A diverticulum (from Latin diverticulum – the road to the side) is a saccular protrusion of the wall of a tubular or hollow organ. A diverticulum can be congenital or develops under the influence of various reasons (damage to an organ wall, scarring, etc.).

Diverticulums in structure are:

True diverticulum, which consists of all layers of the organ wall. False diverticulum , in which only the mucous membrane protrudes.

Diverticulums are:

Congenital and Acquired ,
Pulsation (wall bulging in weakened places) and Traction (connective tissue fusion of the wall with surrounding tissues).

Acquired found in the second half of life. Congenital occur until 20-30 years. Acquired – false, innate – true. Most often, diverticulums of the digestive organs are found: the esophagus, duodenum, small intestines (the so-called Meckel diverticulum), large intestines, and also the bladder. Diverticulums of other organs are rare.

Due to the difficulty of emptying, the contents of the hollow organ are retained in the diverticulum (e.g., food masses in the esophagus diverticulum, fecal masses in the intestinal diverticulum), which can cause mesenteric inflammatory processes, ulcers, pressure sores, perforation, and, as a result, peritoneum inflammation, etc. Sometimes stones form in the diverticulum (fecal, urinary). Occasionally, a malignant tumor may develop in the diverticulum.

DIGESTIVE DIVERTICULES.

Esophagus diverticulum – protrusion of the wall of the esophagus, communicating with its lumen. Esophageal diverticulums are congenital and acquired, pulsion (bulging of the esophagus wall in weakened places) and traction (connective tissue adhesions of the esophagus wall with surrounding tissues).

Zenker diverticulum.
It is localized on the back wall of the pharynx and esophagus, characterized by esophageal dysphagia and regurgitation. The diagnosis is based on an x-ray of the esophagus with barium. Endoscopic examination is less informative and even dangerous. Treatment. More effective is surgical treatment – resection of the diverticulum followed by alloplasty.

Diverticula in the middle part of the esophagus.
The diverticulum of this localization accounts for 70-80% of all DPs. Diverticula with a diameter of up to 2 cm are usually not accompanied by subjective symptoms. Diverticulums, complicated by diverticulitis, are manifested by periodic pain behind the sternum, in the epigastric region, back (pseudostenocardia), dysphagia, regurgitation, subfebrile condition. The diagnosis is based on x-rays. X-ray studies can reveal not only large diverticula (more than 2 cm), but also small (less than 0.5 cm) up to intramural micro-diverticula. Treatment. Local treatment consists in drainage and lavage of the esophagus and DP with warm water. Severe diverticula are subject to radical surgical treatment.

THIN GUT DIVERTICULOSIS.

Diverticulums of the small intestine are more asymptomatic. Only occasionally do they lead to stasis of small intestinal contents (duodenostasis) , excessive bacterial growth and malabsorption (malabsorption). Perforation, inflammation and bleeding are observed much less frequently than with diverticulosis of the colon.

Duodenal diverticulum.
A single duodenal diverticulum is usually not accompanied by symptomatic manifestations and is accidentally detected during an X-ray examination.

Clinic.
It appears when there are complications: diverticulitis, ulceration in the cavity of the diverticulum, rupture of the diverticulum, stones, tumors. With a high diverticulum, the clinic resembles gastritis, ulcerative b-n. With a low location, it resembles intestinal obstruction . At the location in father papilli begins mechanical jaundice . At break – a clinic of phlegmon, penetration, bleeding. Treatment.

The correct fractional diet, food in small quantities, the correct position after eating ( pastoral drainage method ), after 5-6 hours do not eat.
Antacids
Antibiotics (tablets preferably) 8-10 days,
Vegetable laxatives, osmotic,
Enzymes
Duo-drains with a probe, insertion of a probe to a certain level. Soda, mineral water, novocaine are introduced through the probe .
In severe cases, if clinical symptoms do not stop with conservative methods, surgical treatment is recommended .

Meckel’s diverticulum.
2% of people have saccular protrusion in the terminal ileum, called Meckel’s diverticulum (DM), and of these, only 5% of people have clinical manifestations characterized by bleeding.

Bleeding from DM occurs in connection with its inflammation (diverticulitis). Patients usually lose a relatively small amount of blood. Diverticulitis and perforation of DM resembles acute appendicitis in clinical manifestations.
The diagnosis is based on x-rays. In this case, barium is introduced through a probe beyond the ligament of Treitz. Treatment. With complications, it is subject to surgical treatment.

