Medicine

LECTURES

LECTURES 5.

 

Surgical infection classification.
- Acute suppurative disease of purulent tissues: abscess, furuncle, carbuncle, hydradenitis, mastitis, erysipelas, lymphadenitis, lymphangitis, paraproctitis. Acute hematogenous osteomyelitis.
- The acute specific surgical infection. Gas gangrene. Tetanus. Diphtheria of wounds. Anthrax.
- Chronic specific surgical infection. Tuberculosis. Actinomycosis. Syphilis. The general purulent infection. SIRS. Sepsis.

 

Abscess (abscessus) - Separated by a collection of pus in the different tissues and organs due to purulent fusion of tissues and the formation of cavities (unlike empyema in which the accumulation occurs in the natural body cavities and hollow organs).

 

Etiology and pathogenesis. Pathogens purulent infection is staphylococcus - monoculture or in association with other microbes (Escherichia coli, streptococcus, Bacteroides, and others.).

Pathogen infection usually enters from outside (exogenous infection), although possible and endogenous infection - penetration with neighboring or distant organs, metastatic abscesses with sepsis. The cause of the abscess can be input into the tissue kontsentrovannyh solutions of drugs - 25% solution of magnesium sulfate, 24% solution kordiamin, 50% solution of aspirin and others. Purulent inflammation that develops, leading to melting of tissues, and sometimes to the exclusion of necrosis and gangrenous tissue-sequestration. Sequestration could face further enzymatic melting.

Abscess cavity can be as simple rounded and complex, with numerous pockets. The walls of the abscess initially covered with purulent fibrinous layers and remnants of necrotic tissue. Then, on the periphery of the abscess developing area of ​​inflammation, which leads to the formation of pyogenic membrane, surrounded by connective tissue.

Formed as a result of purulent or aseptic inflammation abscesses have different resolution: spontaneous dissection of breakthrough outside (abscess subcutaneous fat, muscle abscess, mastitis, paraproctitis etc..) Perforation abscess in a closed cavity (peritoneal, pleural, in the joint space and so on.) with the development of septic processes (peritonitis, pleurisy, pericarditis, arthritis, etc.). Possible ulcer perforation into the cavity of communicating with the external environment (the cavity intestine, bladder, etc.).. Abscess cavity, which freed, under favorable conditions, reduced in size, and subjected spadayetsya scarring, with incomplete released, the process can go into with chronic fistula formation at the place of abscess.

 

Clinical manifestations and diagnosis. When superficial acute abscesses marked redness, swelling, pain, local temperature increase, dysfunction, sometimes referred floktuatsiya. Inflammation may hold a different area. Character pus abscess (texture, color, smell) contained in the cavity, determined by the type of agent: stinky smell, dirty-gray pus typical putrefactive flora thick yellow-green pus - for staph, blue-green color and sweet smell - for blue-purulent sticks etc.

Common clinical manifestations abscess: fever of sub-febrile to high, malaise, weakness, loss of appetite, headache. In the peripheral blood - leukocytosis with a shift neutrocytosis and leukocyte formula. ESR increased.

 

abscess of neck

 

Left thigh abscess in a patient with diabetes

 

SEVERE abscess dominated phenomena of intoxication may be due as absorption of toxic products from the lesion (purulent resorptive fever), and the development of sepsis (see Sepsis).

Abscess should be distinguished from the hematoma, cysts, tumors that fail. Of great importance is the diagnostic puncture: a manure allows, in addition to establishing the diagnosis in doubtful cases to bacteriological examination - abjection and determine its sensitivity to antibiotics.

If aerogenous flora in the oral abscess may form and accumulate gas - gas abscess. Percussion over the area abscess appears timpanichesky sound, X-ray images of the abscess cavity defined by gas bubbles and horizontal fluid level below it (usually occurs when an abscess caused by septic infection).

Treatment consists in opening the abscess, drainage and emptying his mouth. Not subject to section cold abscesses of tuberculous etiology due to superinfection, which inevitably occurs while hnoyeridnoyu microflora. A small abscess formed, with well-defined capsule removed completely.

For opening an abscess choose the shortest line access including anatomical features and topography of the body. Often used method of opening the abscess by needle, first punktuyut abscess, then the needle cut through tissue. The autopsy abscess possibly suited to its lower pole to create good conditions for drainage.

In order to reduce infection operative field in the course section abscess surrounding tissue carefully isolated gauze napkins and making a small hole in the wall of the abscess, remove manure electric pumps. Aspiruvavshy pus incision expand, the abscess cavity examined finger, sharing existing bridge is removed sequesters tissue. Avoid rough manipulations that violate pyogenic membrane. Abscess cavity was washed with antiseptic solution, then draining one or more rubber or PVC tubes or injected into her gauze swabs soaked solution of proteolytic enzymes and antiseptics. With insufficient emptying of the abscess through the main incision is made additional - counterpuncture. Treatment abscess after opening conducted on the principle of treatment of purulent wounds.

General treatment includes strengthening therapy, blood and plasma, antibiotics considering the sensitivity of the microbial flora of specific therapy (staphylococcal toxoid immunization, the use of specific y-globulin, etc.)..

 

Phlegmon - acute diffuse purulent inflammation of adipose tissue, not prone to separation. Depending on the location distinguish subcutaneous, intramuscular, retroperitoneal phlegmon and others of its species. A sharp localizations are some special names: purulent mediastinitis paraproctitis, paranefryt, paraartykulyarna abscess and others. A sharp that developed as a result of the transition of purulent inflammation of lymph nodes, called adenoflehmonamy. A sharp prone to spread klitkovynnyh spaces, vascular bed, fascial cases.

Phlegmon of the left tibia

 

Etiology and pathogenesis. Causative agent of the disease is different hnoyeridni microorganisms (Gram-positive and Gram-negative, aerobic and anaerobic), but more often - staphylococci, streptococci, enterobacteria, Proteus, E. coli. Microorganisms penetrate into the fatty tissue directly or hematogenous routes. Possible formation of secondary abscess - spreading suppurative inflammation in adipose tissue with osteomyelitis (parakistkova abscess), septic arthritis (paraartykulyarna abscess), pyelonephritis (paranefryt) and others.

Development phlegmon begins with serous infilfatsyiyi subcutaneous fat. Fluid rapidly becomes purulent character, formed areas of necrosis, which are then merged. Necrosis and melting fat lead to abscess phlegmon.

Changes in the tissues under phlegmon depend on the nature of the pathogen: putrefactive anaerobic infection and lead to tissue necrosis with the formation of bubbles of gases. When coccal microflora is purulent fusion of fabrics. The inflammatory process in phlegmon has no tendency to limit, as observed by an abscess, and distributed in the intervals between klitkovynnyh connective tissue.

Inflammation in adipose tissue is certain stage of development, starting with serous edema, with subsequent formation of an inflammatory infiltrate with subsequent tissue necrosis.

 

Phlegmon tibia in a patient with abnormal streptococcal

 

Adenoflehmona right groin in a patient with diabetes

 

Clinical manifestations and diagnosis. Signs phlegmon are the same as the symptoms of inflammatory processes (fever, fatigue, malaise, headache). They determine complaints of patients who also noted pain and swelling at the site of inflammation, pain with movement, change of body position.

Local manifestations subcutaneous phlegmon characterized classical signs of inflammation. Swelling usually increases, the skin over it red, shiny, then gradually fades and becomes a normal color. Palpation determined painful compression without clear boundaries, real, hot to the touch. When abscess phlegmon can determine softening infiltrate symptom fluctuations. Regional lymph nodes are enlarged, painful. In some cases around infilfatu defined mesh red stripes or bands (mesh or tubular, lymphangitis).

Active and passive movements of the limbs, head turns, changes in body position caused a sharp increase in pain in the phlegmon.

 

When deep-seated (intramuscular) phlegmon limbs, its volume increases as compared with the healthy. Measurement measuring tape can accurately determine volume increase limb. Sometimes there is a protrusion of tissue in the area of ​​phlegmon. Palpation defined deep, sharply painful infiltration. Movement of limbs sharply painful, sometimes there is protective (painful) contractions of the muscles in the form of involuntary limb position in which pain is expressed to a lesser extent. Regional lymph nodes are enlarged and painful. Detection by puncture pus confirms the diagnosis of deep intermuscular phlegmon.

On the neck with mild clinical symptoms of purulent inflammation may be determined infiltrate woody texture with bluish color of the skin over it - woody phlegmon. Infiltration malobolyuchyy, fused with the skin, fascia, aponeurosis, absolutely motionless, gradually increasing in size. Suppuration infiltrate observed rarely. Latent disease occurs, the body temperature low-grade, mild symptoms of intoxication.

 

Treatment phlegmon operative. Only in the initial stage, the expected serous inflammation acceptable conservative treatment: bed rest, rest the affected limb, antibiotykoterapiya, UHF-therapy, electrophoresis of chymotrypsin. Effective novocaine blockade packs with antibiotics Vishnevsky. Improve the general condition of patients, reducing local inflammation are favorable signs that indicate a separation or reverse the development process. If no effect within 12-24 minutes or progression shown in operation.

In urgently operated patients admitted late with severe intoxication, progressive process, the presence of purulent inflammation. Under anesthesia conducted autopsy cellulitis, manure removing necrotic tissue. Reveals swelling and pus pocket wound thoroughly washed with antiseptic solutions, drain. To ensure good drainage sometimes make additional cuts - counterpuncture. Treatment after surgery is performed on the basis of treatment of purulent wounds.

 

 

Localization of purulent processes in the skin and subcutaneous tissue (Fig).

1 - anthrax, 2 - hydradenitis 3 - boil, 4-erysipelas, 5 - abscess subcutaneous tissue.


Folliculitis - purulent inflammation of the hair follicle. Available as single and multiple lesions. They are located in any area of ​​the skin where there is a long, well-developed vellus hair.

 

Etiology and pathogenesis. Development of folliculitis is caused mainly Staphylococcus aureus. Penetration of bacteria in the hair sac in disturbed outflow contents causes inflammation. Development folliculitis contribute exhaustion, colds, vitamin deficiency, chronic diseases, metabolic disorders.

 

Clinical manifestations and diagnosis. Folliculitis is a small cone-shaped pustules that appears on the skin, in the center of which is hair. Pustules surrounded by a narrow strip of flushing. Around the small pustules palpable infiltration. After reducing signs of inflammation produced purulent crusts, which vidpadayuchy leaves little morning with red shiny surface. After epithelialization remains for awhile stain bluish-pink. With the localization of follicles on the scalp are determined inflammatory nodes that merge together. Rozm'yakshuyuchys, infiltrates leading to the formation of deep purulent moves. After recovery still infiltrates remain severe scarring.

 

Treatment. Excluded, baths and even moisture follicles. Recommended observance of safety measures. The skin around fires wipe 2% salicylic alcohol, hair short obstryhayut. Follicles reveal a sterile needle and treated with iodine tincture, green diamond to form crust.

In chronic folliculitis being treated comorbidities, antibiotic therapy, immunotherapy, vitamin correction metabolic (eg, diabetes). Use physiotherapy equipment - UV-irradiation of the lesion, electrophoresis of staphylococcal phage or antibiotics to the affected area, diadynamic lesion area and others.

 

Boil (furunculus) - acute necrotic inflammation of the hair follicle, sebaceous gland and surrounding subcutaneous fat. The most frequent localization is boils back of the neck, forearms, back of the hand, hip. The appearance of 2 or more boils shows abrasions. In the occurrence of boils play a role microtrauma, such scratches skin in diseases involving itching.

 

Etiology and pathogenesis. The most common pathogen is Staphylococcus aureus furunculosis, at least – purulent other microbes. Favorable conditions for furuncle is a weakening of the body, metabolic disorders (often diabetes), vitamin deficiency, skin diseases. Development boil begins with festering pustule formation: after distribution of micro hair follicle in the papillary layer of the skin there is an inflammatory infiltrate. The center infiltrate formed foci of necrosis (necrotic core), around the accumulated manure. After exclusion of pus and necrotic skin defect rod filled with the subsequent formation of granulation tissue.

Patients with early disease complain of the appearance of abscess (pustule) or painful compression in the thickness of the skin. With an increasing inflammation align complaints malaise, fever, pain in the seal increases. The most severe pain is the localization boil on the skin are closely adjacent to neighboring tissues: on the scalp, neck, ear canal, dorsum of fingers.

 

Furunculus face under abscessed

 

Furunculus forearm, which was complicated by phlegmon forearm

 

Clinical manifestations and diagnosis. On examination of patients with early disease in inflammation is a small abscess (pustule) with hyperemia of the skin around. Less can be found in the thick seal skin and flushing of skin thickening, abscess while absent. As the boil formed infiltrate cone rises above the skin, with a diameter of 0.5-1.5 cm, with no clear boundaries. The skin over it purplish-red color. In the center of infiltration appears crusty area of ​​softening, from the peel allocated a small amount of pus. After removal of pus in the center infiltrate defined area of ​​green fabric - top necrotic rod. With the formation of necrotic rod of purulent discharge increases with pus and blood is separated and refill. In the center of infiltration after removal of the rod appears fairly deep wound, which quickly filled with granulation and healing in 2-3 days to form embroiled scar that moderate bleeding.

Sometimes when viewed on the site furuncle defined globular swelling, softening, slight purulent discharge. This abscesses boil, formed as a result of complete meltdown purulent necrotic rod and violation of the outflow of pus.

Identified during the inspection of the skin of patients with red stripes running from the boil, suggest joining lymphangitis, increased tenderness to palpation of regional lymph nodes - to join lymphadenitis.

When localization boil on the face (Fig. 97) - the upper lip, eyelids, eyebrow arches - patients sometimes complain of a severe headache, high body temperature, which are signs of complications boil purulent thrombophlebitis facial veins. The latter is sometimes accompanied by a purulent meningitis due to the transition of inflammation in the veins of the face through a vein in the eye cavernous sinus.

Joining such symptoms as intermittent fever, chills, excessive sweating, delirium, dizziness, pale skin, indicating the occurrence of sepsis, and the appearance of abscesses in other organs (metastatic abscesses) confirms the diagnosis septikopiemia.

 

Treatment of furuncle conservative. Patients should be warned about the potentially serious complications of pressing boils, pustules a razor cutting, use warming compresses. At the onset of the disease is treated skin 70% ethanol, 2% salicylic alcohol, spend UHF therapy. After opening the boil make bandages with proteolytic enzymes, hypertonic sodium chloride, used UVR. After removing the rod impose ointment dressings with sintomitsinovoy emulsion metyluratsylovoyu ointment. When complications boil lymphangitis and lymphadenitis shown antibiotic.

    Patients with facial boils subject to urgent hospitalization in the surgical ward, where the local and general treatment, including antibiotics. Patients prescribed bedrest, pureed food.

When abscess furuncle conduct surgical treatment - opening the abscess.

In rare recurrent boils and abrasions require the examination of patients that can detect metabolic disorders (diabetes, vitamin deficiency). In order to increase resistance to infection transmitting staph staphylococcus toxoid immunization.

 

Carbuncle - acute diffuse necrotic inflammation of several hair follicles and sebaceous glands, accompanied by the formation of general infiltration and necrosis of the skin and subcutaneous tissue due to thrombosis.

Etiology and pathogenesis. The most frequent pathogen anthrax, Staphylococcus aureus, at least - streptococcus, sometimes - mixed infection (staphylococcus and streptococcus). Factors predisposing to the development of carbuncle is weakening the overall resistance of the organism with debilitating diseases, hypo-and avitaminosis, metabolic diseases (diabetes).

The main localization carbuncle - back of the neck, neck, upper and lower lip, back, back.

The disease begins with the appearance of infiltration, covering multiple hair follicles and sebaceous glands. There circulatory disorders caused by local thrombosis with the formation of necrotic skin, subcutaneous tissue, sometimes hlybsheroztashovanyh tissues. Together with necrosis occurs purulent fusion of fabrics and oozing pus through the openings of hair follicles. After rejection formed festering wound of deep tissue defects which healing occurs by secondary intention.

Clinical manifestations and diagnosis. Patients complain of severe pain, the presence of painful infiltrate, fever, chills, malaise, fatigue, weakness, loss of appetite, headache. In compiling the history clarify the possible presence of diabetes, beriberi, depletion.

When examining patients, but general signs of purulent inflammation (increased body temperature, increased heart rate), it turns blue and Scarlet swelling in the back of the neck, back, lower back, face, at least - the extremities. At the onset of the disease may be several infiltrations, which are then joined together to form a pronounced swelling, which rises above the surface of the skin. The skin over the infiltrate intense, brilliant, with intense blue-purple color in the center to the periphery, it gradually fades. On the surface infiltration determined several purulent necrotic pustules that are in the center merge together to form extensive skin necrosis. Thinned area of ​​necrosis breaks in several places to form holes (symptom "sieve") who stands manure. Infiltration dense, sharply painful around it - pronounced swelling of tissues. Regional lymph nodes are enlarged and painful (lymphadenitis), rarely observed lymphangitis.

With self-rejection tissues nekrosis, center infiltrate produce large cavity, covered with gray-green necrotic tissue with abundant Department manure.

 

Carbuncle face

 

If the observation of the patient revealed an increase in tissue edema, progression of necrosis, and increased symptoms of intoxication (tachycardia, headache, weakness), chills, excessive sweating, lymphangitis, lymphadenitis, thrombophlebitis, it should be regarded as unfavorable carbuncle, the development of cellulitis, sepsis.

Especially dangerous is anthrax through face may develop meningitis.

 

Autopsy carbuncle (a) and amputation of necrotic tissue (b)

 

Carbuncle should be differentiated from sybirvyrazkovym anthrax, characterized by the presence of hemorrhagic blisters, no purulent discharge, painless infiltration, pronounced swelling of tissues, necrotic tissue black, formed, and surrounded by small bubbles with hemorrhagic content. In content bubbles are sybirkovu stick.

Treatment of carbuncles in early stages conservative. It includes the complete rest of the affected organ. When carbuncles face patients required bed rest. They prohibit talking, prescribe a liquid diet. After processing carbuncle 70% ethanol impose aseptic bandage appoint UHF-therapy. Parenteral antibiotics administered orally - sulfanilamidnye long-acting drugs. When carbuncles in patients with diabetes, the necessary correction of metabolic disorders, careful of insulin, which reduces the development of the inflammatory infiltrate and necrosis.

Failure of conservative therapy within 2-3 days, increase necrosis, purulent intoxication are indications for surgery, which is done under general anesthesia. Cut crosswise cut through infiltration to cut off the fascia and necrotic tissue throughout, separating them from the fascia, skin, revealing purulent edema (Fig. 99). Bleeding with minor (vessels in the inflammatory infiltrate trombovani), it stops when injected into the wound swabs with hypertonic saline or with proteolytic enzymes.

 

Large carbuncle back, in a patient with newly diagnosed diabetes

 

On the face of anthrax reveal linear incision after the abscess. Postoperatively treatment carbuncle conducted on the principle of treatment of purulent wounds for removing necrotic tissue used proteolytic enzymes.

