Chronic hepatitis B transmission

Chronic hepatitis B virus transmission can be done by different ways:

A. Horizontal

-Parenteral or percutaneous ( blood, blood derivates, contact with infected instruments, including tattoos).
-Physical contact (non-sexual) : intrafamilial, children collectivities;
-Sexual contact.

B. Vertical
-Perinatal (from an infected mother to the child).

In areas with high endemicity, the transmission is mainly vertical, while in those with medium and low endemicity the main transmission is mostly horizontal. The serological selection of blood taken for transfusion has led to the decreasing in incidence of HBsAg and of residual risk of transmission of HVB.

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Chronic hepatitis B Epidemiology

Chronic hepatitis B represents a public problem caused by the relatively high carriage.

Epidemiology

At as global level, 2 billions of people in the world have been infected with hepatitis B virus, only in Europe the annual apparition of new cases being more than one million. Nowadays it is estimated that in the whole world there are over 350 millions of chronic carriers HBV, with a tendency to increase to 400 millions. Most chronic carriers are in Asia and Africa, places with high prevalence (over 8 - 10 % ). Our country is considered to have a medium endemicity. There are also zones with a low prevalence (under 2 % ) in Australia, USA and Western Europe.




The natural sources of HBV infection are the infected people, the virus being located in the blood, saliva and other secretions (seminal, vaginal, human milk). The main source of infection is represented by infected blood, so the administration of blood (transfusion) or its derivates (platelets mass, cryoprecipitate, antihemophilic factors etc. ) may produce the infection. This can be also transmitted sexually (by sperm), by different secretions or perinatal.
The receptiveness is general except for those that have already surpassed the disease or the vaccinated.

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Alcoholic fatty liver (alcoholic hepatosteatosis)

Lipids that accumulate in alcoholic fatty liver may come from many sources: diet, adipose tissue, hepatic synthesis of novo from glucide. Predominant source depends on the chronic or acute consumption of alcohol, lipid content in diet. In alcoholics, the majority of the lipids in the liver are derived from diet and from oxidation of fatty acids. Accumulation of lipids during the chronic consumption of alcohol does not continue forever, modification of the redox state of the whole liver will slow down during the chronic consume of the alcohol.

Morphopathologicallys teatosis represents the presence of the lipid in more than 5% of hepatocyte. Macroscopically, the liver is enlarged, firm with a yellowish color. Microscopically it can be observed an increase in fat deposits, later intrahepatic cholestasis, migh appear.
Clinically an asymptomatic hepatomegaly is observed and sometimes stigmas of chronic liver disease like contraction of Dupuytren, testicular atrophy, palmar erithrosis, sidernavy, and gynecomastia. Later, fatigue, cachexia, fever, anorexia, nausea, vomiting, jaundice, painful hepatomegaly, splenomegaly and ascites might appear. Majority of this is associated with alcoholic hepatitis.
Positive diagnosis is done by histological examination and imagistic evidence by doing an ultrasound examination. A particular form is the focal steatosis, which makes it difficult to differentiate with a tumoral formation.
Complications that might appear in patients with alcoholic steatosis are sudden death through fatty embolida, alcoholic cessation syndrome or hypoglicemia.
Treatment consits in stopping of alcohol consumption, correction of malnutrition and drugs so called hepatoprotectors (slimarine and mainly vitamin B complex) with disputable efficiency.

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Pathogenesis of alcoholic liver disease

Metabolism of alcohol in the liver takes place in three ways, result being the same, and in the liver takes place in three ways, result being the same, and acetaldehyde is metabolized with high hepato toxicity. Those three ways are:
1. alcoholdehydrogenasis path is the major way of metabolizing alcohol.
2. microsomal oxidation system - P450, interfere in oxidation of alcohol when its concentration is more than 50 mg/dl.
3. catalyze way, which has a seconday role.

Acetaldehyde is later oxidated up to acetate, but in alcoholics, the capacity of mitochondrion to oxidate acetaldehyde is reduced. Their accumulation leads to the promotion of lipid peroxidates and the formation of complex proteins. Besides the toxic effect of the acetaldehyde, alcohol has its role in developing cirrhosis. It has been proven that adipocytes involved in fibrogenesis are active after chronic consumption of alcohol.