Multiple small bowel diverticulums.
They are almost always located on the mesenteric margin and proceed in a similar manner, until their inflammation joins as a result of microbial contamination of these parts of the intestine. The diagnosis is based on an x-ray.

Treatment. Antibacterial treatment, as this causes excessive bacterial growth. In case of bleeding, for the purpose of diagnosis, angiography is performed, surgical treatment in specialized centers.

DIVERTICULAR PULMONICULAR DISEASE.

Colonic diverticulums are detected in 50% of people over the age of 50, but in most cases they are asymptomatic. Most often diverticula are found in the sigmoid colon, less often in its right parts and very rarely in the rectum. Diverticular colonic disease (DTI) includes protrusion of the intestinal wall (diverticulosis) and its inflammation (diverticulitis).

The diagnosis is based on x-rays . In these patients, diverticula are detected by chance during irrigoscopy for other diseases. Usually two rows of diverticula are found, one on each side of the intestinal wall between the mesentery and the mesenteric ribbons of the colon. When irrigoscopy along with diverticula reveals deformation of the intestinal wall, colonoscopy is also indicated to exclude other diseases of the colon. But colonoscopy should be carried out by experienced specialists in order to avoid the risk of perforation of the intestine affected by diverticulosis.

Clinic.

Regularly occurring pains in the left iliac region, disappearing after the act of defecation and continuing for several weeks, and sometimes several months. The same pain can sometimes appear in the mesogastrum and in the right iliac region.
Constipation associated with diverticulosis is usually characterized by the presence of feces in the form of balls with an admixture of mucus.
Bloating and abundant gas separation.
Dyspeptic disorders associated with concomitant hiatal hernia and cholecystolithiasis (Senta triad).
Rectal bleeding and the appearance of other intestinal symptoms (pain in the epigastric region, diarrhea, tenesmus) cannot be explained only by diverticulosis, without exception of other reasons.

Complicated diverticulosis of the colon.
Inflammation (diverticulitis), suppuration (abscessing), perforation, bleeding, obstruction (narrowing of the lumen of the intestine), fistula.

Pain, fever, leukocytosis, and an increase in ESR appear.
With an abscess, a painful tumor formation can be palpated and symptoms of intestinal obstruction (obstruction) can be detected.
Perforation of the diverticulum can manifest as peritonitis.

Treatment.

The inclusion of dietary fiber for constipation.
Antispasmodics and Prokinetics (debridate, meteospasmil, duspatalin, peppermint oil) can reduce pain.
You can not take stimulant laxatives, as they can increase pressure in the intestine and provoke pain.
You can use osmotic laxatives such as lactulose (if there is no intolerance) – 30-60 ml per day.

With complications.

With diverticulitis, bacteriological blood culture is performed ,
In / in the introduction of plasma substituting and detoxification solutions : reopoliglyukin, hemodesis, “disol” , etc.,
Antibiotics (metronidazole 500 mg and cefuroxil 750 mg 3 times a day),
Anesthesia (IM 1 ml of 2% Promedolum solution every 4 hours).
Surgical treatment is carried out with recurrent diverticulitis complicated by abscess formation, perforation, obstruction, bleeding and fistula formation

VIRAL HEPATITIS .

Viral hepatitis is an infectious disease of the liver that causes diffuse inflammation of the liver tissue. With hepatitis, the entire liver is involved in the inflammatory process and, as a result, liver functions are impaired, which is manifested by various clinical symptoms. Hepatitis can be infectious, toxic, medicinal and others . Viral hepatitis is one of the most common diseases in the world. In most cases, it proceeds subclinically and is diagnosed only on the basis of additional studies, including laboratory data. The range of clinical manifestations varies greatly.

ACUTE VIRAL HEPATITIS

Acute viral hepatitis can be caused by different types of viruses.
These include hepatitis A, B, C, E, D and other viruses.

Causes of Hepatitis.
Common causes of hepatitis :

Viral hepatitis A (enteral, by mouth),
Viral hepatitis B and C (parenteral, via blood),
Alcohol.

Less common causes of hepatitis :

Hepatitis E virus (enteric),
Epstein-Barr virus,
Medication.