When to start treatment promptly carbuncle prognosis is favorable, but in depleted patients with severe diabetes, as well as anthrax face does not exclude the possibility of a bad outcome.

 

Hidradenitis - purulent inflammation apokrynes sweat glands.

Etiology and pathogenesis. Gidradenity caused mainly Staphylococcus aureus, which penetrates through the excretory ducts of sweat glands. Precipitating factor for the development of the disease are non personal hygiene, excessive sweating, skin contamination, skin diseases (dermatitis, eczema).

In sweat glands develop inflammatory infiltration of tissues with subsequent purulent melting.

Clinical manifestations and diagnosis. An examination of patients is painful swelling - often in the underarm, at least in the groin or perianal areas (locations apokrynovyh sweat glands). From history we can determine the presence of triggering factors: increased sweating, rules of hygiene, the use of depilatories, shaving hair in the armpits.

Disease begins acutely, with the appearance of small painful nodule that increases in diameter of 1-2 cm and sharply above the surface of the surrounding skin.

On examination, marked swelling purplish-red color. In engaging in the process of the sweat glands several nodes merge into dense infiltrate, which can hold all the armpit. Single units are superficially fused with the skin. After 10-15 days in the heart swelling appears softening, defined fluctuant with infiltration, disclosed, begins to stand creamy pus. After discharge of pus occurs with the formation of scar healing. The disease can recur.

In engaging in the process of surrounding subcutaneous fat may develop abscess, with involvement of lymph nodes - lymphadenitis.

Unlike boil speaker infiltration has follicular pustules and necrotic center. For axillary lymphadenitis specific location deep infiltration, enlarged lymph nodes, lack of cohesion tumor lesion of the skin.

 

Purulent hydradenitis left axillarise area.

 

To treat gidradenitis using antibiotics, long-acting sulfonamides. Spend staphylococcal toxoid immunization. In the armpit shaved off the hair, skin rubbed with alcohol, cologne, smeared 3% solution of brilliant green. Apply physiotherapy - UHF, UV-irradiation.

When abscess gidradenitis conduct surgery, autopsy abscess manure. With prolonged unsuccessful treatment gidradenity and the threat of sepsis divide all the fatty tissue in the armpit, as in anthrax.

 

Mastitis - inflammation of the parenchyma and interstitial tissue of the breast. Acute mastitis is mainly found in the first 2 weeks postpartum in women who are fed milk - postnatal (lactational) mastitis, at least - in women who are not breast-feeding and very rare - in pregnant women. The incidence of puerperal mastitis ranges from 1.5 to 6% (relative to the number of births). Occurrence of mastitis contributes to change the species composition of agents of purulent infection, their antigenic properties and resistance to antibiotic . Usually mastitis develops in one breast, bilateral mastitis is rare.

Classification of mastitis

I. Swollen form.

II. Infiltrative form.

III. Suppurative destructive form.

1) abscesses mastitis;

2) phlegmonous mastitis;

3) gangrenous mastitis.

 

Etiology and pathogenesis. Causative aureus mastitis is often in the form of monoculture and in association with E. coli and streptococcus, at least - in the form of isolated E. coli or Streptococcus, sometimes found Proteus, Pseudomonas aeruginosa, anaerobic flora, fungi. There are also specific forms which are rare, mastitis - tuberculous, syphilitic. The source of infection is bacteria carriers and patients with sore forms purulent-inflammatory diseases that surround the patient. Of primary importance in causing mastitis is nosocomial infections.

Purulent lactation mastitis

 

Input Worth infection is often cracked nipples. Can also intrakanalikulyarne of infection during breastfeeding or pumping milk, rarely spread of infection is hematogenous and lymphogenous ways of endogenous foci of infection. The presence of pathogenic bacteria on the skin and nipple of the mother, as well as in the mouth of the child does not always lead to mastitis. Contributing points for disease development is the weakening of the mother comorbidities, lower immunobiological reactivity, Running across a difficult childbirth (especially the first or large fruit), various complications of childbirth and the postpartum period (bleeding, infection of the birth canal, and others.). A major factor predisposing disease, is a violation of the outflow of milk from the development of its stagnation, which often occurs in childbirth due to lack of milk ducts, irregular structure nipples and functional disorders of the breast. When ingested bacteria in enhanced milk ducts milk thickens, wall ducts swell, which increases galactostasia and if damaged ductal epithelium promotes penetration of microbes in tissue cancer.

Features purulent process in glandular organs are mild ability to its differences and almost unlimited proliferation involving inflammation is more glandular tissue. This distribution often does not stop at opening fire and then created more new abscesses in the parenchyma of the gland.

The inflammatory process in the gland may be limited by inflammation of mammary ducts (halaktoforit), which is accompanied by milk, whether pus or inflammation of glands in the areola area (areolit). During the transition process in the tissue and its development can be consistently observed phase serous and purulent inflammation, often with marked destructive changes. In the phase of serous inflammation of the gland tissue soaked with serous fluid around the vessels observed accumulation of leukocytes. With the progression of inflammation serous impregnation breast parenchyma changes diffuse purulent infiltration with small foci of purulent fusion, which later merged to form abscesses. Recent dramatic thinning due mizhchastochkovyh walls caused by inflammation and increased secretory apparatus during lactation may coalesce and burst into subcutaneous tissue or retromamarnyy space.

The most frequent localization of ulcers - intramamarna, subareolyarna. When the location of the abscess in pieces on the back of the gland it can be opened in klitkovynnyy space behind it to form a rare form - retromamarnoho abscess. Sometimes due to involvement in the inflammatory process vessels and thrombosis following necrosis of individual sections of cancer developing gangrenosum form of mastitis.

Underlying chronic suppurative mastitis is the formation of small abscesses with marked induration of the surrounding tissues. He develops as a result of improperly conducted the treatment of acute mastitis (irrational antibiotic use by local re-entered them in the inflammatory infiltrate).

There are acute and chronic mastitis. Inflammatory processes may wonder predominantly parenchyma (parenchymal mastitis) or breast interstitium (interstitial mastitis). However, the distinction between these forms on the basis of clinical data is not practically possible, the more frequently they are combined with one another.

For practical purposes, is the most appropriate clinical classification of acute mastitis in view of inflammation: serous (initial stage), acute infiltrative and destructive - abscesses, abscess, gangrenous. In the group of chronic mastitis distinguish purulent and purulent form.

 

Clinical manifestations and diagnosis. Early diagnosis of early forms of mastitis and promptly started treatment in most cases to achieve the reverse of the process, prevent its transition in purulent, destructive phase.

Acute inflammation in the mammary gland must be differentiated from acute congestion of milk. In women after the first birth galactostasia meets 2 times more often. Patients complain of heaviness and tension in the gland that gradually increases. Tumor formation corresponds contours lobules of the breast, it is quite moving, with clear boundaries, uneven surface, painless. When you click on him milk secreted freely pumping painless. After racking comes relief. Overall condition is deteriorating slightly, body temperature, clinical blood tests often are normal. Acute galactostasia more often bilateral and develops in terms of the flow of milk (3-5-day after birth).

 

 

Localization ulcers with mastitis.

1 - subcutaneous, 2 - intramamary

3 - retromamary 4 - halaktoforit.

 

Distinguished initial forms of acute mastitis milk stagnation is not always easy, so any swelling of the breast that occurs with fever should be considered stage serous mastitis. This allows time to start treatment and prevent the transition process in purulent phase.

With the penetration of purulent microflora galactostasia 2-4 days becomes inflammation - phase serous mastitis. Disease begins acutely with chills, fever, sweating, weakness, weakness, sharp pain in the gland. The gland is enlarged, painful on palpation, infiltration is defined clearly. Pumping milk painful and brings relief. In blood leukocytosis to 10,0-12,0 - 109 / l ESR 20-30 mm / h. In late begun treatment within 3-6 days process can go in infiltrative phase with severe clinical signs of inflammation, severe general condition. There is a rise in body temperature to 38-40 degrees. Palpable tumor formation has sharper contours.

The inflammatory process leads to changes in the acidity of milk toward increasing pH, which is associated with increased activity of alkaline phosphatase. Microscopic examination of the cellular composition of breast secretions determined by a large number of leukocytes.

Go early forms of mastitis in purulent inflammation phase characterized by increased general and local symptoms of inflammation. Body temperature is constantly high or hectic nature. Infiltration in the gland increases, flushing of the skin increases, fluctuations appear in one of the areas of cancer.

Critical condition of patients observed in the form of gangrenous mastitis: the body temperature rises to 40-41 ° C, heart rate - up to 120-130 per minute, sharply increased breast, skin swelling, with bubbles filled with hemorrhagic content, with areas of necrosis. Swelling spreads to surrounding tissues. In the blood - high leukocytosis with a shift to the left and leukocyte toxic grit leukocytes, protein appears in the urine.

The course of mastitis may be complicated lymphangitis, lymphadenitis and (rarely) sepsis. After opening the pustules, especially involuntary, can be formed mammary fistula, which closed itself over time.

Treatment of early forms of mastitis conservative, festering - operative. If signs of stagnation of milk glands provide an elevated position by mobilizing bandages or a bra that need support, but do not squeeze the gland. To drain the gland suck milk breast pumps, breast feeding does not stop, limit fluid intake, prescribe oxy-totsyn and no-silos. In serous and infiltrative venerable used antibiotics (semi penitsyllin, aminohlikozid, cephalosporins, macrolides), sulfonamides (in combination with antibiotics), infusion therapy with the introduction blood substitutes liquids gemodez, protein preparations, saline, used as means of improving the body's defenses (γ-globulin, and others.). Mandatory regular pumping milk (to prevent stagnation in the gland). Reverse the development process contribute retromamarni novocaine blockade with antibiotics and proteolytic enzymes: 70-80 ml of 0.5% solution of novocaine, 500 000 ED kanamycin and 10 mg of trypsin or chymotrypsin. In serous and infiltrative forms of mastitis to accelerate the development process used reverse electric field UHF, D, UV irradiation of cancer. All procedures carried out after emptying cancer. In severe mastitis recommend suppress lactation combination of estrogen from androgen.

When purulent mastitis shows the operation, which is done under general anesthesia, only for small surface-located abscess can use infiltration anesthesia, supplemented retromamarnoyu novocaine blockade. Conduct broad and deep enough cuts breast, remove all necrotic tissue and accumulation of pus. Intramamares ulcers reveal radial slits. Manure is removed, the cavity ulcer examined finger, separating bridge washed with a solution of hydrogen peroxide and dried. Then cut edges throw hooks and in good light inspect the abscess cavity, pushing the gland. If you find a connection with another abscess located deep abscess, the hole which receives manure, expanding forceps. Cuts and remove necrotic tissue associated with cancer tissue that hang in the cavity of the abscess. If there are multiple abscesses intramamarise each one revealing a separate incision.

 

The cuts, which are used in mastitis:

1 - radial;

2 - Bardenheyera;

3 – paraareolarese

 

Ductal-aspiration drainage retromamarese abscess.

Retromamares and deeply located abscesses intramamarni reveal semioval section of the lower transition crease. It peeled gland from the pectoralis muscle. Intramamarni ulcers reveal behind abscess cavity drain the wound stitched to drainages. This method of opening the abscess avoids crossing intralobular mammary ducts, providing good conditions for the outflow discharge of pus and necrotic tissue gives a good cosmetic result. In localized forms of acute mastitis, especially in chronic mastitis possible cuts purulent focus within the healthy tissue and blending "blind seam" with leaving small drainage for the introduction of antibiotics.

Treatment of wounds after opening the abscess spend considering phases of wound healing process. The use of secondary sutures reduces treatment time and improves the cosmetic surgery results.

Prevention of mastitis begin in antenatal long before birth. The basis for preventive measures is to increase the body's resistance pregnant woman. An important place is occupied rehabilitation endogenous foci of infection, studies of women, especially those in which the first birth, breast feeding rules, care for breast cancer, hardening of the body, staphylococcus toxoid immunization, UV irradiation of the body, etc. Particular attention should be given to pregnant women with high risk of mastitis (with mastitis, suppurative infections of different localization in history), as well as mastopatiyey, abnormalities of the breast, nipple, with complications of pregnancy.

The complex of preventive measures include preventing injuries and hospital blood loss, anesthesia delivery, combating congestion milk processing nipples before and after breastfeeding breastfeeding, prevention and early treatment of cracked nipples. Given the importance of nosocomial infection in the development of mastitis, an extremely important outlet sanitary-epidemiological profile of hospitals to prevent purulent-inflammatory diseases of infants and mothers. This is particularly timely identification and rehabilitation of bacteria, careful implementation of sanitation requirements in the care of women in labor, regular wet cleaning, ventilation chambers using germicidal lamps etc.

 

Erysipelas - progressive acute inflammation own skin, less mucous membranes.

Etiology and pathogenesis. Erysipelas caused by various forms of streptococcus refers to contagious diseases. As to the antiseptic period it was one of the major complications of wounds in hospitals. Which can lead to nosocomial diseases significant contingent of wounded and sick.

Microflora penetrates the skin from the external environment; lymphogenous, especially hematogenous, route of infection is extremely rare.

In place of getting pathogenic streptococci growing focus serous inflammation localized in the reticular layer of the skin. In fluid determined neutrophilic leukocytes, stasis in blood and lymphatic capillaries. Marked inflammatory changes extend the width, capturing all the new skin. Such changes are characteristic erythematous erysipelas.

As the process occurring epidermal desquamation, exfoliation last inflammatory exudate to form blisters (bullous form of erysipelas). Content bubbles are transparent yellowish fluid, sometimes there is a collection of pus, rarely fluid in the bladder is hemorrhagic nature.

The progression of the inflammatory process in the skin with purulent infiltration of tissues leads to the formation of subcutaneous tissue phlegmon (abscess form erysipelas).

Development of inflammation in the skin can lead to circulatory disorders, thrombosis with the formation of skin necrosis (necrotizing form of erysipelas).

In the pathogenesis of erysipelas importance is allergic factor. Erysipelas prone to relapses, which are based on the state of sensitization of the organism. Relapses inflammation leads to sclerosis subcutaneous tissue and lymph flow disorders of development lymphostasis first and then elephantiasis.

Erysipelas may develop as a result of primary infection with exogenous and endogenous sources. But erysipelas may develop as a manifestation of secondary process - as a result of complications of various inflammatory diseases (furuncle, carbuncle, osteomyelitis, and others.).

Erythematous erysipelas

 

Some forms of erysipelas, diagnosed on the basis of clinical signs, in fact are the phases of the development process, the progress of which can be terminated at any given stage.

 

   

Nodulus erythema left leg requires differential                            Erythematous erysipelas

                                                                                                                diagnosis of erythematous erysipelas

 

Clinical manifestations and diagnosis. The disease occurs with severe clinical manifestations; infringement general condition prior to the development of local symptoms. A small group of patients experienced prodromal period characterized by malaise, weakness, headache. The disease often begins acutely with stunning chills, severe headache. There are sharp tachycardia, rapid breathing, body temperature for a short period reaches 40-41 ° C. From the general symptoms of intoxication observed insomnia, decreased amount of urine, it determined the protein, erythrocytes, leukocytes, hyaline and granular cylinders.

In the blood - marked leukocytosis and neutrophilia, mild anemia, reduced the number of eosinophils, but the beginning of recovery decreases neutrophilia disappears eozynopeniya appears lymphocytosis. Sometimes it may be noted enlargement of the liver and spleen. In some cases, severe intoxication leads to changes in the central nervous system with the emergence of agitation, severe headache, sometimes delirium.

Local symptoms erythematous erysipelas - a burning pain, feeling the heat in the affected area, the appearance of a bright red with sharp, jagged like, outside. Erysipelas often localized on the face, head and lower extremities. For all circuits zone lesions similar to a map, areas of hyperemia resembling flames.

The skin in the area of ​​inflammation swelling, its temperature is increased, pain intensely expressed on the periphery, there is observed a more pronounced redness, whose intensity in the center of lesions gradually decreases. In areas where the skin is inactive, tightly coupled with the appropriate tissues, redness usually breaks. For bullous form of erysipelas, but signs of erythematous erysipelas, characteristic of bubbles of various sizes, filled with serous, purulent or hemorrhagic exudate, which are streptococci; fluid is very contagious and can be a source of transmission of erysipelas by contact. The duration of this form of the disease is usually 1-2 weeks. By the end of the disease is critical body temperature falls with considerable sweating. After calming down local inflammation remains strong exfoliation of the epidermis, the skin on the scalp noted significant hair loss.

Abscess erysipelas changes on the surface of the skin (redness, itching, pain) may be less pronounced, but the common symptoms are stronger than in the erythematous and bullous beshysi. The general condition of the patient difficult: tachycardia, fever, chills. In emaciated, frail and elderly patients with phlegmonous erysipelas form can go into necrotic, which is characterized by the appearance of skin necrosis - black limited painless dense areas in the field of severe congestion, edema, blistering.

Localization erysipelatous inflammation defines some features of its flow. On the face of erysipelas characterized by its swelling. Phlegmonous erysipelas of the scalp accompanied by plenty of pus, purulent edema, exfoliation of skin.

In the trunk of erysipelas characterize active dissemination process, accompanied by severe intoxication. This inflammation can move sequentially capturing all the new skin and even areas previously affected (creeping erysipelas). Erysipelas may affect areas of the body surface at a certain distance between them (erysipelas migrans). With the localization of erysipelas on the limbs mainly observed erythematous and bullous forms of it, but clinically it runs hard, when expressed commonplace. This form is often accompanied by lymphadenitis, phlebitis, thrombophlebitis.

In places where loose connective tissue erysipelas occurs with noticeable swelling of tissues, circulatory disorders and the development of extensive skin necrosis (areas eyelids, scrotum).

Erysipelas mucous membranes characterized by the same general and local symptoms, as in skin lesions: clearly delineated redness, swelling, pain in erytematoznoy phase, the development of blisters containing serous fluid in bullous phase formation of necrosis with necrotic form of erysipelas.

Erysipelas is distinguished by frequent relapses (in 20-25% of cases), recurrence of disease in the extremities lymphostasis lead to the development of elephantiasis.

Erysipelas can spread from the skin to the surrounding tissues to cause metastasis streptococcal infection with the development of foci of inflammation with severe toxemia. The inflammatory process in flehmonoznoy beshysi may apply to tendon sheath, joints, muscles.

In typical cases the diagnosis of erysipelas has no complications. It is based on such manifestations as fever, a sharp increase in body temperature in the presence of pronounced redness with clear boundaries, swelling and hyperesthesia certain areas, abrasions, often located near scuffs, scratches, wounds and so on. No redness observed in rapidly debilitated patients (old and depleted patients), or disguise her scalp greatly complicate diagnosis. In these cases correctly diagnosed erysipelas allow the presence of severe intoxication, fever and detection on the periphery of the inflammatory skin lesions summed shaft, featuring a sharp pain.

Differential diagnosis should be made with erysipelas erythema, dermatitis, cellulitis, limfanhytom in some cases of anthrax.