Morphologic aspects in alcoholic liver: there are three typer of hepatic histologic lesions in consumers of alcohol.
1. Alcoholic fatty liver is a genign reversible form produced by accumulation of some drops of lipids in hepatocyte.
2. Alcoholic hepatic comprise of degeneration and necrosis of the hepatocyte, acute infiltration of neutrophyles sometimes pericellular, sinusoidal line and venular line fibrosis, as well characteristic Mallory corpuscles (alcoholic hialin). Alcoholic hepatitis may be reversible, but the lesions are much more severe being the most important precursors of cirrhosis.
3. Alcoholic cirrhosis comprise of fibrosis in all hepatic tissue, from the portal space up to centrolobular vein, and nodule of regeneration.

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Alcoholic liver causes

Alcoholic liver causes or alcoholic liver disease is represented by a nonspecific total morphological lesion associated with clinical / paraclinical manifestation, among which some are induced by the abuse of alcohol.
Prevalence: alcoholic liver varies from country to country depending on the tradition, religion and especially on the cost of the alcoholic drinks in comparison with the income.

Alcoholic liver causes: excessive alcohol consumption has varied effect on organisms. Due to some unknown cause, 1/3 of chronic consumers of alcohol do not have hepatic consequences.
1. Duration and consumption of alcohol, it is considered that 60-80 ml of absolute alcohol/day for men and 40-50 ml of absolute alcohol women as a toxic dose. The duration of consumption is also important, a consumption of more than 5 years is considered as a risk. Continous consumption is more dangerous than intermittent consumtion. As well, hepatic injury does not depend on the type of drink but in this alcohol content.
2. Gender: females are more susceptible than men are, because at the same quantity of alcohol ingested reach a higher blood concentration. In women, gastric metabolism is reduced comparing to men and cytochrome P450 is less efficient.
3. Genetic factors: although no genetic markers has proved to have a clear association with susceptibility to alcoholism, seems to inherit certain behavior related to the alcohol consumpion.
4. Coinfection with hepatic viruses (B or C) accelerates the severity of the alcoholic liver disease.
5. Nutritional factors: protein caloric malnutrition precedes alcoholism in patients with socio-economic level leading to the appearance of alcoholic liver. It has been proved that healthy diet may protect those who consume alcohol, at least for a period.

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The etiology of chronic hepatitis

Certainly, the most frequent etiology of chronic hepatitis is the viral one.

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Chronic hepatitis diagnosis

Chronic hepatitis diagnosis is clinic, biological, but mostly histological. Chronic hepatitis can often be asymptomatic, or the clinical features are completely nonspecific, and therefore they are sometimes discovered by routine bilogical investigations.
Almost a half of patients suffering from acute hepatitis are discovered by periodical analyses or by a routine ultrasonography, which will show splenomegaly. When presuming the existence of chronic hepatitis, one should start with an exact etiological history, a correct clinical examination, a biological evaluation of the hepatic disease (the four biological syndromes: cytolytic, hepatoprive, inflammatory and billiar), an abdominal ultrasonography to evaluate the spleen dimension and the possible signs of portal hypertension.

The staging of chronic hepatitis is made compulsory by a hepatic biopsy (HBP). The biopsy will allow the correct histological framing, and also a quite exact prognosis, and sometimes will bring important etiological data, and it will allow in the same time a therapeutical decision. Non invasive markers which measures fibrosis were recently introduced. They use biological tests or hepatic elastography.

The histological staging of chronic hepatitis requires a compulsory hepatic puncture. This is a technique with low invasivity and a minimal risk. Lately HPB has been done by ultrasonographic control. THe bioptic fragment, after fixing and coloration with HE or special colorations, will be interpretated by an experimented pathologist. Whis will describe the lesions, a histological classification in chronic persistent hepatitis, in chronic active hepatitis, and the chronic lobular hepatitis, and then will use a quantifying score of lesions. At this moment, there are more histological framing scores.

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Chronic hepatitis definition

Chronic hepatitis represents necro - inflammatory and fibrotic hepatic processes with an evolution of at least 6 months.