Rare causes of hepatitis:

Virus hepatitis D (delta), cytomegalovirus, a virus is herpes simplex viruses, Coxsackie A and B, echovirus, adenovirus (Lassa), flavivirus (yellow fever), leptospirosis, rickettsia (tifus), chemical agents, toxins fungi.

Ways of infection. Infections are transmitted from a sick person to a healthy one. Hepatitis A – feces, saliva; Hepatitis B – blood, sperm, saliva, perinatal (infection of the child from the mother); Hepatitis C – blood; Hepatitis E – feces, saliva; Hepatitis D – blood, sperm. The incubation period varies greatly in duration . Hepatitis A – from 2 to 6 weeks; Hepatitis B – from 8 to 24 weeks; Hepatitis C – from 6 to 12 weeks; Hepatitis E – from 2 to 8 weeks; Hepatitis D – not established.

Symptoms of Acute Viral Hepatitis.

Epidemicity is typical for hepatitis A and E. The
prodromal (incubation) period is characterized by weakness, anorexia, aversion to tobacco, nausea, myalgia, and fever. These symptoms are more common in acute viral hepatitis and are rare in other hepatitis. When the appearance of jaundice symptoms prodromal period usually subside, often becomes dark urine, light stools, sometimes a skin itch, often in alcoholic hepatitis with cholestasis.

Extrahepatic manifestations, including arthralgia, arthritis and an urticarial rash, are usually found only with viral hepatitis B. With this form , the general state of health also worsens in the icteric period, in contrast to viral hepatitis A, in which the condition is icteric Patients are getting better.

Objective physical data.

Jaundice (anicteric forms are diagnosed only on the basis of laboratory data, including the determination of serum virus markers ).
Hepatomegaly (enlarged liver), liver on palpation of “soft” consistency.
There are no extrahepatic “signs” of chronic liver diseases (hepatic palms, vascular “stars” , etc.), with the exception of acute alcoholic hepatitis, which developed against the background of chronic or cirrhosis of the liver.
Splenomegaly is not characteristic of most acute hepatitis. It is often detected in acute hepatitis caused by the Epstein-Barr virus (infectious mononucleosis) and rickettsial infections.

Diagnosis of Viral Hepatitis.

Research.
Increased ALT and AST more than in 10 times higher than normal is a reliable test of acute hepatitis. Bilirubin rises in severe cases. Neutropenia is often detected in viral hepatitis, especially in the prodromal period. Hemolytic anemia is sometimes observed in acute viral hepatitis B. Severe cholestasis, characterized by jaundice and skin itching, is not characteristic of acute viral hepatitis, often occurs with alcoholic hepatitis. It is necessary to examine the level of alkaline phosphatase in the blood. With cholestasis, its level increases 3 times or more than normal.

Enzymatic diagnostics.
Determination of serum enzyme levels : transaminases, lactate dehydrogenases, amylases. The level of these enzymes increases with acute diffuse lesions, acute hepatitis, post-necrotic cirrhosis . A significant increase in these enzymes is also observed in some chronic hepatitis , with portal and biliary cirrhosis.

Serological studies.

All patients should investigate antibody to the virus of hepatitis A class Ig M and HBsAg.
HBeAg should be tested in HBsAg- positive patients to assess infectivity (virus relaxation phase).
D-antigen must be investigated in HBsAg- positive patients, in drug addicts and in severe hepatitis.
Tests for hepatitis C virus are performed if there are no serum markers for hepatitis A and B. There is an assumption of the existence of other forms of viral hepatitis (F, G), i.e. neither A nor B nor C.

Instrumental diagnostics.

Ultrasound: diffuse lesions, focal changes.
Laparoscopy In severe cases, in case of urgent need, a biopsy is taken and under control .
X-ray is of less importance, but in some cases is performed.
Palpation, definition of contours. Riedel share . In asthenics, the edge of the right lobe in the form of a tongue hangs down. This is a fraction of Riedel, which can be mistaken for a tumor, a vagus kidney, gall bladder. The clinic has a decisive diagnosis: examination, palpation, percussion, complaints.