Major complications occur in the differentiation of erysipelas with ordinary phlegmon. When rose process is localized in the skin and more pronounced on the periphery of lesions, in contrast with phlegmon inflammation affects subcutaneous and intramuscular fat, skin changes (swelling, redness) are secondary in nature and amplified from the periphery to the center of the lesion. Maximum tenderness phlegmon also localized in the center of swelling, but not in the periphery, as in beshysi. In addition, the phlegmon in the area of ​​skin lesions observed dense infiltrate in appropriate tissues, which is not the case with erythematous and bullous form of erysipelas.

 

Erythematous-bullous form of erysipelas

 

When abscess beshysi process usually begins with a skin lesion, while abscess - subcutaneous and intramuscular fat skin changes connected to other displays. Suspicion of bullous and gangrenous erysipelas, especially in severe general condition of the patient and contact with animals, skins, wool, should be performed differentiation of cutaneous anthrax. For anthrax is characterized by lesions in the central area nekrotyzo-bathroom tissue with subsidiaries bubbles on the periphery and extensive soft tissue edema (sybirkovyrazkovyy anthrax). In these cases, usually considerably enlarged regional lymph nodes. Local changes in beshysi differ from described the clinical picture.

Result erysipelas depends on the severity of the process and the patient, his immunological forces, the presence or absence of comorbidities on the timeliness and accuracy of treatment. The best results are observed in erythematous and bullous beshysi significantly worse prognosis in phlegmonous and gangrenous forms.

Treatment in hospital. Significant progress in the treatment of erysipelas was achieved after began to use UV rays, especially combined therapy with antibacterials (sulfonamides, antibiotics). When UV irradiation is usually used Erythemic or suberytemni dose. When erythematous or bullous beshysi radiation dosing based localization process: on a limb - 4-5 biodoz on the face - 3 biodozy. If exposure started in the first days of the disease, usually after 1-2 sessions is the body temperature drops, redness is reduced, improving the health of the patient, ie, the process terminates. When abscess beshysi exposure spend carefully because it may lead to increased swelling and thrombosis of small vessels of the skin. When gangrenous beshysi irradiation is contraindicated.

Along with the radiation used antibiotics and sulfanilamide preparations. With antibiotics being used penicillins, semisynthetic penicillins (the disappearance of redness and normalization of body temperature). Effective in these cases, the simultaneous use of sulfonamides prolonged action. The earlier treatment is begun, the faster the recovery comes. In severe cases of erysipelas limbs used Endolymphatic administration of antibiotics.

Wet bandages, compresses, baths absolutely contraindicated. In bullous form of bladder after treatment with alcohol and reveal a plot defeat bandage with sintomitsinovoy emulsion streptotsydnoyu suspension, tetracycline ointment, and others. In phlegmonous and gangrenous forms other than the described treatment, conduct an autopsy accumulations of pus, drainage, removal of necrotic tissue.

Of great importance is the high calorie milk and vegetable diet with a high content of vitamins. Required adherence asepsis, patient better isolate in a separate ward.

Prophylactic treatment of erysipelas is to microtraumas, careful adherence to the rules of asepsis in surgical hospitals, implementation of preventive measures.

 

Eryzepeloyid, pork measles or swine erysipelas, erythema creeping - infectious disease, resulting in inflammation of all layers of the skin.

Etiology and pathogenesis. The causative agent of the disease - swine erysipelas bacillus - crosses mikrotravmatychni skin damage when cutting meat infected animals. The incubation period of 3-7 days. Most affected people directly associated with the processing of meat, fish, fowl, ie working meat, fish, canned and skin industry, domestic housewives and others. The disease is not a rare but often visible or diagnosed as "erysipelas finger", "dermatitis", "felon", "lymphangitis". In the skin develops serous inflammation of all layers of the accession limfangita and tissue edema with congestion in the area of ​​inflammation mast cells.

 

Eryzepeloyid finger of the right hand

 

Clinical manifestations. Most affected fingers. On the 1st day of the disease on the dorsum of the thumb appears painful stain pink-red, itchy, with clear boundaries, towering above the surrounding skin. After a few days of itching increases in 2-3 weeks decreases swelling, itching stops, congestion persists, remains exfoliate the skin. Inflammation can spread to the back of the hand and fingers with the accession of lymphangitis and lymphadenitis. Sometimes acute arthritis of interphalangeal joints. The general condition of almost constant body temperature usually does not rise and only a mixed infection can be high.

When diagnosis is necessary to bear in mind diseases such as erysipelas and acute lymphangitis, but they are accompanied by more severe general symptoms of high fever. From panaritiums erizipeloyid differs less acute course, the presence of itching, lack of local pain. The disease can go into the chronic form, there is also a relapsing disease.

As treatment used immobilization brush antibiotics by intramuscular injection, UV radiation skin effective novocaine blockade packs with simultaneous administration of antibiotics.

Prevention of the disease is to improve sanitary conditions of work in the meat and fish industry, to protect hands from micro-traumas and infection.

 

Paraproctitis. Acute paraproctitis - purulent inflammation pararectal fiber.

Etiology and pathogenesis. Pathogens paraproctitis often are Escherichia coli, Staphylococcus and white staphylococci, anaerobes, and others. Usually defined mixed microflora.

Penetration of microorganisms in the perianal tissue contribute anal fissures, hemorrhoids inflammation, damage to the mucous membrane of the rectum and anal canal, inflammation of crypts, perineum bruising, rozchuhy covers the anus, and others. A sharp navkolokyshkovoyi tissue as possible complications of gunshot wounds, and tumors that splits. The inflammatory process differs edema and purulent infiltration of loose connective tissue. Putrid infection rospovsyudzhuyuchys on navkolopryamokyshkoviy tissue or lymphatic tissue on the pelvis, often causes necrosis - the disintegration of tissue without the formation of abscesses (suppurative necrotic paraproctitis). There are 5 forms of limited perianal abscesses: subcutaneous, ishiorektalis, subcutaneus, pelviorektalis and retrorektalis.

Ishiorektalis paraproctitis left

 

Subcutaneous paraproctitis localized under the skin near pozadoprohidnoho hole. Patients feel a sharp pain in the pozadoprohidnoho channel, especially during bowel movements. Increases body temperature. Clearly defined painful swelling of the skin over her hyperemic. When it abscessed can determine symptom fluktuation.

Ishiorektalis paraproctitis occurs with severe general symptoms. Process, capturing the deeper layers of tissue sciatic-rectal cavities, spreads behind the rectum to the other side to the prostate and, going up, grabs pelvic tissue. Patients noted throbbing pain in the rectum, high body temperature, sometimes chills.

Swelling, redness of the skin at the general intoxication facilitate diagnosis in patients with this form paraproctitis. However, in the early stages of the disease when no external signs of it, we need a bimanual examination, introducing the finger of one hand into the rectum and placing a finger of the other hand on the swelling out. It is possible to define a painful infiltration.

Submucosal paraproctitis localized in submucosal layer of the rectum above pozadoprohidnyh pillars. With digital examination can determine the swelling and soreness in the anus. Unlike subcutaneous abscesses pain pidslyzystiy form paraproctitis less intense.

Pelviorektalis paraproctitis - rare but most severe form pararectalis ulcers. An abscess is formed above the pelvic floor, but may also be located low in front, behind, on the sides of the rectum. Disease at an early stage is characterized by the absence of any external signs of inflammation in the anus, ishyorektalnyh depressions. Later inflammations, punching muscle lifting anus descends down between tendon reflex arc and fascia tissue in the gluteal-rectal cavity, while here there is abscess with characteristic clinical signs ishyorektalis abscess.

If pelviorektalis abscesses are low on soft yazom, raising the anus, then the digital examination of the rectum can be determined relatively early swelling.

Retrorektalis paraproctitis formed as a result of infection in the lymph nodes and differs from pelviorektalis only that originally abscess located in the tissue behind the rectum, and may well go down in ishyorektalis fiber and cause it phlegmonous inflammation.

Treatment. In the very early stage of the disease in the presence of a small infyltratu in perianal area used conservative treatment: sitting warm bath with a solution of potassium permanganate, lumbar novocaine blockade radiators, UHF-therapy and others. All heat treatments combined with antibiotic therapy.

Cutting abscess (at paraproctitis) and abscess.

a - abscess at autopsy paraproctitis: 1 - the cut, 2 - cutting abscess b - opening abscess: 1 - cuts used 2 - opening the abscess

 

Surgical treatment of acute paraproctitis includes early emergency surgery by opening the abscess with removal of manure and nekrosis tissue abscess cavity examination finger separation bridges and drainage cavity.

 

Location ulcers in acute paraproctitis. Lumbar (a) and sagittal (b) sections.

1 - subcutaneous, 2 - ishiorektalis 3 - pelviorektalis 4 - submucosa, 5 – retrorektalis

 

Apply radial, venous, cross sections, the most comfortable with them - venous and radial. They provide an open wound and outflow of purulent exudate, and less traumatic. After surgery, the purpose of delay stool for 3-4 days patients prescribed tincture of opium (5-6 drops 3 times a day). Requires strict bed rest. When reflex urinary retention patients put a heating pad on the area of ​​the bladder or intravenously injected 5.10 ml 40% solution of hexamine.

When putrefactive necrotic paraproctitis during surgery is performed complete excision of tissue that numb within healthy tissue, and do this 2-3 more cuts skin and subcutaneous tissue for drainage.

 

The incisions used in

acute paraproctitis

1 - perianal abscess;

2 - retrorectalis;

3 - ishiorektalis

 

Surgical approach used in

ishiorektalis (1) and pelviorektalis (2) abscesses

 

 

 

 

 

 

 

 

 

 

 

 

Lymphangitis - inflammation of the lymphatic vessels, complicating inflammatory disease. Penetration of bacteria in the interstitial spaces and lymph vessels there always, with any disease, but clinical manifestations are possible only when the inflammatory changes in blood vessels.

Etiology and pathogenesis. The most common pathogen is Staphylococcus limfangita, other pus germs are rare.

Lymphangitis - disease secondary. It complicates the course of this disease, as abrasions, karbunkuloz, abscesses, cellulitis, felons, nahnyvayuchi wounds etc.

Inflammatory process affects both surface and deep lymphatic vessels. In the wall of the lymphatic vessels and surrounding tissue edema, tissue infiltration by lymphocytes with phenomena perylymfanhitis.

Clinical manifestations and diagnosis. Joining acute lymphangitis with varying purulent process indicates the progression of the underlying disease and increases the severity of its occurrence. Typically, the body temperature rises to 39 - 40 ° C, accompanied by chills, headache, increased sweating, weakness, high leukocytosis. When reticular lymphangitis there is a pronounced hyperemia of the skin, similar to erysipelatous, but without clear boundaries, sometimes you can define mesh drawing in a zone of intense redness. When stem (trunkulyarnomu) lymphangitis congestion has some kind of bands, ranging from inflammation to the area of ​​regional lymph nodes - to the axillary fossa or groin folds, skin swelling. Palpation perceptible painful consolidation in the form of strands along the lymph vessels. Regional lymph nodes are enlarged, thick, painful on palpation. In engaging in the process of deep lymphatic vessels dermahemia absent, defined pain in extremity, swelling, tenderness on deep palpation and early appearance lymphadenitis.

When perylymfanhitis defined areas induration along the lymph vessels.

 

Infected wound of forearm, complicated truncus lymfanhitis forearm and shoulder

 

Treatment is directed primarily at eliminating the primary lesion: an autopsy abscess, cellulitis, purulent swelling, drainage of abscesses. Antibiotic therapy prescribed by the nature of the microbial flora and its drug resistance. Important creating calm, elevated position affected organ, for this purpose, using immobilization of the limb.

Prevention lymfangitis reduced to a thorough and timely primary surgical treatment of wounds, limb immobilization, timely incision and drainage of purulent foci, regional antibacterial therapy.

 

Lymphadenitis - inflammation of the lymph nodes. Arises as a complication of various purulent-inflammatory diseases (festering wounds, furuncle and carbuncle, felon, erysipelas, osteomyelitis, thrombophlebitis, venous ulcers, and others.) And specific infections (tuberculosis, plague, actinomycosis).

Etiology and pathogenesis. Pathogens are disease festering germs penetrating the lymph nodes in the lymphatic vessels. Extremely rare microorganisms penetrate the nodes hematogenous route. Possible contact spread of infection.

The inflammatory process starts with serous edema (simple catarrhal lymphadenitis), which can go into festering and purulent inflammation in the surrounding tissue develops adenoflehmon.

 

   

Cervical lymphadenitis left without abscess                    Purulent lymphadenitis neck left

 

 

Clinical manifestations and diagnosis. Acute lymphadenitis begins with pain and swollen lymph nodes, headache, weakness, malaise, fever. Often, the disease occurs simultaneously with lymphangitis. When catarrhal lymphadenitis general condition of patients suffering enough. They note a dull pain in the area of ​​regional lymph nodes, the latter enlarged, tight and painful on palpation, not soldered to the surrounding tissues, the skin over them is not changed.

When purulent lymphadenitis pain is sharp. The skin over the nodes hyperemic, painful palpation sites previously lymph nodes, clearly palpable and merge with each other and surrounding tissues become immobile. When adenoflehmoni determined diffuse hyperemia of the skin, tight, without clear boundaries infiltrate with foci of softening. Body temperature is high, there are chills, tachycardia, headache, severe weakness. When putrid phlegmon palpation reveal crepitus in the lesion. Purulent lymphadenitis may lead to the spread of purulent process tissue spaces (for peritoneal spaces, mediastinum, and others.) And sepsis.

 

Treatment of early forms of lymphadenitis conservative: the creation of peace to the affected organ, UHF-therapy, active treatment of the underlying source of infection (timely opening of abscesses, phlegmon, efficient drainage of abscess, incision purulent edema) antibiotic therapy. Purulent lymphadenitis treated with surgical method: reveal abscesses, adenoflehmon, remove pus, wound drain. Further treatment is carried out according to the principles of treatment of purulent wounds.

 

 

Osteomyelitis

 

The term "osteomyelitis" was introduced in 1831 Reynaud.

Osteomyelitis - an acute purulent inflammation of the bone marrow with involvement in the actual process of bone nadkistnytsi and often characterized by the generalization process.

 

Classification of osteomyelitis.

According to the International Classification of Diseases Injuries and Causes of Death osteomyelitis classified:

 

I. For reasons (for agents):

1. Monoculture (staphylococcus, streptococcus);

2. Mixed or associated culture (double, triple Association);

3. The causative agent is not known.

II. Clinical

1. Acute hematogenous osteomyelitis

  a) generalized form;

b) local (focal) form.

2. Posttraumatic osteomyelitis:

a) after fracture;

  b) firearm;

  c) post radiative.

3. Atypical forms of osteomyelitis:

a) Brodie abscess ( intraosseous abscess);

 

абсцесБроді

 

 

Brodie abscess .

No specific complaints and characteristics of the disease. The disease begins in early childhood and is manifested in many years. Appearance - slight tenderness to percussion bones.

Notable changes in the blood were detected.

The X-ray is a hotbed of enlightenment in the metaphysis or epiphysis femoral, tibial.

Shape rounded pockets, clear sclerotic border, empty cavity, bone tissue along not changed peryostal reaction is absent.

Treatment - Surgery: trepanation bone curettage inner wall of the cavity, with muscle plastic.

 

 

 

 

Fig. 12. Brodie abscess.

 

 

 

 

 

 

 

b) Sclerosing Garre;вогн

Starts subacute, with pain in extremity, there is dysfunction, mild fever.

General effects pass quickly and prevailing local features:

    1) swelling

    2) infiltration soft tissue

    3) sometimes intermuscles phlegmon, fistula.

Course of long-term with remissions and exacerbations.

X-rays pronounced fusiform thickening of the diaphysis with areas thinning and small sequestra. Channel completely obliteration (hard bone, with small cavities and sequestration).

Treatment: 1) conservative - Antibiotic

2) surgery - removal of small lesions osteomyelitis

 

 

 

 

 

 

Fig 13.  Sclerosing Garre;

 

 

 

 

c) albuminous osteomyelitis Ol 'are;

d) antibiotic osteomyelitis.

 

III. Stages and forms of osteomyelitis:

 

1. Acute phase:

a) intramedullary phase;

b) extramedullary phase.

2. Subacute phase:

a) phase recovery;

  b) phase continue.

3. Chronic phase:

a) acute phase;

b) the phase of remission;

c) phase recovery.

 

IV. For localization process:

 

1. Osteomyelitis of long bones:

a) epiphyseal;

  b) metaphyseal;

  c) diaphyseal;

  d) total.

2. Osteomyelitis flat bones

a) Pelvic;

  b) blade;

  c) iliac;

  d) skull.

 

V. morphological forms:

 

1. Diffuse;

2. Alopecia.

 

VI. Complications:

 

1. Local:

a) pathological fracture;

  b) pathologic dislocation;

  c) false joints;

d) contracture;

  e) ankylosis.

2. General:

a) amyloidosis;

  b) destructive pneumonia.

 

  Hematogenous osteomyelitis.

 

Statistical data.

Ill mostly children, mostly boys.

Seasonality - winter - summer - about 28%, Fall - Spring - 72%.

Localization.

Most affected thigh and shin, namely the Department of bones that more is involved in the growth in length (distal metaphysis of the femur and proximal tibia metaphysis). They account for 2/3 of all cases of osteomyelitis.

 

Variants of acute hematogenous osteomyelitis.

 

1. Breakwire (49%) - vyzdorovlennya occurs within 2-3 months of onset.

2. Protracted (36%) - vyzdorovlennya after 6-8 months of treatment.

3. Lightning (2%) - usually fatal and happens when toxic and septic forms.

4. Chronic (13%) - formed sequesters, voles, broken limb function, marked by periodic worsening in terms of more than 6 months.

 

Etiology.

 

The main causative agent is Staphylococcus aureus (61%). Less is streptococcus, pneumococcus, intestinal bacterium, Proteus, Pseudomonas bacterium. Recently, along with aerobes planted and clostridial anaerobes.

Pathogenesis of acute hematogenous osteomyelitis (MGO).

MGO - heavy SEPTIC bone lesion that develops on the background modified reactivity ohanizm and accompanied by a violation of homeostasis.

 

Theories of pathogenesis.

 

1. Vascular (embolic). Founder - A.A.Bobrov (1888). In children, bone vessels depart at an acute angle in the metaphysis forming an extensive network and end blindly. This contributes to a sharp slowdown in blood flow and sedimentation of bacteria in the blood vessels.

2.Alergic (S.M.Derezhanov, 1940). Osteomyelitis developed on the basis of sensitization of the organism. There is a fireplace aseptic inflammation of vasoconstriction and impaired blood supply.

3. Neuro-reflex (N.N.Yelanskyy, 1954). Reflex vasospasm due to external stimuli leads to impaired blood flow.

The author does not exclude the role of sensitization and the presence of covert infection .