Hepatitis may occur with limited or no symptoms, but often leads to jaundice, anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but it can also be due to toxins (notably alcohol, certain medications, some industrial organic solvents and plants), other infections and autoimmune diseases.

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Foods to Eat and Foods to Avoid after Gallbladder Removal

After a cholecystecotmy, it is important to eat foods that will help support the liver, and minimize the workload of digestion. Healthy, unprocessed vegetable oils, particularly those rich in omega-6 and omega-3 fatty acids, such as flax seed oil and hemp seed oil, should be consumed on a regular basis.

Image source: Wikipedia.org

Both of these nutritious oils are available in supplement form, or they can be used to make salad dressings; they should not be used as cooking oils. These oils, as well as other vegetable oils such as olive oil, help the body naturally eliminate unhealthy LDL cholesterol build-up. Being of a slippery nature, and liquid at room temperature (as opposed to saturated fats, which are solid at room temperature), unsaturated fatty acids slide through the body's pathways with ease, taking toxins and harmful build-up with them.

Lemon juice and vinegar are also helpful foods to eat after gallbladder removal. The acid helps to break down the fatty acids in digestive bile. Try mixing fresh lemon juice with two tablespoons olive oil in a glass of water. Drink this solution in the morning and in the evening.

A diet after gall bladder surgery should include fruits and vegetables, with raw, fresh, organic foods being the most beneficial. Eat plenty of avocados, beets, cucumbers, sweet potatoes, grapes, apples, berries, and artichokes. They will provide fiber, which the body needs to aid in digestion and help cleanse, as well as the nutrients that the body needs to restore itself after gallbladder removal surgery. Other beneficial foods to eat after a cholecystectomy are yogurt, fish, and cottage cheese. As time passes after the surgery, start introducing whole grains, eggs, and some poultry and low-fat milk.


There are a number of foods to avoid after gallbladder removal, the most important being red meat, which is high in difficult to digest animal protein and animal fat. Also minimize pork, poultry, dairy, chocolate, and refined carbohydrates. Choose foods without hydrogenated or trans fats - this means no margarine, and few processed foods. Fried foods, spicy foods, and soft drinks should be taken out of the diet after gallbladder surgery altogether.

A cholecystectomy may be effective in masking the symptoms of a bile imbalance, but the only way to return to a true state of well-being, and to prevent the formation of more stones is to choose a healthy diet.

See more about gallbladder disease:

• Gallbladder pictures
• Gallbladder surgery VIDEO
• Gallbladder cancer treatment
• Gallbladder diet

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Gallbladder pictures

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The recto colonic neoplasm diagnosis

The rectocolonic neoplasm diagnosis is made by the following diagnostic procedures:

• rigid rectoscopy
• flexible rectosigmoidoscopy
• colonoscopy
• irigography
• hemoccult test

Rigid rectoscopy requires a rigid metallic rectoscope and allows the examination of approx. 20-25 cm of the rectosigmoid. The device is not expensive, the technique is easy and it allows the diagnosis of rectal cancer. In addition to the anal examination and anoscopy (which diagnose the pathology of the anal channel and rectal ampoule), it may correctly evaluate the distal region of digestive tube.

Flexible rectosigmoidoscopy uses the flexible sigmoidoscope for the diagnosis. It allows the exact evaluation of the left colon (most often up to the splenic angle of colon), where 70-80% of colon neoplasms are only two enemas and the discomfort of the patient is not very high.

Barium enema evidences the colon by retrograde fulgilling of colon with barium. The double contrast technique is useful. It does not allow biopsy from suspect lesions and it does not allow therapeutic measures. The technique is the most widespread method of colon evaluation, but gas a diagnostic sensibility clearly inferior to the colonoscopy.

In the future it is anticipated the using of CT spiral (virtual colonoscopy) to reconstruct the colon and to diagnose the neoplasia or big polyps). Also in some dedicated centers, the abdominal ultrasound examination and especially hydrosonography may sometimes diagnose the colon neoplasm. Echoendoscopy allows the evaluation of the extension in layers of the neoplasm.

