver cirrhosis

Liver cirrhosis (stiffness of the liver) is the consequence of many chronic liver diseases. Normal liver tissue will be replaced by soft tissue and local production of collagen leads to stiffness and hardening of the liver. This results in an elevated resistance of the liver towards blood flow and leads to elevated blood pressure in the splanchnic veins (portal hypertension). In order to drain blood out of the bowels collateral veins predominantly in the lower part of the esophagus widen and form esophageal varices. Those varices might rupture and cause acute bleeding (bloody vomiting, black stools) which poses the patient at great risk. The elevated portal blood pressure also leads to accumulation of free water in the belly (ascites). Further complications are water retention in many tissues such as legs (leg edema), reduction in kidney function, an elevated risk for bacterial infection especially in the ascites (spontaneous bacterial peritonitis, SBP), a reduction of proteins produced by the liver (diminished blood coagulation, reduction of albumin) and an impairment of detoxification by the liver with increased blood ammonium levels and symptoms such as inability to concentrate, dizziness and even coma. In addition, liver cirrhosis impairs excretion of bilirubin into gall fluid and leads to an elevation of bilirubin in blood which results in yellowish discoloration of the skin (jaundice). A further complication is the development of a malignant tumor in the liver (hepatocellular carcinoma, HCC).

The goal of therapy is reduction of symptoms by using diuretic medication, by administering beta-blockers and treating esophageal varices by ligation to reduce the bleeding risk and by measures aimed at reducing ammonium production. In severe cases of liver cirrhosis liver transplantation might be necessary.

Hepatocellular carcinoma (HCC)

Hepatocellular carcinoma is a late consequence of liver cirrhosis; in >90% of the cases liver cirrhosis is the underlying disease. Frequently several tumor nodules are found in the liver, distant metastases are relatively rare. Treatment has not only to consider tumor size and numbers, but also reduced liver function due to liver cirrhosis. Several treatment options are available and include surgical resection, liver transplantation, local ablative therapies such as radio frequency ablation (RFA), percutaneous ethanol instillation (PEI), or microwave ablation (MWA), further transarterial chemoembolization (TACE) and systemic treatment with the tyrosin-kinase-inhibitor sorafenib (Nexavar).

Endoscopy

Gastroscopy

Gastroscopy (inspection of the stomach) is used to look into the esophagus (foodpipe), the stomach and the upper part of the duodenum. The gastroscope is a flexible device of small diameter, which brings light into the stomach and captures live pictures and projects it in large magnification on a monitor. The patients swallow the scope after local anesthesia of the throat with an anesthetic spray, sensitive patients might also get sedation with midazolam (Dormicum) or diprivan (Propofol). The investigation is painless and lasts for about 7 to 10 minutes. Routine biopsies will be taken out of the mucosa of the stomach and will be investigated by a pathologist. Gastroscopy is able to detect changes in the mucosa such as gastritis, erosions (superficial defects in the mucosa), also ulcerative disease (defects in the mucosa), bleeding sites, tumors, stenosis and tears in the mucosa. It is also possible to perform a local treatment of some of the detected changes. The patient should be without food for at least 6 hours before investigation. Clear water or tea is allowed until one hour before investigation. Similarly, routine medication should be taken as usual. After the investigation the patient spends about one hour in the recovery room, thereafter food intake is again possible. It is advisable not to drive by car to the investigation, the patient should be accompanied by someone or use public transport.

Colonoscopy

Colonoscopy is the endoscopic investigation of the colon. It is very important that the colon is completely cleansed from feces. Cleansing is usually done by a so-called wash-out solution of which three liters should be taken the day before investigation and the last liter in the morning of the investigation. The solution stays in the intestine, it will not be taken up into blood and washes the feces out of the colon. This method of colon cleansing does not produce any circulatory problems and is well tolerated. Only the neutral or unpleasant taste and the large volume might be a challenge for some patients. The colonoscope will be inserted into the colon via the anus and pushed along the whole colon. On the way back the mucosa of all colonic regions will be inspected. Colonoscopy is able to detect polyps, tumors, diverticles, angiodysplasias, sources of bleeding, inflammation, fistula and so on; biopsies can be taken out, polyps can be removed with snares.

During the investigation air will be insufflated through the colonoscop into the colon to inflate it and to improve the view. That might lead to bloating and sometimes crampy pain after the investigation. Nowadays, CO2 will be used instead of air, which produces less bloating and crampy pain. Colonoscopy is usually done in sedation using Dormicum or Propofol and lasts for about thirty minutes; the patient is sleeping during the procedure. After the investigation the patient stays in the recovery room for one hour and might be dimissed at home. It is advisable not to drive by car to the investigation, the patient should be accompanied by someone or use public transport. If larger polyps are detected and removed a hospital stay overnight is usually recommended to monitor the patient. Complications after colonoscopy are rare, sometimes bleeding after endoscopic removal of polyps is seen, which can be stopped by endoscopic means.

Screening colonoscopy

Colon cancer develops in most of the cases from a benign adenoma (polyp).Those adenomas enlarge over years, if they are bigger than two centimeters in diameter the risk of a malignant change within the polyp leading to colon cancer increases. The aim of screening colonoscopy is to detect all polyps and to remove them before colon cancer develops. In Austria, screening colonoscopy is recommended to start with the 50th year and should be repeated every 5-7 years. In addition, testing for occult blood in stool should be done on an annual basis starting with the 40th year of life.