4.M.V. Green (80th years of the twentieth century.) Believes that the MGO based osteonecrosis is not intra-vascular circulatory disorders (embolism) and external compression of vascular inflammatory infiltrate.

 

Patients MGO significantly depressed cellular immunity.

None taken separately theory can not explain the overall pathogenesis of the disease and its versatility.

MGO develops on the background of nonspecific resistance, previous sensitization when exposed to an infectious agent.

 

Predisposing factors.

 

1. Endogenous focus in "Running across yalo infection.

2. Sensitization body.

3. Nonspecific stimuli (trauma, hypothermia, exhaustion, illness, weaken the body).

 

Pathological Anatomy.

 

By the 5th day of onset observed reactive inflammation (hyperemia, vasodilatation, blood stasis using formennyh elements intercellular infiltration).

Up to 15 day - marked bone marrow necrosis, focal hemorrhage, accumulation of fluid destruction leukocytes.

After a month (35 days) necrosis extends to all elements of the bone.

Based on shared etiopathogenetical factors should be considered that MGO starts in metaphysis bone marrow inflammation. Increases pressure in the closed space marrowy channel. Disturbed microcirculation (blood stasis, thrombophlebitis shallow vessels). Developed intramedullary abscess with subsequent formation subperiosteum and intermuscular phlegmon.

 

пош

With the development osteomiyelitis phlegmon in the process of sequestration of bone.

Sequestration - a fragment of the affected bone pathological process that separated from the parent base. They are divided into:

cortical (outer) intracavitary (side endosteum), penetrating (the entire thickness of the bone in a segment) pervasive (across the circle diaphysis).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Fig.14. Development osteomiyelitis phlegmon

 

 

вили секвестрів

 

 

Fig.15. 1 cortical.

              2.Central.

              3. penetrating

              4. total

 

The formation of sequestra from 4 weeks to 4 months.

 

Clinic MGO.

 

The clinic depends on:

virulence of microorganisms, reactivity and localization process, the patient's age, presence of complications.

The local (focal) form of the disease is characterized mainly by local suppurative inflammatory changes.

Pain is constant. After 2-3 days of the "edema is soft tissue (density, intensity). At the end of the week infiltrate captures all tissues.

Acute onset after triggering factors (trauma, hypothermia). Prodromal period - 1-2 days. Increases body temperature to 38.5-400C. It is noted intense pain in extremity. Palpation and percussion determined greatest tenderness over the fire ignition

ост

Generalized form.

1. Toxic (lightning) form a very serious infection, complicated toksytchnym shock.

Getting rough with hyperthermia and fever. Muscular pain, agitation, delirium, seizures, a symptom of severe intoxication. Leather gray, cold, collaptoid condition oliguria. Manifestations trombohemorahic syndrome. Local signs do not have time to develop, or are minimal. Often death occurs in the coming hours or days.

2.Septykopiemia form. Getting sharp. Fast-paced intoxication. The emergence of other purulent lesions in bones (multiple osteomyelitis), in other organs. Body temperature is a constant 39-400C with fever (fever), vomiting, diarrhea, severe pain in the injured limb.

On "objectively: swelling, palpation - severe pain. Possible appearance of complications - pneumonia, pleurisy, meningitis, pielonephritis.

 

Diagnosis.

 

1.General blood (hyperleukocytosis, shift to the left, toxic granularity neyrofililes, erythrocyte sedimentation rate).

2. Biochemical analysis of blood (hypoproteinemia by reducing fine factions, hypokalemia, hyponatremia, hypercalcemia).

3. Radiography (swelling soft tissue, peryostitis, availability sequestration).

4. Puncture bones (search and evacuation of pus, measuring intraosseous pressure, it is possible an increased to 200-400 mm water column

5. Rheovasography (increased vascular tone, spasm and contraction of tissue edema).

6. Ultrasonic echolocation (presence osteomiyelitis fire)).

7. Skin thermometry (body temperature over the fire at 2-40C higher).

8. Thermography (increase the intensity and duration of infrared radiation).

9. Cytological method (accumulation of neutrophilic leukocytes in bone marrow punctate).

10. Computer "tomography (serial sections).

11. Densitometry (determining the degree of bone demineralization).

12.Osteomedulohrafiya (Normally contrast resolves after 10-30 min. When osteomyelitis - more slowly).

13. Radionuclide imaging.

 

Figure 16. Osteomyelitis of the tubular bones:

1. subperiosteum abscess.

2. metaphyseal focus

3. Purulent fistula

4. diaphyseal fireplace

                                       5. epiphyseal center

                                       6. sequestration

 

Treatment.

 

I. Effect on Macro-organism.

II. Effect on microorganism.

III. Treatment of local focus.

       I. Effect on Macro-organism.

1. Detoxification therapy;

2. Reducing or eliminating dysfunction of vital organs;

3. Increasing the body's defenses.

Intensive care.

1. Correction of homeostasis.

2. Therapy dysfunction of vital organs.

3. Increasing imunorezystance and maintain energy balance:

a) non-specific immunotherapy (adjuvants);

b) specific immunotherapy (impact on active immunity, the impact on passive immunity).

4. Desensibilization body.

 

II. Effect on microorganism.

1. Fast (the first hour) antibiotics;

2. Determination of sensitivity to antibiotics;

3. Creating a high concentration of antibiotics in inflammation (intraarterial administration).

4. Duration of antibiotic therapy in optimal doses (up to 6 weeks).

 

Indications for discontinuation of antibiotics.

1. Satisfactory condition of the patient.

2. Stance (10-14 days) normalization temperature.

3. Normalization leukocyte reaction and SHOYE.

III. Local treatment.

1. Rest and immobilization limb plaster splints (from the onset).

2. Surgical treatment - in advanced cases, phlegmon:

 a) osteoperforation (application holes in the bone with the production of drainage tubes for flow irrigation and the introduction of antibiotics);

b) disclosure subperiosteum and intermuscular phlegmon with active and running catchment.

 

остеоперф

Fig. 17. Surgical treatment of osteomyelitis

 

Chronic osteomyelitis.

Forms:

1. secondary chronic hematogenous osteomyelitis;

2. chronic osteomyelitis after traumatic injuries;

3. atypical forms of chronic osteomyelitis (primary chronic osteomyelitis).

 

Prehid MGO in chronic occurs from 3 weeks to 4 months. The process of sequestration lasts months and sometimes years. Sequestration become infected stranger body. Formed long healing fistula (tens of years). The ongoing changes in parenchymatous organs (liver, kidney failure, amyloidosis).

 

Clinic.

Characterized by mild symptoms - aching pain at the site of the fire, purulent fistulas, severe postoperative scarring.

At aggravations - pronounced pain, fever to 390C, flushing of the skin in the area of ​​fistula.

Diagnosis.

The main importance is radiography. The X-ray observed:

thickening of the bone, the presence of cavities in it and sequestration; osteosclerosis, narrowing marrowy channel; thickened periosteum.

          With modern methods of diagnosis using computer "tomography.

Treating complex.

Radical surgery, targeted antibiotic therapy, detoxification therapy, activating the body's immune.

Radical surgery is the excision of fistulas after previous coloring them trepanation bone sequestrectomy the removal of granulation and pus to normal bone flowing drainage of suturing wounds.

With a large cavity in the bone using plastic muscular flap on the middle leg bone or plastic (own bone or canned demineralized bone).

 

 

   Total purulent infection (sepsis). Endogenous intoxication in acute surgical infection.

 

The word "sepsis" Greek origin, means decay, decomposition and is associated with illness and death. After the discovery of the role of microbes in putrefactive processes, sepsis has become synonymous with heavy, deseminovanoyi infection, "poisoning" of blood. For a long time considered the pathogenesis of sepsis according to the classical definition of N. Schottmuller (1914): "On the sepsis can say when the body is the focus of infection from which continuously or periodically enter the bloodstream bacteria, and as a result, there are both subjective and objective 'objectively symptoms. " This definition, which many clinicians have not given up and now, almost reflecting the clinical situation, and thus appear as clinical and medical errors that lead to late diagnosis and inadequate treatment of pain. Despite the fact that the problem of sepsis remains very relevant for many decades, in terms of terminology and understanding of the essence of sepsis still remains unclear and much disputed.

Despite the use of new antibiotics, the introduction of new methods of medical and surgical treatment, the incidence of sepsis and its complications is reduced. In Germany from sepsis die each year 75,000 patients (the same patients and dies from acute myocardial infarction). Overall in Europe, nearly half a million cases of sepsis, a condition diagnosed in one patient in a thousand hospitalized. In the United States registered 300 thousand cases of gram-negative sepsis.

Evidence of the complexity and the many unresolved fundamental issues pathogenesis of sepsis and its terminology is holding 5 of the World Congress on the issue of sepsis, shock and inflammation, held in Munich from 1988 to 2000, the Organization of the Academy of multiple organ failure in Trieste (Italy).

In Soviet literature for a long time used the terminology and classification of sepsis suggested M.I.Kuzinym and BM Kostyuchenko (1981).

Determining driven them talk about the difficulties of this controversial problem. On the one hand, sepsis should be considered as a consistent link in the development of surgical infection as a result of generalized infection that initially localisation in the primary focus, with the rest, "sepsis - a heavy nonspecific infectious process occurring against the backdrop of changes in reactivity." Classification MI Kuzin and BM Kostyuchenko contains a number of provisions which do not have proliferated like "purulent resorptive fever", on certain terms, such as "chronic sepsis," the authors themselves refused.

MI Kuzin and BM Kostyucheno (1990) find that from a practical point of view can be guided by the following time parameters:

1) fulminant septicemia - clinical picture unfolds within 1-2 days (2% of patients);

2) acute sepsis occurs within 5-7 days (39-40% of patients);

3) subacute sepsis lasts 7-14 days (50-60%);

On the development of clinical disease after infection infestations should, according to M. Kuzin and BM Kostyuchenko (1990), to provide:

- Early sepsis arising in terms of 3 weeks after injury, when the role of the primary lesion is undeniable;

- Late sepsis, such as that developed after a month or more similar conditions when the primary focus is losing its clinical significance, which often leads to misconceptions about acute cryptogenic sepsis.

In addition, based on the phase character of biological responses that sometimes is not related to temporary factors, the authors consider clinically reasonable to provide 3 phase sepsis:

- Tension;

- Catabolic disorders;

- Anabolic.

 

In everyday clinical practice to classify sepsis by type of microbe-agent:

- Staphylococcal

- Kolibacillus

- Pseudomonas etc.

Since the species of microbe has a significant impact on hospital sepsis, this division has a certain practical significance for physician directs for the most rational antibiotic therapy. As you know, microflora in monoculture occurs in less than half of the patients. Species composition of its stake in the blood is often not the same as in the treatment process quickly changing. Clinical course of sepsis is determined not only the kind of pathogen and its "dose", but pretty much the nature of reactions to the infection, as well as a number of other factors, such as primary and secondary septic foci, concomitant diseases, age of patients and others.

Depending on the location of the primary vohnyscharozriznyayut:

- Odontogenic

- Otogenic

- Obstetric and gynecological

- Urological

- Surgical and other types of sepsis.

The feasibility of such a division is due to the fact that the course and outcome of sepsis is largely determined by the success of treatment of the primary lesion, and how his treatment is very different: obstetric and gynecological sepsis should be treated with gynecologists and surgery - surgeons, etc.

The concept of surgical sepsis usually include sepsis that developed as a result of acute and chronic suppurative surgical diseases (furuncle, carbuncle, abscess, cellulitis, osteomyelitis, peritonitis, and others.) And required local surgical operation and general intensive treatment. Very close to the surgical wound sepsis that develops against the backdrop of various, mainly severe gunshot wounds and traumatic. This also should include cases of sepsis that developed after surgery, intensive care and diagnostic procedures, intravascular manipulation, etc. This type of sepsis called nosocomial (hospital acquired within the institution).

 

 

Modern terminology and the idea of ​​Sepsis

 

Insight sepsis goes along with the desire to give a clear definition of this pathology. The literature continues to debate on modern terminology and understanding of the essence of sepsis.

Complexity of the problem stems from the fact that patients with clinical proyavamysepsysu only 45 - 48% of cases can be detected bakteriyemiyu. It appeared that a large array of damaged tissue (necrotizing pancreatitis, polytrauma, abdominal aortic rupture, burns) may be replaced as bacteria trigger a generalized response.

Exceptional achievements in theoretical and practical point of view, that changed the whole concept of sepsis was the opening number of endogenous mediators of systemic inflammatory response. At present, the common view that sepsis can not be the result of direct action of microorganisms on Macro-organism as a result of significant disturbances in the immune system that are in its development over the state of activation ("phase hiperzapalennya") to the state of immunodeficiency ("phase imunoparalisis" ). The body, therefore, is an active member autodestruktyvnoho process. Septic "autokanibalizm" - a concept that was introduced to describe the metabolism of the patient with sepsis. Nowadays the leading role played by gram-negative flora (Escherichia coli, Bacillus blue-green pus, Klebsiella, Proteus).

One of the most powerful agents of starting sepsis is lipopolysaccharide membrane of gram-negative bacteria, designated as endotoxin. Note especially spending antibiotic that endotoxin is released in the process of microorganisms, and because their death under the influence of antibiotics, and the degree of unequal allocation of endotoxin by the action of different antibiotics.

In order to eliminate differences in terminology and in accordance with modern ideas about inflammation conciliation conference the American College of Physicians and Thoracic Association for the treatment of patients who are in critical condition (American Colledge of Chest Physicians / Society of Critical Care Medecine Consensus Conferens, 1992), decided to standardize the terminology used in assessing the severity of the inflammatory response and diagnosis of complications that eliminate existing ambiguities.

At the suggestion of the conciliation conference, severe body's response to inflammation caused by infection, severe trauma, burns, acute destructive pancreatitis and other tissue damaging factors recommended called syndrome of systemic response (reaction) on inflammation - Systemic Inflammatory Response Syndrome - SIRS.

But we should celebrate this concept as "systemic inflammation". This term in general pathology there. Inflammation is a local, protective, controlled immune system reaction to the above damaging factors. The response to inflammation depending on the severity of the latter may be primarily a local or systemic, total, such, accompanied by dysfunction of several organs and systems. It should be emphasized that SIRS is a set of symptoms rather than a diagnosis, and his presence should make the doctor find the cause of this symptom, which does not identify a specific disease and is the basis for a treatment.

Definition of sepsis adopted North American consensus yesamym reasonable, though not disclose all the features of the pathogenesis of this condition. Sepsis - a systemic response to infection. To put this diagnosis must be at least two of the following four characteristics and the presence of foci of infection:

- Body temperature> 38 ° C or <36 ° C;

- Heart rate> 90 in 1 min.;

- The number of breaths> 20 min., Or pCO2 <32 mmHg;

- WBC> 12000/ml or <4000/ml, more than 10% immature neutrophils.



Tab. 1 The terminology adopted by the North American Conference of Reconciliation, 1991

 

infection

The inflammatory response, stimulated by microorganisms by the invasion of the usual tissue intact microorganism

Bakteriyemiya

The presence of bacteria in the blood

Systemic inflammatory response syndrome

Differs severe clinical occurrence, harakteryzuyetsya2 or more clinical signs: body temperature> 38 ° C or <36 ° C, heart rate> 90/hv, respiratory rate> 20/hv or pCO2 <32 mmHg, WBC> 12000/ml or <4000/ml or immature forms of> 10%.

Sepsis

Systemic response to infection, which is characterized by 2 or more signs of SIRS.

Severe sepsis

Characterized by organ dysfunction, hypoperfusion of tissues and hypotension. Possible laktatatsidoza, oliguria, impaired consciousness.

Septic shock

Sepsis with hypotension, which develops despite adequate infusion therapy, tissue hypoperfusion, laktatatsidoza, oliguria, impaired consciousness. If inotropic support can stabilize blood pressure, but hypoperfusion remains.

Arterial hypotension

Systolic blood pressure <90 mm Hg or decreased> 40 mmHg the average in the absence of other causes for hypotension

The syndrome of multiple organ failure |

The presence of acute lesions function of organs and systems, while the body without the aid can not alone stabilize homeostasis.

 

The severity of the syndrome is determined by the number of available evidence of dysfunction in this patient. If two signs syndrome assessed as moderate (mild) severity, 3 - as medium severity, 4 - as heavy. At 3 and 4 signs of the syndrome of systemic responses to inflammation of the risk of disease progress, the development of organ failure, sepsis and death increases dramatically.

Obviously, the criteria for severity of systemic reactions are more objective than subjective opinion of the patient's condition as satisfactory, moderate, heavy. Assessment of severity of the patient may be supplemented by a number of other criteria (impairment of mental status, presence of oliguria, metabolic acidosis, increased bilirubin and transaminase), counting the number of points on a scale SOFA (Sepsis related Organ Failure Assesment) adopted by the European Society of Intensive Care in 1994 for evaluation of organ failure associated with the presence of sepsis or APACHE-II, which takes into account not tilkyhostri violation of physiological functions, but also the patient's age, the presence of aggravating chronic diseases.

In recent years, in connection with the study of the role of different cytokines in the pathogenesis of sepsis gaining, with SIRS, another concept, as proposed by RC Bone - CARS (compensatory antiinfammatory response syndrome). This well-connected phase winding, anti-inflammatory responses, early and late multiple organ dysfunction and nosocomial infection.

 

Untitled-1

Fig. 1. Relationship SIRS and CARS (no RC Bone et al., 1996)

 

 


Statistically S. Wade et al. (1998), the incidence of SIRS in ICU patients in the surgical clinic reaches 51.1%: 335 of 656 patients, in 65 (19.4%) of 335 patients with blood isolated microbial culture and diagnosed with sepsis, in 47 of 65 patients sepsis developed septic shock mortality 53.2%. Cooperative research covers several medical centers in the U.S., showed that the total number of patients with SIRS only 26% developed sepsis and 4% - septic shock. Mortality increased depending on the severity of the patients. When SIRS she was 7%, with sepsis - 16% in septic shock - 46%. Because of the low specificity of symptoms that characterize SIRS, without additional clinical and laboratory data is difficult to predict the possibility of sepsis or septic shock. Multiple studies of blood for the presence bakteriyemiyi in combination with other biochemical and instrumental studies can provide additional information for the prediction.

There are several options for assessment septic state. Clinical interpretation depends on microbiological data (or is no invasive infection, positive blood culture) and the presence of these or other signs of systemic inflammatory response (Table 2). Certain clinical and tactical assistance can provide diagnostic use matrix (Nystrom, 1998).

 

Tab. 2. Matrix diagnosis of sepsis (Nystrom, 1998)

 

invasiveness infection

Синдром системної запальної реакції (SIRS)

Clinical interpretation

No

Present

SIRS is infectious nature. Cultures negative sepsis.

Present

No

Infection without sepsis

Present

Present

Sepsis

 

 

If the findings of microbiological studies of absence invasive infection (no blood culture), but there are clinical signs of SIRS, we can assume that either it SIRS infectious nature (eg, traumatic) or this - culturally negative sepsis.