The Hemoccult test allows the determination of occult hemorrhages in the stool. It is rather a screening test, in general population; it helps to discover suspect persons that will be afterwards examinated endoscopically. The Hemoccult test is recommended every year, generally after 50 years of age. The Hemoccult test II, more modern, does not require special preparation and has a superior sensibility.

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The predisposing causes for the colon neoplasm

The predisposing causes for the colon neoplasm are:

• colocrectal polyps
• familial colic polyposis
• inflammatory bowel disease
• familial predisposition
• Lynch syndrome

Colorectal polyps represent a frequent situation in the gastroenterological practice, almost 10% of people 50 years - old and up to 30% of people over 70 years present colonic polyps. These polyps may be adenomatous (adenoma) and hyperplastic.


Adenomatous polyps (real polyps) are of many histological types: tubular, tubulo - villous and villous. The villous polyps have the most increased potential of malignity. The hyperplasic (inflammatory) polyps have no malignant potential.
The evolution of polyps towards malignity seems to be linked to genetic factors (familial), metabolic factors (the co- carcinogen effect of billiary acids) and alimentary factors (the negative effect of lack of vegetables and fibers). The bigger the polyps are (generally over 2 cm diameters), the more numerous and the more severe dysplasia is found at biopsy, the highest is their malignant potential. Starting from these data concerning the relationship polyp - neoplasia, searching polyps by colonoscopy and the endoscopic polypectomia has become a necessity, because it is the best prophylaxis of rectocolic neoplasia.

Familial colic polyposis represents a pathological situation with a genetic character, defined by the presence of more than 100 polyps in the rectum and colon, appearing before the age of 30 years. The genetic transmission is autosomal - dominant and the evolution of polyps to cancer is the rule. Therefore, it becomes a necessoty to check - out actively the transmission is autosomal - dominant and the evolution of polyps to cancer is the rule. Therefore, it becomes a necessity to check - out actively the transmission in the affected families and the most precociously total colectomy, before the malignization.

Inflammatory bowel diseases with prolonged evolution increase the risc of colon neoplasm. This risk is of approx. 10% after 25 years of evolution in ulcero - hemorrhagic rectocolitis (becoming significant after more than 10 years of evolution). The risk is smaller in Chron's disease with prolonged evolution.

Familial predisposition represents an increased risk for the descendants of a family with colon cancer (the frequency of cancer is 2-3 times bigger in first - degree relatives).

The Lynch syndrome or the hereditary nonpolypoidal colorectal cancer (without the intermediate state of polyp and with important hereditary involvement) is characterized by presence in more members of a family, the apparition of cancer at young age and frequently associates other neoplasms (the most eften ovary and endometer).

The Amsterdam criteria for diagnosis of Lynch syndrome are at least 3 members of a family with diagnosis of colonic carcinoma, one of which must be a first-degree relative, in a generation; the transmission be done at two succesive generations and at least one of the casees to be diagnosed before 50 years.

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Colon cancer Diagnosis, Evolution and Complications

The differential diagnosis problems in colon cancer depend upon the differentiation of rectal bleeding. The main causes are:

• hemorrhoidal disease and anal fissure
• Chron's disease
• ulcerative colitis
• colonic diverticuli
• ischemic colitis and irradiation colitis
• colonic angiodysplasia

In front of an anemic syndrome, it should be controlled if the anemia is by iron deficiency, and in this case, the most probable and most evidently it is related to the digestive tube (esogastric, intestine or colon).

Evolution of colon cancer
The evolution of colon neoplasia depends of the moment of its discovery and operation. On the Dukes A stage, the 5 years - survival is about 90%, and in Dukes C approx. 50%. In front of a neoplasm with hepatic metastases (Dukes D), the survival is very low.

Complications of colon cancer
The most frequent are: metastases, intestinal occlusion and perforation.

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Gallbladder Surgery VIDEO

What peoples says:

Had my GB removed a week ago. Pain lasted a few days but nothing that paracetamol couldn't deal with. Still have the staples which should be removed in 3 days from now. I didn't want this operation but after 4 seizures my wife got fed-up with taking me to the emergency services in the middle of the night and insisted I take the doctor's advice. Feel much better now! Glad I had it done.
If you have a GB stone/s causing you trouble, don't hesitate, just get it done.