Outcomes.
Complete recovery from acute hepatitis usually occurs within a few weeks, less often months. Fatigue and anorexia (lack of appetite) often persist in most patients for a long period. Acute viral hepatitis B, C and D often turn into a chronic form. Fulminant hepatic failure due to massive necrosis, almost never is not the case with viral hepatitis A and meets with about 1% of cases of viral hepatitis B, 2% of viral hepatitis C and more often in viral hepatitis D. Acute hepatitis sometimes characterized by a relapsing course. The most unfavorable outcome of acute hepatitis is chronic disease.

TREATMENT OF ACUTE HEPATITIS.

There are no specific treatment methods and therefore most patients undergo basic treatment (see treatment of chronic viral hepatitis, below).

Bed rest is not mandatory for most patients.
Careful observance of personal hygiene (hand washing, separate dishes, etc.).
Hospitalization is necessary in severe cases of the disease and in the absence of the possibility of ensuring the regimen at home. Caring for patients should include measures to avoid transmission of infection (disinfection, work gloves, etc.)
A strict diet is not necessary, but you need to exclude fats from the diet , drink juices.

Contact with sick persons.

With viral hepatitis A, people in contact with the patient, usually by the time of jaundice, may already be infected and therefore do not need isolation and treatment . For prophylactic purposes, it is possible to administer IM administration of human Ig (5 ml once).
Sexual partners of patients with viral hepatitis B are subject to examination with determination of serum markers and in their absence, these persons are shown the introduction of the Recommended HBV vaccine. Perhaps the introduction of hyperimmune HBV immunoglobulin in 2-4 weeks.

Observations of patients after acute hepatitis.

Abstinence from alcohol intake to the full normalization of liver function (normalization of AlAT, AsAT, GGTP , etc.), but a small amount of alcohol (4-8 servings per week) does not adversely affect the course of the recovery period. Complete abstinence from alcohol is necessary only for alcoholic hepatitis.
Moderate physical activity may resume after the symptoms of the disease disappear.
A second study of liver enzymes, mainly AlAT and AsAT, is carried out after 4-6 weeks from the onset of the disease, and if they remain unchanged, then they are repeated in 6 months later. Increased transaminases more than a 2-fold after 6 months, is the basis for carrying out in-depth studies, including liver biopsy.

Immunization.
Hepatitis A.
Passive immunization / m introduction of 5 ml of normal human Ig is effective during 4 months. It is carried out for preventive purposes. 1. Persons traveling to epidemiological regions (Indonesia, the Middle East, South America, Mexico , etc.). 2. Persons in; close contact with patients.

Hepatitis B.
Passive immunization is carried out to persons in close contact with patients. In / m administration of hyperimmune HBV immunoglobulin 500 IU twice with an interval of 1 month.

CHRONIC VIRAL HEPATITIS.

Chronic Viral Hepatitis B.

It develops in the outcome of acute viral hepatitis B. The hepatitis B virus (HBV) does not have a cytopathogenic effect on hepatocytes, and their damage is associated with immunopathological reactions. The dramatic enhancement of the immune response leads not only to the massive damage to the liver parenchyma, but also to the mutation of the genome of the virus, resulting in further to the hepatocyte destruction in for an extended time. Possible effects of the virus and is the liver: mononuclear cells, the sex glands, thyroid gland, salivary gland (immunological aggression). Symptoms of CVH- B. Associated with asthenovegetative syndrome (weakness, fatigue, nervousness, etc.), weight loss, transient jaundice, hemorrhages, pain in the right hypochondrium, dyspeptic disorders (bloating in the abdomen, flatulence, unstable stool , etc.). In some patients with low activity, the disease may be asymptomatic. Of the objective symptoms – hepatomegaly. The appearance of “spider veins”, hepatic palms, splenomegaly, itchy skin , transient ascites indicates, as a rule, transformation into cirrhosis of the liver (CP). In a small number of patients with CVH-B , extrahepatic systemic manifestations (arthritis, vasculitis, nephritis, “dry syndrome” , etc.) are detected . There may be an increase in ESR and lymphopenia, an increase in the level of serum aminotransferases (up to 2-5 or more norms in proportion to the activity of inflammation), high hyperbilirubinemia, hypoalbumin and hypoprothrombinemia, choleraemia, an increase in alkaline phosphatase (not more than 2 norms) and gamma globulins. Virus replication phase markers (HbeAg, anti-HBg Ig M, DNA virus) are detected in serum .