 

Etiology SEPSIS

 

Difficulties of early diagnosis of sepsis associated often with insufficient ob'yektyvnoyuotsinkoyu changes occurring in the wound - the local focus of infection, which under certain circumstances becomes primary septic foci that late, and then develops generalization process.

Complexity of the problem stems from the fact that patients with clinical proyavamysepsysu, only 21-48% of cases can be detected bakteriyemiyu. It appeared that a large array of damaged tissue (necrotizing pancreatitis, polytrauma, burns, positional compression syndrome, and others.) Can be replaced as bacteria trigger systemic inflammatory response. In addition, the presence of membrane potential and heterogeneity of the surface of blood cells leads to the microorganisms penetrate into the bloodstream, is soon fixed on the membranes of blood cells. Granulomas and lymphocytes can get rid of foreign elements adsorbed by phagocytosis and other factors of cellular and humoral immunity. Only red blood cells is to be inferior to cleanse itself and so become carriers of infection in sepsis. It is on their membranes "dormant" organisms.

"Entrance gate" in sepsis

 

The most common cause of sepsis is acute purulent diseases of soft tissues that make up the structure sepsis 44.3% - 52% - of the so-called "Wound sepsis."

Second in frequency cause of sepsis are patients with purulent peritonitis as a complication of inflammatory processes in the abdominal cavity.

Something specific group of patients with clostridial infection. Overall clinical presentation of this infection is so bright that comes to the fore and obscures the role of primary site of infection.

 

Reasons generalization of infection

1) Wrong surgical tactics and inadequate volume of surgery;

2) The wrong choice of size and antibacterial components, dezintoksykatsiynoyii symptomatic therapy;

3) Reduced or distorted imunnoreaktyvnist microorganism;

4) presence of severe comorbidities (diabetes, alimentary dystrophy, and others.)

5) Wide dissemination of antibiotic-resistant strains of bacteria;

6) Change the etiological structure of pathogens of purulent surgical infection.

 

Hospital sepsis

 

Problem nazokomialnoyi (nosocomial) infection for surgery is of particular importance. According to statistical studies, the incidence nazokomialnoyiinfektsiyi in surgery an average of 6 - 8% with variations depending on the nature of the surgery. The frequency of wound infection complications in various fields of surgery in the 80 years ranged from 1 to 14%, 42% lethal rezultativpislya operations was due to purulent-septic complications.

The highest level of infectious complications that have no connection with the transaction, was in the surgical intensive care unit (VAIT). The average rate of infection in nazokomialnoyi VAIT is 25% and is directly related to the duration of stay of patients in the department.

 

Sources nazokomialnoyi infection causing factors pathogenesis

 

There are two main sources of nosocomial infection hirurhichnohohvoroho - exogenous and endogenous. Any external sources (air, food, water, contact with staff and visitors, invasive medical diagnostic procedures) may lead to colonization of the patient with podalshymrozvytkom infection.

In modern hospitals, which built and operated withcompliance all sanitary-epidemiological and health requirements, external sources of infection persists reliably. However, in such offices, patients develop nazokomialni infectious complications and deaths appear related to septic multiple organ failure, and external infection with careful analysis excluded.

Many bacteria live in the gastrointestinal tract of healthy humans - both anaerobic and aerobic. Normally they get along just fine with each other, but also support adequate motor, secretory and metabolic functions of the gastrointestinal tract. However, under the influence of surgical stress, shock, protein deficiency, massive antibacterial such a state of "biological comfort" is broken and there are conditions for the translocation of toxins, cytokines not only in the portal system, but also directly through the intestinal wall. This release of endogenous bacteria or their toxins can cause septic and non-specific organ damage. In these cases, it is the intestine, figuratively speaking, "motor" that runs and supports multiple organ failure (MOF). Therefore, the gastrointestinal tract, usually first damaged by surgical stress.

There is a condition that clinicians still treated as a mysterious "sepsis without primary focus" and is called "sepsis intestinal origin".

New perspective on organ failure is the evaluation of mesenteric nodes as a link between non-functioning intestine and MOF. Experimental studies have shown that mesenteric lymph nodes play an important role in the occurrence of acute phase inflammatory response, as a link between the intestine and damaged internal organs. Lymph containing activated lymphocytes, neutrophils, cytokines enters the lungs, which in this case are between the intestine and the liver on the one hand and the systemic circulation from the other and take the first hit itself, being the primary filter.

 

Etiological and nosological structure nazokomialnoyi infection

 

With more than 400 species of bacteria that live in the human body, only about 15 play an essential role in the etiology nazokomialnyh infectious complications. Gram-negative enteric bacteria, Pseudomonas aeruginosa, staphylococci, enterococci, some anaerobes - that's almost the entire range of pathogens obligatory complications in abdominal, cardiovascular and other major fields of surgery.

Recently, most authors are more common with epidermal staphylococcus as an etiological factor catheterization complications vascular and endovascular cardiac surgery. And it is not only microbiological phenomenon or a consequence of poor asepsis.

As nosological structure nazokomialnoyi infection, it is in surgery differentiates its widest range; any organ and anatomic area may be included in the scope of surgical infection, even regardless of the location and nature of the surgery.

The main pathogen was Staphylococcus aureus osteomyelitis - 83.4% of crops. When crops bile in patients with acute cholecystitis was obtained nehatyvnyyrezultat in 69.3% of cases, and the growth of flora found in 30.3%. With the positive response in 47.8% detected E.coli, and in 26% - Klebsiella pneumonia.

Thus, we can assume that a significant proportion of "negative" results of crops may be associated with the presence of anaerobic microorganisms, which are available at our disposal methods are unable to detect.

To date, a number of isolated components of microbial cells that can directly cause the formation of so-called prozapalnyhtsytokiniv-IL-1, IL-6, tumor necrosis factor, and run SIRS.

Dive proteins (Fig. 1), which are localized in the cell membrane of gram-negative bacteria, and proteins villi also have high enough resolution to induce proinflammatory cytokines.

 

Untitled-2

Fig. 1. Simplified diagram of the structure of the cell membrane of gram-negative bacteria (by Brooks GF, et al., 1994).

 

The outer membrane, which is a lipid bilayer is in Gram-negative but not Gram-positive bacteria. It permeated Plunge - special proteins that provide penetration of hydrophilic substances to the membrane cytoplasm. Peptydohlikanovyy layer inherent only bacteria and is thinner in gram-positive organisms than in gram. The outer membrane with peptydohlykanovym layer is the cell wall.

Lipoprotyeyiny, glycoproteins, lipids, peptydohlykany is in gram-negative and gram-positive bacteria in. All of them - the components of the cell wall. Specific surface proteins found only in gram-positive bacteria.

Obviously, the potential for induction of proinflammatory cytokines in gram-positive microorganisms is much lower. For example, the concentration teyhoyevyh acids needed to trigger the induction of tumor necrosis factor is 1000 ng / ml.

Microorganism adapted to in order to develop a pathological reaction in the human body, and between the human body and the microbe is a constant dialogue. Of course, ongoing dialogue is mainly due to surface structures. These proteins bind to immunoglobulins, and a large group of proteins that recognize the extracellular matrix, ie those proteins that allow microorganisms to attach to the extracellular matrix, intercellular spaces in the human body. By surface structures include a number of surface enzymes.

One of the main conditions for the successful treatment of purulent-septic patients is effective in suppressing these microbial pathogen that feasible only after his identification. Guess the character pathogen in some cases can be features on clinical manifestations of his life in the wound (general view of the wound, the nature of the discharge, smell them, and others.), But the final vysnovokrobytsya according to bacteriological examination.

 

 

 

PATHOGENESIS OF SEPSIS

 

The pathogenesis of sepsis play an important role not only pathogens but also the reaction of the immune system that is caused by bacterial toxins or products of inflammation (necrosis), passes in its development path from excessive activation state (phase hiperzapalennya) to a state of immunodeficiency (phase imunoparalichu) ( fig. 3). The body is an active member of the destructive process, rather autodestruktyvnoho process, or as it is called, "autokanibalizmu."

The main factor initiating SIRS is endotoxin, which is lipopolisaharydnoyu substance (LPS), the toxic effect of which is due to lipid A, which is included in its composition. Isolation of endotoxin observed during the destruction of microbial cells, especially under the influence of antibiotic therapy. Value is how "aggressive" antybyotykoterapiya, leading to a cascade of receipt of endotoxin into the bloodstream from the destroyed microbes and use subterapevtychnyh doses of antibiotics used prophylactically. This is because most antibiotics subterapevtychnyh doses have high affinity for protein PSB-3, causing inhibition of bacterial cell separation, sharing with the formation of long threadlike structures - filaments. Consequently, the observed increase in biomass production and endotoxin. A special role is played by the functional reserves of the spleen, which provides not only general detoxification, but also the appropriate level of antibodies to LPS.

Endotoxin, which separated, activates multiple biological systems: kinin, coagulation system, contact, complement, peripheral blood cells - neutrophils, eosinophils, monocytes, macrophages, and endothelial cells from initiating the release of many neurotransmitters which vividly called "metabolic anarchy." Metabolic anarchy accompanying Spohn and found increased levels of lactate, total liposaharydiv, prostacyclin, zrostannyamaktyvnosti cyclooxygenase, coagulopathy, low levels of circulating antibodies, reflecting excessive uncontrolled activation моноцитмакрофагальнихцитокінов, lack of control which is the basis for SIRS in critically different etiologies.

Toxic effects LPS is a complex of disorders caused by simultaneous damage as cells circulating in the bloodstream and endothelial. Damage to endothelial cells acquires special importance in the development Spohn, as opposed to pre-existing views on the endothelium as a passive barrier, now known for its essential role in the regulation mikrotsyrkulyatsiyishlyahom impact on the balance of relaxation and reduction of vascular permeability (Fig. 4).

Among the many metabolic breakdown of particular note is the so-called oksyradykalnyy stress that forms autoposhkodzhennya in sepsis and SIRS. Free radicals and hipohlorna acid damage endothelial cells of various organs as a result of lipid peroxidation layer membranes, which leads to the formation syndrome VET (Spohn) in patients with hypertension, liver failure, diabetes, and atherosclerosis. This is due to the normal flow, which is not provided due to the instantaneous and complementing each other disorders of lipid prostacyclin PGJ2, supportive and tromborezystentnist protyzhortannya and free-N0, which provides a vasodilator effect.

Under the influence of lipid A endotoxin disrupted the integrity of the membrane of red blood cells, eosinophils, neutrophils, macrophages, polymorphonuclear leukocytes, resulting in the release into the bloodstream a number of biologically active agents - cytokines such as TNF-a and TNF-p, interleukin (IL) 1-6 and others. TNF - tumor necrosis factor - the initiator release phospholipases, violations products N0, inhibition of angiotensin II, which leads to damage of systolic and diastolic function of the left ventricle, inhibition of the contractile ability of the myocardium and arterial hypotension.

Excessive systemic cytokine activation monotsytmakrofahalnyh is very harmful because it stimulates the synthesis of additional natural inflammatory mediators such as leukotrienes (LTC4, LTD4, LTE4), eicosanoids, interleukins, thromboxane, bradykinin, microcirculation involved in the destruction, permeability and edema formation by increase in hydrostatic capillary pressure and activation vasodilation. At the same time changing the activity of cellular calcium and protein metabolism in skeletal muscle, increased breakdown of glucose increases acidosis, increases the concentration of acute phase proteins.

Most cytokines - is endogenous pyrogens that are responsible for the development of a model for sepsis and SIRS hyperthermic syndrome. Thus, the activation of monocytes in the blood enters the IL-1, which penetrate the blood-brain barrier to neurons of the hypothalamus, stimulates heat and breaks behavioral processes.

Although the exact mechanism of destruction of hepatocytes and sinusoidal liver cells under the influence of cytokine unknown, found that TNF in combination with IL-6 shows a direct hepatotoxic effect. The basic mechanism of endothelial damage renal tubules influenced TMF leukotrienes and LPS microbes consider local changes fibrinolytic activity and endothelial damage withsubsequent intracellular edema, increase in the number of lysosomes that attack membrane deposition of fibrin.

Since the main point of impact of endotoxin and TNF is endothelial cell activation leads to the release of prostacyclin (PGS2), allocation of elastase, toxic oxygen metabolites, platelet activating factor and complement with the release of anafilaktoheniv as S3A, S4a, S5a, a terminal complement, bradykinin followed by the formation of a syndrome of increased capillary permeability. The release of subendothelial collagen accompanied kininohenu action against platelet adhesion by von Willebrand factor and the presence of thrombin. It promotes the release of thromboxane Ah, strengthens capillary hydrostatic pressure increases swelling and permeability in the presence of leukotrienes (LTC4, LTD4, LTE4) and bradykinin.

Thus, the severity of disturbance of microcirculation and the formation of multiple organ failure in sepsis and SIRS depends on the combined damage under the influence of cytokines hemostatic system and immunity.

Coagulation disorders accompanied by thrombocytopenia, the advent of fibrinogen degradation products, and fibronectin - a key modulator of the immune response that provides the bacterial invasion and activation of T-lymphocytes, activated clotting protein depletion with anticoagulants, increased levels of binding protein. Damaged endothelium is able to produce platelet activating factor - a strong stimulant of aggregation, thromboxane Ah, serotonin, fibronectin. In the presence of thromboplastin entering the bloodstream from damaged tissues and cells against endothelial function affected both by coagulation forming block capillary circulation - the basis SPON.

Immuno paralysis - response to infection and extreme action. It is called the phenomenon of change in the ratio of cells of the immune response, unnatural increase in complement activation and lymphocytes. This is the T-cell dysfunction - defective proliferation to the stimulus, until the stage of deep stress by two cytokines - IL-2 and interferon-g, because of their inadequate product. Along with this excessive systemic hyperactivation monotsytmakrofahovyh cytokines harmful, as it stimulates the synthesis of additional natural inflammatory mediators, such as eicosanoids, IL-8 and others.

Endotoxin is very immunogenic and stimulates B-lymphocytes, enhances helper function, stimulates plasma cells and the formation of immunocytes. In this process, endothelial cells are involved, highlighting influenced cytokine activation of tissue compatibility antigens class II, which can be a source of cytokine stimulation, leading to disruption of leukocyte-endothelial interactions.

If normal nonspecific natural immune mechanisms provide adequate protection against local infection, localized inflammation, limit excessive production of inflammatory mediators, prevent the development of severe general (systemic) reactions vital organs in response to inflammation, in terms of SIRS, - a massive inflammatory reaction, resulting in the release of cytokines, leading to multiple organ failure.

Inflammatory reaction rid of the pathogenic factors distinguished "foreign" from "his", what promotes recovery.

 

The most studied natural defense mechanisms include:

1) reaction of the central nervous system, the sympathetic and neuroendocrine systems that regulate hemodynamic and metabolic disturbances in the body in response to inflammation, trauma, presence of nonviable tissue in the body;

2) natural nonspecific immune responses, such as chemotaxis, opsonizatsiya, phagocytosis, activation of complement, immunoglobulins, produce histamine, serotonin, prostaglandins, and others;

3) inflammatory mediators produced by cells (cytokines), discovered recently thanks to the success of molecular biology and molecular genetics.

 

Clinical picture and diagnosis of sepsis

 

Sepsis is a clinical syndrome is difficult to define. The above mechanisms of inflammation suggest that SIRS is clearly delineated pathophysiological settings. SIRS, which develops due vazhkoyiinfektsiyi, no different from a syndrome that occurs in response to other damaging factors because of their pathophysiological mechanisms involved in the same inflammatory mediators. The syndrome of systemic inflammatory response can not consideredas sepsis, because to some extent, damage to the immune system, it essentially means the only useful defensive response against infection and other harmful factors. It becomes dangerous to the patient's life in cases where excessive production of cytokines and other mediators of inflammation and an imbalance between pro-and anti-inflammatory mediators damage control function of the immune system. In these circumstances, SIRS may be complicated by the development of sepsis, septic shock, multiple organ failure.

 

Clinic SIRS varies depending on four stages, isolated in the course of the syndrome.

 

Phase A, which is a normal response to stress after major surgeries, injuries and diseases, is characterized by a moderate decrease in systemic vascular resistance and a corresponding increase in cardiac output. Oxygen consumption that increases are hipermetabolichna response to stress, the concentration of lactate remains within normal limits. This is a normal reaction, which can be observed in each patient after major surgery and severe trauma. Assuming that the attendant complications missing transient SIRS, which reflects the systemic effects of generalized inflammatory response solved as the patient return to normal physiological state.

 

Phase B is excessive stressful response. Loss of systemic vascular resistance becomes excessive. When supported by adequate preload by increasing intravascular volume and at normal physiological reserve left ventricular cardiac output increased significantly to meet the needs created by a significant decrease in load due to systemic vasodilatation. Combination vasodilation of blood vessels and a significant expansion of extracellular volume due to systemic edema creates the need for large volumes of additional preload for patients in stage B. If achieving adequate preload (preferably crystalloid solutions) fails, it can lead to hypotension, even in patients with parameters this stage of SIRS.

Phase B is also characterized by a significant decrease in arteriovenous difference of oxygen.

This is the stage in the beginning to show the development of multiple organ dysfunction syndrome. With increasing excess lactate in the peripheral blood appears decrease arterial blood oxygen saturation. The level of serum bilirubin begins to rise. In the absence of measures to prevent the development of acute gastric ulcers and erosions, these symptoms appear complications. Serum creatinine level greater than 90 mm / l. If the main trigger factor stage in SIRS persists, further evolution stage of B leads to a detailed organ failure and death. It is important to emphasize that while the systemic blood pressure at first supported adequately, organ damage is occurring during stage V.

 

Phase C is decompensated SIRS response to stress. Loss of systemic vascular resistance pronounced. Physiological reserves left ventricle can not maintain pressure because of the very pronounced decrease stress. Cardiac output is normal or slightly elevated, so we can assume "normal" physiological state of the patient, but in rezultatinadmirnoho reduce the load pressure can not be supported adequately. Downgraded BP is maintained even in conditions of adequate preload. This condition hypotension traditionally attributed to septic shock or shock that occurs when the "natural" development of sepsis. Clinically, these patients have a paradoxical combination of hypotension and warm skin.

Combination of bacterial infection and other potential activators of the inflammatory response may play synerhytycheskuyu role in the development of septic shock. Shock (clinical stage I) is a set of effects of all potential activators of inflammation, often bacterial nature. Not surprisingly, the combination effects of peripheral oxygen utilization and humble blood pressure leads to severe laktatatsidoza. Patients with septic shock really (Stage With SIRS) require aggressive and rapid treatment.

 

Phase D is preterminalnoyu stage of SIRS. Available hypodynamic circulation with low cardiac output, which seemingly caused by self vasoconstrictor effect. Systemic vascular resistance increased sharply above the norm. Stage D, perhaps, is the superimposition of heart failure expressed SIRS. The total oxygen consumption extremely low utilization due to violation of the periphery, inadequate cardiac output and peripheral vasoconstriction. Lactate concentration significantly increased. Death at this stage likely in most patients.