PBCaurillac
 ---------------------------------------------------------------

had mine done on wednesday. was very sore for 1 day, then the wind trapped inside my body wasa bit awefull. but after just 3 days i can say i am allready feeling alot better. no longer feel like i have poison running through my vaines and feel alot more happy in myself. if in pain get it done. good luck.

wetstocks
 ---------------------------------------------------------------

Before you consider doing this operation you should find out what happens when you no longer have this important organ. You need to be rid of the STONES, not the gallbladder. This can be done simply at home with nothing more than epsom salts, olive oil and grapefruit. I had a severe attack of gallstones but refused surgery and got the stones out myself. I am 100% recovered. Google liver cleanse if you want to know more.

pelhosaini

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Gallbladder cancer treatment

Nowadays there is almost a consensus that asymptomatic gallstones be only watched and not surgically solved. Reminding that only 1 - 2% of the asymptomatic cases  become symptomatic annually the expectative appears to be the most logical and economical solution. If the symptoms appears to be the most logical and economical solution. If the symptoms appear, a therapy will be initiated.

The symptomatic gallstones will be treated. Most often this treatment is surgical and more rarely treated by nonsurgical techniques. Since the laparoscopic colecistectomy was introduced, the trust of patient into the intervention has increased. It involves a safe intervention, a short hospitalization and minimal postoperatory inconvenient (when the surgeons are well trained in this technique). The uncomplicated cholelithiasis cases are usually treated by this technique, but also the acute cholecistitis or vesicular hydrops. In the scleroatrophic lithiasic cholecistitis or when there is a suspicion of common bile duct lithiasis, the classic technique of open colecistectomy is preffered. In case of common bile ductolithiasis suspicion the exploration of common bile duct is mandatory.

The nonsurgical techniques of treatment of gallstones are the medicamentous litholisis and the extracorporeal lithotripsy.

Medical therapy (gallstone dissolution) is effective in the cholesterol calculi, preferably small, those fill in less than a half of the vesicular volume and when the gallbladder has a permeable infundibulo - cystic zone. The therapy consists in the administration of ursodeoxycholic acid (10 mg / kg body / day) - Ursofalk or its combining with chenodeoxycholic acid (10 - 15mg / kg body / day) - Litofalk for 3 - 12 months, up to the complete solubilisation of calculi. The overseeing of the results is made by ultrasonography.

Extracorporeal lithotripsy consists of fragmenting the cholesterol calculi by extracorporeal shock waves; it addresses to the unique or less numerous calculi, preferable under 15mm. The fragments resulted from lithotripsy will then be solved by administrating billiary acids up to the complete disappearance of all calculi fragments from the bladder. Both nonsurgical techniques are relatively-expensive.

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Colon cancer, Epidemiology, Etiopathogenesis

Colorectal cancer represents a public health problem, considering that in most European countries it is the first on the list of neoplasms. Even if the bronchopulmonary neoplasm is prevalent in men and the genital tumors in women, totalizing their prevalence on both sexes makes the colorectal cancer the first cause of malignancy in many states.
 
Epidemiology

In France the incidence of colorectal cancer is 15% of all cancers, in Romania it is the first among the digestive cancers. Its frequency varies with the geographic area being very frequent in Europe and USA but less frequent in South America and Africa. These geographic differences are firstly related to the alimentary habits and in a certain measure to genetic factors.

The special problem in this cancer is that it is somewhat forewarned, since at this moment the filiations is clearly established (adenoma carcinoma), thus the endoscopic finding an will prevent the apparition. The role of genetic factor (Lynch syndrome) in the apparition of colon neoplasm is also known.