Chronic Viral Hepatitis C

It develops in the outcome of acute viral hepatitis C, chronicity in 50% of patients. The virus has a cytopathogenic effect on hepatocytes . Symptoms of CVH-C . Most patients are characterized by moderate asthenic and dyspeptic syndromes, hepatomegaly. The course of the disease is wave-like with episodes of deterioration, when hemorrhagic manifestations ( nosebleeds, hemorrhagic rash), moderate jaundice, pain in the right hypochondrium, etc. appear on this background . CVH-S can remain in active form for up to 10 years or more without transformation into CP. Extrahepatic manifestations can usually occur during the transition to CP. There is an increase in the activity of aminotransaminases, the level of which fluctuates, not reaching a 10-fold increase even during a period of noticeable deterioration of the patient’s condition , and moderate and transient hyperbilirubinemia are occasionally noted . Identification of the RNA virus and antibodies to it confirms the etiological role of hepatitis C.

Chronic Viral Hepatitis Delta (D) .

The disease is the outcome of OVH-D, proceeding in the form of superinfection in patients with CVH-B. Virus D has a cytopathogenic effect on hepatocytes , continuously supports activity and, consequently, progression of the pathological process in the liver, suppresses hepatitis B virus replication . Symptoms of CVH-D . Most have a severe course with severe symptoms of liver cell failure (severe weakness, drowsiness during the day, insomnia at night, bleeding, a drop in body mass , etc.). At most there is jaundice, itchy skin. The liver is usually enlarged, but with a high degree of activity, its size decreases. Often patients appear systemic lesions. In most cases, the disease acquires a progressive course with the rapid formation of CP. The study revealed necrosis of the parenchyma. In the blood , there is a constant increase in the activity of aminotransferases, bilirubin, less often alkaline phosphatase (usually not more than 2 norms). In most of the detected mild hypergammaglobulinemia, disimmunoglobulinemiya, increased erythrocyte sedimentation rate. When transitioning to CP in the blood , markers of integration of hepatitis D virus and antibodies to it (Ig G, Ig M) are detected .

TREATMENT OF CHRONIC VIRAL HEPATITIS.

All patients undergo basic therapy, antiviral therapy. The main components of basic therapy are diet, regimen, exclusion of alcohol, hepatotoxic drugs, vaccination, saunas, occupational and domestic hazards, treatment of concomitant diseases of the digestive system and other organs and systems.

The diet should be complete: 100-120 g of protein, 80-90 g of fat, of which 50% are of vegetable origin, 400-500 g of carbohydrates. When prescribing a diet, it is necessary to take into account the individual habits of the patient, tolerance of food products and concomitant diseases of the digestive system.
Course treatment with antibacterial drugs that are nonabsorbable and have no hepatotoxic effect (one of the following drugs is streptomycin sulfate, chloramphenicol stearate, kanamycin monosulfate, phthalazole, sulgin inside, 5-7 days).
With the subsequent use of biological preparations ( bificol , lactobacterin, bifidum-bacterin, bactisubtil – one of the drugs) for 3-4 weeks.
Simultaneously administered Enzyme preparations , does not contain bile acids, which have a damaging effect on the hepatocytes.
Detoxification measures. 1) intravenously administering to 200-400 ml gemodez for 2-3 days, 2) Inside Lactulose (Normase) 30-40 ml 1-2 times a day, 3) Did 500 ml of 5% w / w Glucose solution Vitamin C 2-4 ml and Essential 5.0 ml. The duration of basic therapy is an average of 1-2 months.
Antiviral therapy.
The leading role in antiviral therapy belongs to Alpha-Interferon , which has immunomodulating and antiviral effects – inhibits the synthesis of virus proteins, enhances the activity of natural killers. It is indicated for B and hepatitis C. Uses for the purpose of Interferon Alfa: Absolute: a chronic course, the presence of serum blood HBV (HbeAg replication markers and HBV- DNA), increased levels of serum aminotransferases more than a 2 fold. Doses and treatment regimens depend on the activity of the process, the level of serum DNA of HBV.
Pegasis is indicated for viral hepatitis B and C. It is used for combination and monotherapy.
Zeffix (Lamivudine) is highly active in viral hepatitis B.
Rebetol, in combination therapy with Alpha-Interferon for viral hepatitis C.
Copegus, in combination therapy for viral hepatitis C with Alpha-Interferon and Pegasis.