It is important to recognize this syndrome in the early, early stages of development when there is only 2-3 signs in order to determine the cause of its origin, to take measures to stop its progress and prescribe adequate treatment to the development of severe systemic dysfunction of organs and systems.

 

Markers of sepsis. As soon as identified mediators of sepsis, there were proposals to use some of them as markers of sepsis. Raising the level of many cytokines, including tumor necrosis factor, interleukin - 6 -8, -10, indeed observed in many septic patients and some of them are associated with a poor outcome. Often used as a marker of sepsis IL-6. However, increased cytokines varies and, in addition, there may be other conditions that cause an inflammatory response.

Among other biological markers known and widely used C - reactive protein. This acute phase protein, increased in parallel vmistyakoho growth cytokines. Several authors considers this figure as sensitive for infections than the number of white blood cells or temperature.

Prokaltsytonin, the precursor of calcitonin, is also offered as a marker of sepsis. Origin and its function in sepsis are not clear, but the level rises several hundred times in patients with severe sepsis and its use to differentiate infection from other causes of inflammation, as well as a marker of severity of infection. Potential markers of sepsis include neopterin, elastase, phospholipase-2.

The syndrome of systemic reactions may last only a few days at a favorable course of the disease, but can exist for a longer time. Symptoms can go gradually to decline, in these cases the danger of complications decreases sharply and you can expect to recover. In severe syndrome (3-4 signs and more) excessive production of cytokines and other mediators of inflammation may disrupt immunological control the development of inflammation. Pro-and anti-inflammatory mediators may reinforce each other, creating a growing immunological dissonance. There is a direct correlation between the content tsytokinivv blood and severity of the syndrome and its complications.

Conciliation Commission U.S. physicians defines sepsis as very vazhkuformu SIRS in patients with primary site of infection, confirmed by blood cultures. T and Blackwell et al. (1996) define sepsis as clinical signs and symptoms that occur as a result of excessive systemic inflammatory response to the introduction of infection. However, in the 20 - 30% of patients zsepsysom blood cultures may be negative. Perhaps this is due to insufficient persistent search bakteriyemiyi or defects in the transportation and cultivation made by the material. If the source of infection and severe SIRS blood for culture should be taken at least 3 times a day, and in severe cases - vprodovzh3 - 7 days. With this persistent search bakteriyemiyi it can be detected in sepsis more often.

Do not forget about the possibility of translocation of intestinal bacteria in the blood. In such cases, the intestine is the source of infection, which is not considered when searching for the cause of bacteremia. Translocation of bacteria and endotoxin in the bloodstream becomes possible with violating the barrier function of the intestinal mucosa because of ischemia of its walls with peritonitis, acute intestinal obstruction, shock and other factors. Under these conditions, the intestine becomes like "undrenaging purulent cavity." According to A. Pollock (1996), sepsis and septic shock can occur without infection or after the elimination of infection with antibiotics. The mechanism responsible for this phenomenon carefully studied, but still can not determine when infection sepsis becomes noninfectious SIRS. We only know that they are the same frequency deaths. MI Kuzin (2000) repeatedly observed patients successfully cured of widespread purulent peritonitis but died of sepsis (peritonitis at autopsy evidence they were found).

   For the doctor is important to identify early symptoms of sepsis according to the criteria of the conciliation conference.

Fever - the most common clinical finding in sepsis and it is main symptom for the diagnosis of sepsis. Increase body temperature due to the influence of pyrogenic cytokines, including interleukin-1 (direct and indirect, especially prostaglandin E2) in the hypothalamus, although other endogenous molecules may lead to the development of hyperthermia. By itself, the fever can be a favorable sign, judging by the results of the disease: higher mortality noted in the absence of feverish reactions in patients with sepsis. The difference in mortality forces show evidence to prescribing, lowering the temperature in sepsis.

In sepsis, and, rarely, with SIRS, often in elderly patients with disorders of thermoregulation, hypothermia can occur.

Respiratory disorders in the early stages of sepsis occur hyperventilation, which leads to respiratory alkalosis and respiratory muscle fatigue.

Dysfunction of the cardiovascular system can carry diverse nature. In the initial stage there is a decrease in peripheral vascular resistance and hypotension on the increase in cardiac output. Further, under reduced vascular resistance, although it can occur and peripheral spasm, decreased cardiac output and blood pressure remains low.

In the later stages of sepsis associated failure function nyrokz azotemia and oliguria, when liver damage occurs hyperbilirubinemia, the syndrome of disseminated intravascular coagulation. It is also possible central nervous system dysfunction in violation of consciousness (disorientation, agitation, psychosis). In typical cases, the symptoms associated with the presence of the primary source of infection, although the systemic inflammatory response center can not be determined. With the progress of pathological states show signs of failure, such as hyperlactatemia, hypoxemia, oliguria, impaired consciousness. In laboratory studies revealed leukocytosis or leukopenia, thrombocytopenia and reduction of other factors in the blood hemostasis.

Coordinated concept of sepsis requires a systems assessment of severity of the patients, which will give the ability to objectively assess the severity of the patients, the effectiveness of the therapy, to predict the level of mortality and length of intensive care.

The systems proposed for assessing the severity of the patients can be divided into 3 groups:

♦ methods based on the collection of objective clinical and laboratory data (APS; APACHE I, II, III; SAPS; SOFA);

♦ methods based on statistical modeling - MRM system;

♦ system to evaluate the severity of the patients according to the number and complexity of research methods and treatment necessary for its maintenance - the system TISS.

Studies have shown statistical significance and the importance of these systems and no significant difference in criteria such as sensitivity, specificity, and overall correctness of the method.

 

METHODS OF INTENSIVE CARE

 

Most of the patients with sepsis requires prompt readjustment purulent-inflammatory foci, which lays the foundation for the effect of intensive therapy. All methods of intensive therapy used in the treatment of sepsis, the degree of priority can be classified into two groups:

• methods, efficacy demonstrated broad clinical practice (the preferred method);

• methods, which use appropriate from the standpoint of pathogenesis, but their effectiveness is not recognized or proven only experimentally (Supplementary Methods).

This separation is useful from a practical point of view, because it allows to concentrate efforts on the most important areas of treatment, without the realization that you can not count on the effect of the other, especially in terms of time and shortage of medicines.

 

Tab. Treatment of patients with severe SIRS and septic shock.

Control of septic focus |осередок|

Includes resection, plikatsiyu, eksteryryzatsyya firmware or perforation of hollow organs, drainage and necrosectomy in necrotizing pancreatitis, drainage of abdominal abscess or empyema; aggressive rehabilitation bronhialnohodereva with severe pulmonary lesions, drainage blocked urinary tract, replacement of infected vascular grafts.

The patient, who is in septic shock, intensive therapy should be limited in time and aimed at stabilizing vital functions for further surgery, without which all resuscitative measures are doomed to failure.

Supportive therapy

Respiratory System

Requires use of mechanical ventilation with PDKV and / or other modes of ventilation to maintain oxygenation, but with minimal risk of lung barotrauma.

BCC |

Introduction sufficient volume of fluid (preferably crystalloids) to maintain adequate preload and optimize cardiac output. Wedge pressure pulmonary capillaries must be maintained at 15-18 mm Hg

Hemodynamics

Patients with septic shock (stage C) requires an increase in cardiac output due to lower peripheral vascular resistance. In stage D, cardiac output should be increased, but in this case you need to use vazodylyatatorov due to the pronounced increase in afterload due to peripheral vascular spasm.

kidneys |брунька|

Often requires the use of one of the many methods of hemofiltration and / or hemodialysis.

Stress bleeding

Requires use of a H2-hystamynoblokatora or sucralfate. Introduction antacids through nasogastric tube is usually ineffective.

Antibiotics

Shall be used or the results of bacterial studies, or against the most likely infectious agents.

 


Primary methods of intensive care

 

Antibiotic therapy (ABT)

 

Despite the emergence of new, fundamental understanding of the nature and systemic organ damage in sepsis, antibiotics continue to play a critical role in treatment.

Selection of ABT "first day" (before the results of bacteriological examination) is dependent on the location of the source of infection on the basis of known options domination of microorganisms and their sensitivity to antibiotics, and the severity of the immune status of the patient, pharmacokinetics, potential side effects and cost.

 

TERMS ABT sepsis:

 

1. For empirical antibiotic ABT choose a wide range of bactericidal action type or combination of drugs that have activity against potentially possible in this clinical situation pathogens.

 

The lack of protection mechanisms antiinfection sepsis requires reaching perhaps more complete eradication of microorganisms and thus antibiotic with bactericidal action type (b-lactams, aminoglycosides, fluoroquinolones).

In recent years, increased the number of observations that show high efficacy of monotherapy of severe sepsis carbapenems (imipenem, meropenem). This fact is connected with ultra range of products, low-acquired resistance, the ability to use in patients with multiple organ dysfunction.

Prediction result of septic process is largely determined by the severity of homeostatic disorders before treatment. There is a direct correlation between the number of organ dysfunction syndrome severity and probability pon fatal. For example, in sepsis with MOF 2-3 systems, septic shock, mortality ranges from 35 to 75%. In this regard, the choice of optimal starting circuit ABT should be carried out taking into account the risk of death: the higher the likelihood of an unfavorable outcome, the greater are the arguments in favor of the appointment of agents with the highest activity and lowest ability to increase the content of endotoxin in the blood. In these categories of patients justifiably use carbapenems as the primary scheme ABT. Similar tactics are justified and in postoperative abdominal sepsis.

Dyskutabelnym remains the question of the admissibility of monotherapy with carbapenems Escherichia infection. Perhaps this should be discussed on a case-by-case basis, based on the severity of the patient's level of resistance of microorganisms. In severe angiogenic sepsis associated with central venous catheterization when there is a high risk of the presence of staphylococci metytsylinorezystentnyh should begin therapy with vancomycin.

 

2. Intravenous route of administration of antimicrobial agents is mandatory in patients with sepsis.

 

3. Selection of dose and multiplicity of administration depend on the type and availability of bactericidal antibiotic effect and sensitivity of microorganisms.

 

Before antibiotics are bactericidal concentration dependent, include aminoglycosides and fluoroquinolones. Therefore, they should be given the maximum allowable dose for a particular patient. For aminoglycoside antibiotic characterized by a long effect. In this regard, rational bolus aminoglycosides, which creates a short-term high concentrations of drug in the blood and tissues.

Detection of antibiotic in the aminoglycoside antibiotics led to a number of one-time (1 per day) entering all the daily dose of gentamicin, netilmicin, amikacin. Results of multicenter studies demonstrate at least as clinical efficacy and reduced toxicity. However, you need to very thorough approach to calculating creatinine clearance, especially in syndrome MOF.

Bactericidal b-lactams time-dependent effects. Increasing concentrations not accompanied by accelerated destruction of microbes. It is believed that one should strive to maintain a constant concentration of the IPC, which exceed in 2-5 times. To use this dosing infusion device. Precisely the pharmacodynamics b-lactams in many clinical situations do not apply to the maximum dose.

Yes, there were conclusive studies that demonstrate the same clinical efficacy medium (1.5-2.0 g / day) and maximum (3.0-4.0 g / day) doses of imipenem in severe infections. Ceased used megadoses of penicillin: most modern protocols guiding the daily dosage not exceeding 20 million units. Exceptions should be made during treatment with penicillin antysynohnoynymy due to higher IPC for P.aeruginosa, and meningitis caused by Gram-negative microorganisms.

 

4. After clarifying the nature of the microflora and its sensitivity if necessary, make adjustments to treatment: a transition to monotherapy, narrower spectrum drugs or less expensive (eg, oxacillin instead of vancomycin in detecting metytsylinochutlyvoho S. aureus).

 

In most situations, except for infective endocarditis should not be long-term (> 7 days) used aminoglycosides. The use of gentamicin as a component of combination empirically ABT possible only with community-acquired sepsis origin. With hospital infections preferred amikacin or netilmicin.

 

Infusion therapy

 

Fluid therapy in sepsis promotes restoration of adequate tissue perfusion, correction of homeostatic disorders, reducing the concentration of toxic substances and mediators of septic cascade.

Heart failure is the reason for adding dobutamine infusion 5-7,5 mg / kg / min dopamine or 5.10 CIM / kg / mhv. With the development of septic shock choice sympathomimetics determined by specific hemodynamic situation.

All infusion environments have both their advantages and disadvantages. Given those that have to date, there is no reason to prefer any of infusion medium.

 

Respiratory Support

 

Adequate and timely respiratory support - one of the highlights of the treatment of sepsis. In recent years, along with well-known arguments in its favor (support oxygen transport, reducing the work of breathing) was obtained by another: in hypoxic conditions dramatically increases the reaction rate of septic cascade.

 

Restoration of organ and tissue perfusion

 

Restoration of adequate tissue and organ perfusion may contribute to the use of low molecular weight dextran plasma substitutes from starch, heparin 10-20 ths. / D / v, dopamine 0.5-3 mcg / kg / min, dobutamine 2.5-5 mg / kg / min and others.

 

Nutritional support

 

The development of sepsis syndrome pon usually accompanied by manifestations hipermetabolizmu. In this situation, covering energy demand is due to destruction of their cellular structures (autokanibalizm), which exacerbates existing organ dysfunction and enhances endotoxemia. Because of artificial nutritional support is a very important component of treatment.

The optimal value of the daily calorie - 40-50 kcal / kg. Emphasis should be put on enteral nutrition special blends (Izokal, Nutrilan, Nutrizon et al.). These mixes are balanced by major nutritional components, high-calorie containing supplements of trace elements and vitamins. In enteral path must be brought to 80% kalorazh entered.

 

 

Correction of immune disorders

 

In severe sepsis, there is the development of secondary immunodeficiency. His appearance is most typical for surgical infection. Extensive festering wounds with high bacterial invasion leads to intensive use of factors of cellular and humoral immunity. The basic principle imunokorektsiyipry sepsis - filling in the missing parts of the immune defense. However, its adequacy in surgical sepsis, primarily depends on the radical reorganization of purulent lesions. In the acute phase of pathological process shown passive (replacement) therapy immunoglobulins intended for intravenous administration: intraglobin (IGG) 2-5 ml / kg for 2-3 days pentahlobin (IGG and IGM), 5 ml / kg / day three times.

 

Additional methods of intensive care

 

Extracorporeal detoxification

 

After performing a radical reorganization foci of infection, elimination of hypovolemia, recovery of peripheral microcirculation, eliminate hypoxia ensure optimum ABT, caloric support, immunotherapy and in the absence of gross disturbances in the hemostatic system in the treatment of sepsis with MOF can be used extracorporeal detoxification methods: hemofiltration and plasmapheresis.

 

Glucocorticoids

 

Glucocorticoids are used in the treatment of septic shock, since the 50-ies. But in 1987 after the publication of the results of two multicenter studies concerning evaluation of the application of pharmacological doses of methylprednisolone (30 mg / kg or more), much of the resuscitation of using glucocorticoids refused. Their effectiveness could prove only with meningococcal.

In deciphering the mechanisms controlling the synthesis and secretion of cytokines new arguments in favor of their use, but in very moderate doses of 60-120 mg prednisone or hydrocortisone 200 mg per day.

 

Inhibitors of free radicals

 

Their purpose is shown in sepsis through activation processes of free radical oxidation and the development of an imbalance in the lipid peroxidation, which increases structural organ damage. The most dramatic increase in the rate of free radical oxidation observed in sepsis, combined with respiratory distress syndrome. To increase the antioxidant capacity of the possible use of vitamin C, tocopherol.

 

 

Endotoxemia |

Under endogenous intoxication (EI) understand the revenue in the internal environment and the preservation of its surplus substances generated in the body as a result of systemic disorders and metabolic disorders excretion of metabolic products or processes under the influence of hypoxia and inflammation necrobiosis.

Manifestations EI depend on the depth and extent of damage increase with failure and, especially, the failure of organs and systems, providing immobilization, biotransformation and excretion of ETR.

Massive and continued receipt of such substances in the internal environment of the body (tissue fluid, lymph, blood) is another factor damage. Pathological effect of ETR on the body depends on the main road of income - through the thoracic lymph duct or through the gantry section of the circulatory system. Organ and systemic effects EII implemented in typical pathological condition of the body, which is so called endotoksykozu.Zatempom ETR accumulation in the body of the patient and the development of body's response to EI distinguish acute, subacute and chronic endotoxemia.

Depending on the basic mechanism of EI allocate productive, retention, resorptive and infectious or microbial, intoxication.

Productive: EIvyznachayetsya foremost factors aggression, largely characteristic damage to many organs. Under general inflammation productional EI supplemented resorption decay products of damaged tissue. Severity rezorbtsiynoyi EImozheminyatysya depending on the rate of melting and sequestration foci of necrosis.

Retention EIvynykaye primarily for violations of due process dezyntoksykatsiyi functional failure of organs and systems that provide immobilization, biotransformation and excretion of ETR (lung, liver, kidney, reticuloendothelial system, etc.).

InfektsiynaEIpov'yazana from entering the blood of toxins and microbial pathogenicity ynnykiv microbes and found in purulent-putrefactive infection.

 

Diagnosis of endotoxemia

Diagnostic severity EI seems easy task and requires a combined approach. Often a combination of several types of EI in one patient in the real world of clinical practice determines the severity and stability of endotoxemia and difficult removal of the patient from this often critical condition requires early use of intensive treatment. Out of endotoxemia achieved the support of vital functions of the patient's normal activities intensive care and special assistance, including surgery on fires and tanks EI, increasing opportunities dezyntoksykatsiyi and conducting active detoxification.

Expression of EI is determined by the clinical manifestations of this pathological condition and laboratory criteria. Encephalopathy and hyperthermia, respiratory and circulatory (dyspnea, tachypnea, tachycardia, deviation from normal for the patient blood pressure, signs of peripheral blood flow disorders), yellowness of the skin and reducing the rate of urination - clinical signs of EI. Laboratory studies of blood and urine can specify the primary medical review data and assess the severity of EI and endotoxemia.

Among the routine laboratory criteria most accessible EI EI hematological parameters that assess oferythron circulating concentrations of hemoglobin and red blood cells, peripheral blood hematocrit, erythrocyte sedimentation rate, the concentration of blood leukocytes and wbc of podalshymrozrahunkom several indices: the ratio of neutrophils / lymphocytes, leukocyte intoxication index (LII ), hematological toxicity and rate others.

Evaluation of srednomolekulyarnyh polypeptides (IMS) by Gabriel screening method (spectrophotometry TCA-supernatant plasma at 254 nm). More informative method can be achieved, for example, research content MSM at two wavelengths with the calculation of the ratio E254/E28O or even receiving the data but the entire spectrum spectrophotometer with an interval of 8.4 nm. The study of these parameters in plasma, erythrocytes and urine washings patient extends the idea of ​​the severity of EI and endotoxemia and enables us to monitor the effectiveness of intensive therapy and individual treatment.