Etiopathogenesis

More factors are involved in the producing of colon neoplasm:

• the role of alimentary factors
• the role (controversial) of billioary acids
• the role of predisposing causes

a) Alimentary factors are involved in the etiopathogenesis of this neoplasia (based on epidemiologic studies), the vegetables, fibers diet, calcium and vitamins are considered as a protective diet. Negative alimentary factors are the considered as a protective diet. Negative alimentary factors are the excess of animal fats and proteins, red meat, alcohol and excessive caloric intake.

b) The role of billioary acids in the etiopathogenesis remains controversial, but there are experimental studies showing their involvement. Some epidemiologic and clinical studies have shown a relationship between cholecystectomy and the increasing of frequency of the colon neoplasm.

c) The predisposing causes for the colon neoplasm are:

• colocrectal polyps
• familial colic polyposis
• inflammatory bowel disease
• familial predisposition
• Lynch syndrome

Colon Cancer Treatment

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Colon Cancer Treatment

The treatment of colon neoplasia is surgical. The intervention should be done as soon as possible, its type depending on the tumor location. The preoperatory evaluation will include the evaluation of lymph node extension and of metastases (pulmonary, hepatic or peritoneal). The postsurgical chemotherapy is indicated to patients in stages Dukes B2 and C. Schemes including 5 fluoro-uralic, asociated with folinic acid are used. considering the increasing survival postchemotherapy, it is indicated that, after surgery, the patient is sent to continue the treatment to the oncologist.

                                                          Fig.1 Colon Cancer
Radiotherapy is addressed especially to the rectal cancer, which, by its position in the small pelvis, cannot always be correctly eliminated.

The prophylaxis of colonic cancer represents an actual requirement of the medicine, regarding the place ranked by this neoplasia in the world.
- primary prophylaxis consists in measures of nourishment education, over a big number of years  trying to educate the population to consume mostly vegetables, a fibers - rich diet (whole meal, cereals), calcium and to reduce the fats, the protein excess (especially red meat).
- seccondary prophylaxis consists the removal of causes that might lead to a colonic neoplasm, especially the discovering of polyps and endoscopic polypectomia. The discovering of polyps in general population is quite difficult because of the immense number of endoscopic explorations that should be done. Therefore, tests type Hemoccult are recommended followed by colonoscopy in the persons found positive. The prophylactic colonoscopy must be also performed in persons with high risk of cancer: inflammatory bowel diseases, descendents of persons with colon cancer, colonic polyps history.

The molecular screening will represent in the future the ideal method of secondary prophylaxis, by noticing the genetic mutations predisposing to colon cancer.
After the surgical resection of a colon neoplasm, CEA may be used to show the possible local recurrences. The ultrasonography and CT for possible hepatic metastases are also useful.

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Ulcerative Colitis, Physiopathology, Diagnosis, Treatment

Definition
It represents an intestinal inflammatory disease, characterized by recurrent attacks of diarrhea with mucus and blood, alternating with periods of silence.

Clinical features of ulcerative colitis
Digestive manifestations consist in episodes of diarrhea with blood, mucus and pus. The diarrheic episodes consist usually 3-10 stools/day, and in the severe cases there may only appear emissions of blood, mucus and pus. Abdomen on being palpated is painful in the hypogastric area or along the course of the colon.

Extradigestive manifestation are: anemia, fever or low-grade fever in the episode, weight loss, and fatigue. Sometimes arthritis, erythema nodosum, uveitis may appear.

Physiopathology
In the physiopathology of inflammatory bowel disease, more factors are incriminated:
a) Environment factors: the normal intestinal microflora
b) Immunologic factors: defects of local immunity of the mucosa.
c) Genetic factors.

Paraclinical findings
Laboratory data: iron-deficiency anemia,with hypochromia and low sideremia, hypoalbuminemia, inflammatory syndrome (ESR increased,sometimes leukocytosis, reactive C protein increased).
Stool examination is useful in order to exclude an infectious disease such as bacterial dysentery.
Endoscopic data.Typically for ulcerative colitis is the permanent involvement of rectum (recto-colitis), the continuous character of endoscopical lesions. The endoscopy shows the typical aspect of the episode: the mucosa “cries blood”. The mucosa is frail, with superficial ulcerations, diffuse erythema, loss of typical vascular pattern, covered with mucus and pus. The pseudopolyps may be present.
The biopsy proving an inflammatory infiltrate with polimorphonuclear cells at the level of mucosa,  the presence of cryptic abcesses, exulcerations.

Radiological examination. The barium enemawill show, in chronic stages, a granular aspect of the affected mucosa, the pseudopolyps, and the loss of normal colonic haustrations, with a tubular aspect of the colon.