Patients biological methods for evaluating the toxicity of the internal environment for large animals (mice with blocked RES) readily available, and simple (parametsiyi, tetrahimeny) informative. In clinical practice to assess the severity of endotoxemia can be used some indicators that characterize the response of the immune system to toksynemiyu and, above all, nonspecific immunoreactivity (concentration of fibronectin and lysozyme, phagocytosis), the functional state of neutrophils (cationic-lysosomal indicator NBT-test) content of circulating immunocomplexes. Wider research immunogram blood allows to evaluate immunosuppression and metabolic and immune deficiency do directed immunotherapy.

Functional studies in the medical surgical control of OP patients using rapid methods to assess the reaction of the vital functions on EI and identify a number of clinical syndromes that are determinants of acute endotoxemia: cerebral syndrome and fever, respiratory syndrome, circulatory disorders, hepatorenalnyy syndrome and dynamic ileus syndrome, syndromes water and electrolyte disorders and diffuse intravascular coagulation).

 

Active detoxification

 

Rate of EI depends not only on production, resorption ETR, but also on the efficiency of protective detoxification mechanisms of the patient: their failure with respect to growth toksynemiyi or failure due to the same disease are forced to use special therapeutic measures. The objectives of such medical care includes supplementing or replacing natural detoxification mechanisms: dilution and immobilization ETR, biotransformation them, especially withdrawal.

To clinical waste activities may include:

- Detoxification infusion therapy, as well as methods that provide increased natural excretion ETR (forced diuresis);

- Methods sorption ETR as intracorporal (enterosorption) and extracorporeal (hemosorbtion, plazmosorbtion, limfosorbtion);

- Removal of part of the ETR components of the internal environment (blood replacement, plazmoforez and plasma replacement, external lymph drainage);

- Methods that provide simulation excretory mechanisms of detoxification as intracorporal (peritoneal dialysis), and extracorporeal (hemodialysis, hemofiltration, ultrafiltration of blood).

By biotransformation ETR can be attributed to connect isolated homo-or ksenoorhaniv (liver, kidney, spleen). Before therapeutic interventions actually active detoxification methods aimed adjoin change the internal environment through the so-called hemocorrection. Hemocorrection achieved by oxygenation, magnetic treatment or irradiation photo-modification of blood who perform as extracorporeal, after a temporary blood collection and intracorporal, intravascular route.

The most widely used forced diuresis, plasmapheresis, hemodialysis and plazmosobrtsiya, external drainage of lymph and limfosorbtsiya, peritoneal lavage and peritoneal dialysis.

 

Detoksykatsyonnaya infusion therapy. Even a simple increase in blood and extracellular fluid space expansion by infusion of crystalloid solutions krovozaminnyh help reduce the severity of EI. Especially clearly detected against the background of hypovolemia and dehydration. Detoxification is achieved by reducing the extracellular and intravascular concentration ETR that facilitates their transition to the mobile extracellular fluid from the surface of the cell membrane and ground substance tissue, as well as cellular fluid space. Meaning is not only a simple dilution ETR, but also improve the system and peripheral circulation, disaggregation of blood cells that committed normalizing effect on metabolic processes at the cellular level, including the processes of biotransformation ETR.

In the simplest version infusion detoxification using isotonic sodium chloride and glucose but preference should be given polyionic solution, simulating the composition of the extracellular fluid (Ringer-lactate or Ringer-acetate hlosol, atsesol et al.). The application of infusion medium, providing corrective action for disorders underlying the development of EI, such as the severity and tolerance of hypoxia. This perspective can be mafusol environment, the active ingredient of which is sodium fumarate. Ability infusion detoxification greatly expanded through the use of colloidal blood substitutes that will not only increase the software, improve microcirculation but also linking some ETR. These substitutes detoxification is gemodez and Neogemodez, polidez and zhelatynol.

Using these substitutes can not only stabilize at a certain time of blood, promote movement of fluid between the sectors of the extracellular fluid space, but also increase the income of albumin from the interstitium into the bloodstream, which facilitates the processes of dilution and immobilization ETR. The main result of these substitutes is the ability of their active substances form complexes with many toxic ETR, circulating with the blood. Besides infusion detoxification is largely determined by that environment inherent ability to stimulate diuresis, and promote suppression readsorbtsionyh opportunities renal tubular epithelium, for example, by proteinuria imposed in connection with an infusion zhelatynolyu. Efficiency increases detoxification using polivisolinu in which polyvinyl alcohol is combined with glucose and glutamine, which facilitates not only immobilization ETR, but their biotransformation due to the stabilization of the detoxification function of the liver due to these additives.

Dose infusion depends on the severity plazmovtraty and dehydration and should be at least 20-25 ml / kg MT patient in 1 day. The main route of administration of these environments - intravenously through a peripheral or central vein. In some cases, especially when circulatory failure may be used by regional intraarterial administration through catheterized aorta, abdominal artery or its tributaries. Detoxification dose of such solutions is 5-10 ml / kg MT patient in 1 night for gemodez and Neogemodez, 10-25 ml polidezu and polivieolinu and not less than 20-25 mL in 1 day for zhelatynolyu.

Amid infusion detoksykatsiynyhh plazmozameniteley or for 2-3 hours. after the completion of infusion should not be used a lot of drugs (antibiotics, cardiac glycosides, hormones, etc.). due to their ability to bind the active substance and reduce the expected therapeutic effect. Synthetic detoxification solutions should be applied only at the height of EI, no longer than 3 - 5dib. One must consider the possibility of downloading RES velykomolekulyarnymy fragments colloid and iatrogenic damage to the immune system with prolonged use of infusion medium, especially gemodez.

The direct effect of detoxification infusion therapy is reduction of clinical signs of EI (nausea, vomiting, tachypnea, tachycardia, hyperthermia, and others.) And clear growth rate of urination, which can be further enhanced by using special therapeutic action. This approach is the basis of such medical care as forced diuresis (PD).

 

Forced diuresis system infusion, medication and those that adjust the internal environment of therapeutic actions aimed at active detoxification by maintaining a high rate of urination for several hours or days. In clinical practice, forced urination is more than 2 ml / kg body weight of the patient in 1 hour. It is believed that in the course of PD increased output not only water, but all osmotically active substances that are in this pathological condition components of the internal environment of the patient or received it with infusion media.

Prerequisite forcing diuresis is no deep dystrophic and necrobiotic changes in nephron filtration and renal tubular apparatus, as well as maintaining adequate hyper-reaction to the infusion blood pressure, hypervolemia and hemodilution.

There are two basic types of PD: infusion-forced and drug-forsovanyy.U first case, the water load diuresis stimulated by infusion or izoosmolyarnyh slaboosmolyarnyh infusion medium. In a medykomentozno FD used drugs that significantly increase the diuretic effect of water stress. Detoxication PD due not only simple filtration increased urine output and passing ETR, but a decrease in their readsorbtsiyi, changing the molecular state. To facilitate excretion through the kidneys ETR than stimulation using the principle of competition in the processes of proximal tubular readsorbtsiyi. Thus, the maximum glucose transport through the kidneys, achieved against a background of moderate hyperglycemia and glycosuria ceases readsorbtsiyu polysaccharides, including microbial and proteinuria imposed, for example, through the use of hemodilution during zhelatynolyu prevents the reuptake of primary urine protein substances. Plan of PD are different, but more or less certainty in each of them provides three main stages.

Beginner - phase hydration and hemodelyutsiyi-achieved by loading infusion, during which examine the reaction of the circulatory system is to load data CVP, and ECG. An important technical terms because catheterization is considered one of the central veins, which provides a high rate of infusion (not less than 6.7 ml / kg of patient MT per hour), the total dose of about 30 ml / kg. In fact, at this stage, conducting primary infusion detoxification.

Rational scheme hydration and hemodilution involves injections of saline crystalloid solution (Ringer-Locke optimally, laktasola, atsesol), alternating with poliionym solution of type mortar laboratory. Hydration should be combined with stabilization of blood by colloidal substitutes detoxification action (gemodez, zhelatynol), and the presence of distinct signs of hypovolemia - mostly volemichnoyi action (albumin or protein volekam or oksiamal, less polyglukin and reopolyglukine). Already at this stage is justified gradual drip infusion medium consisting of aminophylline in doses up to 480 mg.

The duration of the initial phase PD defined tolerance rate infusion (in response CVP, central hemodynamic parameters). With expressive heart failure hydration and hemodilution as further medical forcing diuresis can be undertaken as quickly intra infusion at a rate of 50 ml in 1 min if the patient for therapeutic purposes catheterized by this time the abdominal aorta. In many cases, the initial stage of complete PD buffering internal environment infusion proofreaders (sodium bicarbonate or trysaminolu), preferably under the control of acid-base status of blood and urine. In identifying the patient's metabolic acidosis dose buferovanoho solution should provide not only the correction of acidosis, but also create a small surplus bases in the extracellular fluid.

The second stage of PD - direct forsuvannyasechovydilennya - usually achieved by injection stapedius 15-20% solution of mannitol or sorbitol dose of 1-1.5 g dry matter per 1 kg of the patient. In the absence of the necessary response to the introduction of osmotic diuretic and intolerance strumennoyi infusion forcing ensure rapid drip infusion saluretics usually furosemide (Lasix) at a dose of 1-3 mg / kg MT patient.

At long sessions FD these medications should be used consistently, given the weak hope of repeating the same type of diuretic effect in their repeated use for one day. Detoxification effect is most pronounced at FD rate not less urine 4-5 ml / kg MT per hour, ie 3.5-4 ml / kg for the first 12 hours for adult patients with an average body weight.

The third stage PD - Support diuresis-provided polyionic infusion solutions and is to maintain homeostasis. Requires accurate records diuresis achieved continuous bladder catheterization throughout the PD, because it allows to control how hidrobalans the patient, and partial renal function in concentration indices. Maximum water retention in the body for a session FD should not exceed 2% of MT patients.

This is the most effective therapeutic measure when removed, drained or blocked fireplace productive EI, no deep lung damage and infarction.

Using FD method as active detoxification contraindicated in:

- Acute heart failure syndrome metabolic origin of small ejection;

- Severe congestive heart failure, decompensated valvular heart defects;

- Myocardial infarction;

- Cardiac tamponade;

- Alveolar edema or progressive compression of the lungs;

- Acute or chronic renal failure.

 

 

External drainage of lymph

 

External drainage of lymph (ZVL) catchment thoracic lymphatic duct (HLP) is used in the treatment of EI. Inflammatory and destructive processes are accompanied by increased revenues in the lymph and then the blood products of impaired metabolism (bilirubin, ammonia, bile acids, phenols) and tissue destruction. Increased limfoproduktsiya characteristic of these conditions leads to increased pressure in the HLP to 25-30 cm of water. century. providing its expansion, facilitating its identification and catheterization.

When catheterization HLPduzhe desirable use of microsurgical instruments and devices that facilitate precision engineering intervention. In general terms, it is bare left venous angle by horizontal incision 5-6 cm long, 1 cm above and parallel to the left clavicle outward from the jugular notch. Pushing out the inner edge of the left sternum-clavicular-soskovydnoho muscle or passing between his legs in the loose tissue peredshodovoho seek space left venous angle. Pulling out the left internal jugular vein and carotid artery medially zblukayuchym nerve, oholyayut arc HLP. In this position, cut through the wall of the duct and drain its distal respectively caliber plastic (preferably Teflon) catheter to a depth of 2-2.5. Catheterization carried through the main trunk HLP or through one of its large lateral tributaries. Approximately 10% of cases kanyulyuvaty HLP fails.

Proceeds from catheter with high speed lymph flow, often muddy, gray-yellow or even red, which contains decomposition products, tissue detritus and erythrocytes, confirming indications and success drainage. To attach a catheter system for blood collection, which comprises a container with a solution stabilizer. Average extract 2-3 l of such lymph leads to a striking reduction in the severity of EI and endotoxemia, reduces pulmonary manifestations of dumping into the bloodstream of pancreatic enzymes, restores renal function, which allows the program to include treatment of such patient forced diuresis. Conversely, inadequate drainage, less than 0.5 liters per day, resulting in the fact that this therapeutic measure the expectations placed upon him. The same can happen if you accidentally remove the catheter, but in this case, especially after 1-2 days after surgery, lymph drainage can be saved if they removed a few stitches on skin wound and put a plastic drainage diameter of 8-10 mm and venous angle: in such cases limfostoma can efficiently operate a few days. Sometimes after dekanyulyatsiyi Strait 3-4 days some time stored on the allocation of lymph drainage channels, which may require special measures.

 

Periodic determination in lymph protein concentration, potassium, sodium, glucose, cytology central lymph and determination bullets EI it can control the intensity of production ETR and compensate for the loss factors of the internal environment infusion of protein and poliionyh solutions, prevents dehydration of the patient is necessary not only to maintain homeostasis, but also to maintain a high lymph. The latter may increase the introduction of 5 - 6% solutions of polyhydric alcohols (mannitol and sorbitol), dextran, Trental, ergotamine or even just hypertonic solutions of sodium chloride.

Indication NOL are pronounced manifestations of EI toxic effects which can not reduce conventional treatments. This is reflected in the progress of enzyme intoxication, and an increase holemiyi hiperamonemiyi, azotemia with a decrease in urine output, despite adequate volume infusion in the manifestation of disorders of higher nervous activity as a toxic encephalopathy.

Relative contraindications to this method of active detoxification find a steady decrease in peripheral blood pressure, a sharp drop in the concentration of potassium, magnesium, and total protein and albumin in the blood, a clear suppression of cellular immune responses to infectious component of EI. Loss of essential components of lymph and inadequate infusion limfozamischennya at ZVL than 3 days can lead to significant iatrogenic disorders of homeostasis and decrease imunorezystentnosti. Loss of lymphocytes from lymph may contribute to the development of infectious complications require transfusions leykolimfozavysi significantly worsen the underlying pathological process, if its development is essential microbial factor.

These shortcomings external lymph drainage can be largely overcome by using limfosorbtsii by coal hemosorbent and ion exchange resins, such as KU-2-8-2 or MHTY or napivselektyvnyh sorbent type ovosorba. This approach should be preferred in all cases of therapeutic catheterization HLP, although the process of limfosorbtsii still about 1/3 limfotsytivruynuyetsya. As a rule, use the indirect method limfosorbtsii, passing through the column with the sorbent lymph, harvested aseptically in fluid container (bottle, bag). Only at very high pressure in the lymphatic system (more than 16-17 cm of water. Cent.) And relatively low CVP can use significant limfovenoznyy gradient and spend some time limfosorbtsiya direct method, masoobminnyk connecting directly to a catheter inserted into the inferior vena cava.

 

Enterosorption

 

Enterosorption (EC) - the active detoxification method based on output factors EI through the gastrointestinal tract by oral administration of traditional and specially developed for this purpose sorbents. Enterosorbents can be both nonspecific and selective, but must meet several requirements:

- High sorption capacity with respect to the components of the intestinal contents, which are removed with minimal

loss of mineral components;

- Lack of desorption agents in the evacuation of the sorbent and depending on changes in the reaction medium;

- Good opportunities izoperystaltychnoyi evacuation without dyspeptic disorders and trauma of the mucous membranes;

- Non-toxicity and a favorable effect on the processes of secretion and intestinal biocenosis intestinal microflora.

The reason for entersorbtsiyivvazhayut revenue opportunity in the intestine ETR expressed homeostatic disorders, frequent dynamic ileus with disorder and cavity wall digestion, ascending colonization paretic intestine pathogens and related fermentation and putrefaction processes, leading to increased flatulence and dyspeptic disorders.

Among absorbents for use with this may be recommended carbon sorbents based on carbon - (NCS P1.SKN P2), industrial activated carbon (SCT 6A HF), fibrous sorbents (Vualen) liquid chelators based polivinilpirolidoua (enterodez and entesorb) and Powder from lignin (polifepan). Most effective in patients in this category is now considered polifepan which provides the almost all requirements.

Polifepan milkodyspersnym powder is odorless tasteless and has on its surface a large number of active groups, suggesting the possibility of chemisorption and complex, not only physical absorption as using carbon sorbents. In this in terms of the specific sorption of low-and srednomolekulyarnyh substances polifepan not inferior coal, and sorption capacity relative to bacterial toxins and even microbes greatly exceeds them. These same properties and paste polifepana - lihnosorb. The daily dose is 1 - 1.5 g / kg body weight of the patient and should be divided by 4-5 methods, each of which lags by about 1.5 hours of oral administration of other drugs and food. Duration enterosorption about is not less than 5 days.

Detoxication enterosorption on the background of the other components of the treatment of these patients is the rapid decrease of EI in mild and average degree of endotoxemia. Detoxication provided by adsorption of excess intestinal contents of biologically active substances that enter the bile, pancreatic and intestinal juices. Simultaneously, the sorption products of protein metabolism, bilirubin, oligopeptides. In addition, there is a significant (80-90%) sorption intestinal bacterial toxins and prevent their arrival in circulating blood clearly reduces the burden on natural processes dezyntoksykatsiyi ETR. Intense absorption eliminates intestinal gas bloating, eliminates blockage of microcirculation in the intestinal wall and restores the barrier function of the latter.

By stimulation of receptor zones chelators have distinct ability to enhance intestinal motility and evacuation content. In severe stages of endotoxemia can use active methods of detoxification (hemosorbtion, plasmapheresis, external drainage lymph), thus providing consolidation achieved effect.

 

Hemosorbtion

 

Hemosorbtion (HS) - One of the most common methods of active detoxification, which simulate the mechanisms of immobilization ETR. Due to the relative simplicity of this extracorporeal operation, high degree of sorption of different ETR, the possibility of removal from the blood of microbial substances, including the blood circulating macromolecular compounds and even microbes, HS often include program efferent therapy for EI.

Essentially all sorption methods conducted one perfusion circuit: through sorption column (masoobminnyk) from Vitro, alone or with a device forced circulation (pump) leaking blood of the patient (or blood components). Depending on the location of adsorption column in relation to the circulatory system of the patient distinguish the following options for the connection: arteriovenous, venovenoznyy, venoarterialniy, pendulous, portokavalnyy and kavoportalnyy, limfovenoznyy. When arteriovenous connection adsorption column may conduct HSsamoplyvom using haemodynamic factor. In all other ways the movement of blood through sorption circuit is achieved by force, by using different perfusion devices - from simple roller pump type APPK-3, SC-2, SC-196 to the most complex machines with computer regulation regime gemoperphusion - var-1, UЭH -1, Hemosorb and others.

Hemosorbenty.V currently in broad clinical practice often use nonspecific sorbents, which include activated carbon and ion exchange resins, their action is based on mechanical and chemical sorption. In physical adsorption characteristic of activated carbons, the fixation substance that is circulating blood in the pores of the sorbent, and the molecule substances sorbed not undergo structural changes. In chemical adsorption, which is typical for ion exchange resins, formed the link between molecules of a substance that is sorbed and active chemical groups on the surface of the sorbent. Most nonspecific sorbents aggressive towards the formed elements of the blood and clotting factors, which makes use heparinisation. In this regard, together with the ETR can absorb vitamins, hormones and even dissolved oxygen in the blood. Being developed sorbents aimed at selective sorption of one substance, or at least groups of substances that determine the specificity of a particular EI. So hemosorbent relatively trypsin and other proteinases may sorbent duck protein - ovosorb.