Transabdominal ultrasonography  showing the thickness of colonic wall in the acute phase of the colonic extension. The colonic mucosa is thickened more than 5 mm (mostly 7-10 mm).

Positive diagnosis: diarrhea with blood, mucus and pus, the endoscopically, followed by the biopic confirmation.

Clinical forms

• Fulminant
• Chronic intermittent
• Chronic continuous

The assessment of severity is made by number of stools and intensity of clinical signs. Therefore, there are moderate, mild and severe forms:

• the mild form presents up to 4 stools/day, with only little blood and mucus, general state is good, without fever or denutrition, the anemia is discrete;
• the moderate form with 4-6 stools/day, anemia, low-grade fever
• the severe form with more than 6 stools/day, fever over 38 grade Celsius, anemia, hypoalbuminemia, big amount of blood in the stools, general feeling of illness.

 Based on the location of ulcerative colitis there are three forms:

• proctitis or proctosigmoiditis (rectal or rectosigmoidian location)
• left colitis (involvement up to the splenic angle)
• pancolitis (involvement of the whole colon).

Differential diagnosis:

• colon neoplasia - the endoscopic examination will certify the diagnosis
• bacterial dysentery or other infections causes: Salmonella, Shigella, Campilobacter jejuni, Clostridium difficile - the stool examination will prove the germ
• ischemic colitis - endoscopic and bioptic diagnosis
• irradiation colitis - history of therapeutic abdominal diagnosis
• collagen colitis or lymphocytar colitis-with a normal endoscopic; the biopsy will reveal the presence of submucosal collagenous bands or a rich lymphocytary infiltrate.
• Chron’s  disease -characterized by discontinuity of lesions, endoscopically deep ulcerations, sometimes linear.

Evolution
The evolution is cyclic- acute episodes of variable duration, usually weeks or months, followed by remission.

Complications

• the toxic megacolon
• intestinal stenosis
• massive bleeding with severe anemia
• colon cancer
• extradigetive severe manifestations. 

Treatment ulcerative colitis
a. Hygienic and dietary

The diet during the episode will be sparing the digestive function, by avoiding milk and dairy meals  (cream, fermented chesse), raw vegetables and fruit, concentrated sweets.

b.Medication - it depends on the episode severity.
In the severe episode, parenteral nutrition must be used, with liquidian and electrolytes correction, corticotherapy pev. -100-200 mg hydrocortisone hemisuccinate/day and in toxico-septic forms, antibiotherapy, especially against anaerobic germs (Metronidazole). In refractory fulminant Ulcerative colitis, cyclosporine has effectively induced remission, obviating immediate surgery. Because cyclosporine is such a potent immunosuppressive agent, the psysician must be absolutely certain that an infection is not contributing to the colitis. Infliximab is a monoclonal antibody against tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine that occurs early in the inflammatory cascade. Infliximab has only recently been approved for use in ulcerative colitis. The drug is given as an intravenous infusion, typically in an induction regimen of 2 infusions over 2 weeks. In several reports, refractory ulcerative colitis responded to infliximab, and emergency colectomy was avoided.
In moderate forms of ulcerative colitis (4-6 stools/day) the treatment is using prednisone 60mg/day; the doses sre tapered with approx. 10 mg/week, so that after approx. 4-6 weeks the necessary dose to suppress the disease activity is 10 mg/day; the treatment is continued, even if remission is evident, for more than 6 months. The alternative is treatment with Salazopirine 4-6g/day or, more modern, 5-aminosalicylic acid (Mesalazine) 3-4g/day.
In distal forms (rectosigmoidian) a local treatment with suppositories, foam or Salazopirine or 5-aminosalicyclic enemas may be  used, or topic corticoids (Budesonide).
In mild forms, a treatment with mesalazine 2-3g/day or Salazopirine 3-4g/day is administered.
In continuous chronic forms, the treatment is indefinite.
In discontinuous chronic forms, the acute episode is treated with higher doses, and with endoscopic and histological remission, it keeps up with Salazopirine 4-6 g/day or Salofalk 3-4 g/day.

c. Surgical treatment in case of toxic megacolon, when there is a perforation or an uncontrolled bleeding a total colectomy or proctocolectomy has to be done

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