There are three classes of widely available carbon sorbents:

- Derived from natural raw materials (SCHT-6A - peat coal, CAU - coal from fruit stones);

- Sorbents that produced by a carbonated synthetic copolymers (SUHS, various modifications of the spherical karbonitu NCS SCS);

- Carbon fiber sorbents with knitted fiber (aktylen).

Carbon sorbents with maximum speed and low-absorbing compounds srednomolekulyarni branched structure and virtually inert with respect to substances such as ammonia, urea, bilirubin, phenols. Practical use of ion exchange resins are less developed, although some of them are quite promising, such as KBS-m. Among the ion exchange resins are sorbents with a considerable degree of selectivity, such as KU-2-8 (the vast sorption of ammonium) or MHTI-2 (for sorption of bilirubin and ammonium).

Access to the vascular system of the patient for hemosorption must be optimal to ensure unimpeded bloodstream through sorption column. When arteriovenous connection options desired overlay arteriovenous shunt, although it can be used catheterization puncture of the abdominal aorta cannula large caliber. When venovenoznomu connectivity options hemoperfuziynoho circuit kateteryzuyut central vein, the optimal intake of the inferior vena cava (catheterization via femoral vein) and injection into the upper vena cava catheterized. In severe heart failure and stagnation in the large circulation, by contrast, blood sampling is carried out from one of the hollow vein and injected sorbed blood into the aorta. In some clinical situations, the possible use of regional HS bypassing the liver or, alternatively, through the liver.

Mandatory heparinisation total during the whole session, HS (200-300 IU / kg body weight). Less use regional heparinisation.

Apparent speed gemoperphusion at GS 60-120 ml / min (depending on the type and characteristics of sorbent hemodynamic disturbances), optimum about 100 ml. Duration of perfusion 40-60 minutes, sometimes longer. It is determined by the severity of EI, if necessary in the course of HS Possible Replacement adsorption column.

Effects hemosorbttsiyimozhut be recorded as a change in the clinical condition of the patient, typical for this variant of EI, and on laboratory criteria, for example, the level of aggression factors in the blood, to change the content of polypeptides.

Given the characteristics of the kinetics and distribution of ETR between tissues and blood, in the case of fuzzy clinical improvement acquitted of two operations HS intervals of 18-24 hours diseconomies of efferent therapy conducted, suggesting conservation in this patient active nedrenovanoho fire EI or inadequacy of the selected sorbent and forced to change his treatment program.

Complications HS should be divided into two groups: the complexity of the gemoperphusion (thrombosis masobminnyka or so-called sintering of sorbent) and complications associated with patient response to extracorporeal gemokorrektsiya. Among them the most important are: fever, increasing hypoxemia, hypotension and vascular collapse. Causes of fever are: getting pyrogenic substances with sorbent microparticles through the filter (schilynovydnu hemoperfuziynoyi nozzle system) and dyzelektremiya example, hipokaltsiyemiya. These complications prevent thorough laundering masoobminnyka isotonic saline perfusion circuit before connecting to the patient.

Deepening hypoxemia determined sorption of oxygen, adverse effects which may occur against violations of pulmonary gas exchange. Clinically distinct hypoxemia and hypoxia require special measures in the form of pre-saturated sorbent or, in the most patients, included in the perfusion circuit malopotokovoho membrane oxygenator, which can be used by standard dialyzers for hemodialysis

The appearance of hypotension associated not only with possible hypovolemia, but with the sorption of vasoactive substances and hormones. Therefore justified routine administration of therapeutic doses of glucocorticosteroids (GCS) with the threat of such complications and venotonizuyuchyh means (sulъfokamfokayin). Mandatory infusion support along the HS. Ekstravaskulyarnaya blood loss in masoobminyku have to be compensated for blood transfusion after a session of HS in the volume corresponding to the volume filling perfusion circuit, or a bit more.

 

 

Plasmapheresis

 

Plasmapheresis - Operation extracorporeal gemokorrektsiya, in which partially or completely removed plasma. Although this operation is aimed mainly at removing EI factors contained in the blood, further movement of ETR tissue pool of blood as a decrease in their plasma concentrations significantly unloads cells and interstitium. Expressive detoxification effect Plasmapheresis is when plasmoexfusion volume reaches 40-60% of the blood, ie 1 - 1.5 liters for an adult patient. In combination with other methods of active detoxification such action Plasmapheresis in many cases, EI can be and at lower volumes infusion. Plasmoexfusion more than 1,8-2 liters of plasma in the adult patient is called plasma exchange and provides the most expressive detoxification, though aggressive towards the patient.

 

Fig. 7. Apparatus for plasmapheresis Russia – 05

 

In clinical practice, using several techniques Paphos. In discrete or stepped, variant Paphos perform incremental blood sampling on 0.4-0.5 liter twin in plastic bags or bottles with stabilizer (sodium citrate, heparin). Then these capacity centrifuged in refrigerated centrifuge, plasma merges and resuspenzovani crystalloid solutions in erythrocytes reinfuzuyetsya patient. Continuously or hardware, technique Paphos spend using devices - separators blood - both domestic (PC-05, FC-3, 5) and foreign (Aminko, 5S-3000, Koba spectrum, Dideka, Feng shaft, Fresenius, Hemonetiks, 1VM 1992). These devices are also centrifuge principle and allow you to quickly extract plasma from the patient's blood, which is continuously removed from the bloodstream in quantities necessary to achieve detoxication up to a total plazmozaminy. Optimum performance is achieved with approximately 1 liter of plasma for 1 hour. of the device that is connected to the vascular system of the patient. Ryeinfuzovannnya erythrocytes in such devices occurs in closed systems, which eliminates a number of discrete Paphos complications (infection reinfuzatu, significant fluctuations in CBV, damage to red blood cells).

The third method yemembrannyy Paphos, where plasma separation is achieved by filtering it through the semipermeable membrane in lamellar or fiber plazmofiltrah. These filters are designed by many foreign firms (Altino, Asahi, Hambro, Fresenius) and in our country (PMF-800, BP "Optics"). Average productivity plazmofiltriv - about 15 ml of plasma in 1 min. Selecting membranes can achieve not only plazmoeksfuziyi blood flowing through the filter, but the separation of the plasma albumin and the fraction containing the large-molecular pathogenic factors (fibrinogen, enzymes, antibodies, and especially immunocomplexes). This cascade plazmofiltratsiyadozvolyaye achieve isolated removal of pathogenic factors of EI without reducing labile plasma proteins.

In the management of patients with significant in severity and long flowing endotoxemia in the intensive care unit can be used multiple sessions Paphos. The frequency of sessions depends on the severity toksynemiyi, especially during prolonged endotoxic at which additional sources of EI can be damaged organs livelihood. The possibility of the next session Paphos defined stabilization of vital functions, although rational support these functions using general measures of intensive therapy, this method of active detoxification can be used in the most critical situations, such as recovering from clinical death. Preferably be applied in Paphos productive, retention and infectious EI.

Security Paphos depends not only on the technique of extracorporeal surgery itself, but also the choice of methods plazmozameny. If a high level of plasma protein and small volume plazmoeksfuziyi (20%) may replace the loss of plasma exclusively by crystalloid substitutes, then the intense Paphos to use colloidal environment. Their size must be at least 30% of the total volume of infusion required to stabilize hemodynamics and should constitute a significant part of natural colloids (albumin, protein, native plasma). When plazmobmini dose of natural colloidal plasma substitutes should reach 60% of the infusion and more.

Dangers and complications of Paphos can be divided into two groups. The first group is determined primarily features access to the vascular system (peripheral or central vein arteriovenous shunt) and the effect on hemocyte and clotting factors. The emergence of these complications depends on the method of Paphos. The second group of side effects and complications determined plazmoeksfuziyi impact on the patient and the initial, preoperative condition of vital functions and internal environment (protein and fluid and electrolyte disorders), size and choice ob'yemuplazmoeksfuziyi infusion program to run the operation and after its completion. It requires prompt medical monitoring of the patient in the course of Paphos and after. With intensive Paphos necessary gradual determination of central hemodynamics, especially in patients in critical condition, the dynamic control of laboratory plasma protein clotting factors, plasma electrolytes major.

Despite the fact that Paphos is considered one of the safest methods of active detoxification, this operation is contraindicated with significant heart failure, hypoproteinemia less than 52 g / L, hypoalbuminemia less than 25 g / l and especially while maintaining active (nedrenovanoho or neblokovanoho) foci or sources of EI.

Portability detoxification greatly enhanced when combined with perfusion plazmoeksfuziyi plasma taken through hemosorbent - plazmosorbtsiyi. This operation can be performed in a single path separator with blood or perform separately, after Paphos, in order to use adsorbed or otherwise modified autoplazmu for compensation in subsequent plasmapheresis. The effectiveness of detoxification and sorption greatly increased after prior freezing eksfuzovanoyi plasma. Effect krioplazmosorbtsiyi largely determined by the loss in rozmorozhuvaniy plasma cryoprecipitate, which contains much of the ETR. When plazmoobmini dose of natural colloidal plasma substitutes should reach 60% of the infusion and more.

 

Immunotherapy, immunoprophylaxis, immunocorrection

 

Immunotherapy (IT) as a concept combines different methods of action on the immune system (SI) to stop the pathological process in the body.

Immunisation (IP) includes similar steps used to prevent disease or relapse. Usually it is used to prevent infections in healthy people as a vaccine. Her other option - to prevent recurrence of allergic diseases (asthma, hay fever, and others.) By alerhovaktsynatsiyi.

Earlier immunotherapy and immunoprophylaxis considered only those treatments in which no specific biological agents: antigens, vaccines, toxoids, allergens, immunoglobulins and others.

Immunocorection (IMC) - a set of therapies that provide correction of defects in SI.

This concept emphasizes the commitment of used vehicles for color correction, restoration immunoreactivity, although these tools and methods are no different from immunotherapeutic immunocorrection but includes such methods do not recover or therapeutic inhibition of immunoreactivity as reconstructive surgery - transplant organs and cells of the immune system and, conversely, removal organs, cells, molecules CI patients. Thymus transplant, bone marrow, and especially gene therapy immunodeficiencies (eg deficit adenozyndezaminazy) - the most striking examples immune.

Immunomodulation (MI) - not a temporary increase or decrease in these or other indicators of immune reactivity.

Terms of substances with immunomodulatory properties, continuously growing. Often these properties are found in drugs previously used for other purposes - for the treatment of certain diseases. This indicates that the immune system vysokotropna to various substances, especially xenobiotics that enter the body. They or their biotransformation products interact with receptors on cells and extracellular factors SI and disrupt indicators of immunological reactivity, usefulness or harmfulness of which can be assessed only in specific situations.

Immunorehabilitation (IP) - a complex immunological, imunokorrehuyuchyh, social, environmental, biomedical immunization activities aimed at restoring altered immunological reactivity of the patient population or specific population of the continent.

Appointment immunocorrective, immunomodulating agents must always be justified as clinical and laboratory data of the patient examination. It depends on the severity of the disease and its course - acute, chronic. Selecting immunomodulating agents are not always logical enough, since they have a wider range of effects on the body than that of which would be judged by their origin and data annotations. Immune system and the only change some of its parameters are usually induce other changes.

 

The main objectives of immunotherapy and immunocorection:

 

• increase with lowered immune responsiveness and substitution insufficient factors in SI immunodeficiency;

• inhibition increased reactivity in allergy and autoalerhih. Due to the nature of immunotherapy and immunoprophylaxis of different diseases it is necessary to distinguish the following groups:

 

1) immunotherapy of diseases with high reactivity (allergic and autoimmune diseases);

     2) immunocorrection primary and secondary immunodeficiency diseases

     3) immunotherapy of tumors and lymphoproliferative disorders;

 

     4) immunotherapy transplantation reactions;

     5) imunokorektsiyaya violations reproduction.

  Immunotherapeutic effect can be obtained through the application of specific or non-specific tools.

 

The nature of the immune system to distinguish the following types of IT and IP:

Stimulant - used to activate immune responses in a healthy body to prevent infectious diseases and with immunodeficiencies.

Depressing, used for depression of immune responses in allergy and haveautoallergicheskie systemic (autoimmune) diseases.

Specific - used drugs antigens or antibodies specific against the pathogen or antigen.

Nonspecific include effects on the immune system chemicals, physical factors and antigens, nonspecific arisen in relation to the pathological process.

Mechanism of action distinguish active IT and IP, when the immune system actively responds to the drug (usually antigens, vaccines) and passive IT and IE when injected into the body in the form of antibodies prepared antisera or antibodies.

If categorize IT for the disease, it can be identified: 1) IT primary and secondary immunodeficiency diseases involving infection, 2) IT noncommunicable diseases: with increased reactivity (allergic and autoalerhychni disease), tumors and imfoproliferatyvnyh diseases; transplantation postreaktsiy; disorders of reproduction.

On features of IT application can be local (regional), combined and monotherapy. Total IT is that the drug or other agent that is introduced into the body, uniformly valid for all SI. In regional PI preparation or action is applied to the local cell damage, for example by electrophoresis substances through the skin, by inhalation aerosol preparations, washing their lacunae of tonsils, regional perfusion, etc.. Thus, firstly, reduced total resorptive, sometimes toxic effects of drugs (corticosteroids, immunosuppressive drugs) on the body, and secondly, is the most intense of their impact on local mukozalnyy immunity, which often plays a leading role in the pathological process, and especially promising for tsytokinoterapiyi.

Combination therapy in contrast to the use of certain drugs (monotherapy) includes both the use of multiple drugs acting on different parts of the SI, and the combination of different ways and means of general and local action.

 

The means, determine the type and method of immunotherapy

 

         The proper choice of IT and immunotherapy requires accurate diagnosis of the type, form, version, severity of the disease. Therefore, the purpose of treatment prior to general clinical and immunological examination, establishing not only clinical but also immunological diagnosis.

Successful IT is impossible without immunodiagnosis that, firstly, determines to IT and its kind, and secondly, allows you to monitor its implementation, thirdly, to evaluate the effectiveness of IT, fourthly, to determine the need for maintenance and IT immunorehabilitation.

 

         Before IT should evaluate immune status, ie objectively reveal that link CI violation which caused the disease and its recurrence.

Agents selectively affect one or another level of immune system enough, and although we know that some of them are focused on T-and B-lymphocytes as well as macrophages in vitro, or in animal experiments, it is not means that their therapeutic effect in patients is due only so, but not any other effect. The same applies to certain types of IT that are traditionally considered to be focused on the pathogen or its toxins. Antitoxic effect of antimicrobial agents may be due not only to the direct bactericidal (static) or toksynneytralyzuyuchoyu effect, but stimulation of the relevant subpopulations of leukocytes.

The question of the appointment of a particular drug is solved by studying the nature of violations of immunological reactivity, which is used as a common clinical and laboratory diagnosis, and a corresponding set of immunodiagnostic methods.

If necessary immunostimulation or immunosuppression should advance to test the impact of second-hand vehicles on leukocytes by skin tests and "windows" of patients as well as in tests in vitro. This testutvannya helps in some cases to predict efficacy and avoid possible complications. It was found that the effect of drugs on receptors in leukocytes of patients varies.

Found that many drugs (timalin, taktyvin, levamisole, and others.) In therapeutic doses did regulating effect: they strengthened economy mode expression of receptors on T-and B-lymphocytes of patients, and conversely, reduced its under normal terms. In addition, the effect of the drugs was uneven in different individuals, both donors and patients. In some patients the drug leucocytes showed a stimulatory effect on leukocytes others - depressing. The effect of the action of the complex effect of different drugs when exposed them apart. Thus, the required selection immunomodulators each patient by evaluating their effect on the receptors and their functional activity of leukocytes, production of antibodies, cytokines, metabolism.

However, data on the positive effects of the drug in vitro, unfortunately, not always confirmed the effectiveness of treatment. The drug that stimulates the increase of T cells in vitro, to be clinically effective only in cases of T-lymphopenia, when it is the main pathogenetic mechanism of the disease, ie T-cell immunodeficiency disease. Diseases such suprovodzhuyutsyanayavnistyu recurrent infection, and laboratory - a significant decrease in the level of T-cells (the level is above 45%), impaired phagocytosis.

However, please note that the effects of immunomodulators multifaceted and final of their impact in vivo is usually the result of direct and indirect effects not only on the alleged target cells Cl, but also on its other cells, and the endocrine and nervous systems. Therefore, to determine the clinical effectiveness of the drug can only trial treatment. Moreover, the assessment of effectiveness should be conducted by specially designed cards in which each symptom is characterized by points, and the result - total score reflecting clinical improvement. These laboratory evaluation of IS prominently in the characterization of SI and can be included as an integral part of or be considered independently.

 

The main clinical indications for immunotherapy, immunotherapy and immunorehabilitation:

 

Immunostimulation appointed in protracted, slow pathological processes accompanied humbled indicators leukocytes, T-, B-lymphocytes, monocytes, macrophages, or granulocytes and complement. This therapy is also indicated in the treatment of chronic immunosuppressive agents.

Imunodepresyvnimetody used mainly in autoimmune and allergic diseases, as is typical for these changes in immune status including increasing the level corresponding antibodies and high T-cell sensitization.

It is important to assess the relation of the form IT major phases of the immune response: inductive, proliferative, effector. As IT is used usually in the middle or in the early period of the disease, it operates in the effector phase of the immune response, less than in the previous two. This should be considered when using certain drugs, some of which affect mainly on cell proliferation, others - on the selection of mediators, and others - on the last interaction with target cells.

In appointing IT and IP should it justify and plan according to the type of immunopathology.


 

Anaerobic infections

The first mention of anaerobic infection is found in Hippocrates. Ambroise Pare described the disease in the form of hospital gangrene. Presented in sufficient detail the clinical picture of anaerobic gas infection in the works M.I.Pirohova who watched definite pathology during the Crimean War and called her "local stupor," "mephitic gangrene", "acute malignant edema".

In 1899 Lidental Hihman and found that the main role in the occurrence of gas infection belongs Cl. perfringens, which opened seven years earlier. Later it was found that the main pathogens anaerorbnoyi gas infection are: Cl. perfringes (44-50%), Cl.oedomatiens (15-50%), Cl. septicum (10-30%), Cl. Hystolyticus (2-6%). All these organisms are spore-forming bacilli.

In the last decade, with the development of anaerobic technology in patients with gas gangrene were sown Cl. soldelli, fаluх, sporogeneus.

The idea of ​​the genesis anaerobic infection connected with the above mentioned mikroorganisms kept the 70-y of XX century. At this moment with robortam Faingold separated somewhat different to the clinic pathology with special course that caused nosporogeneus (clostridial) anaerobes.

Therefore, at the present stage of development of the doctrine of surgical infection separately allocate appropriate anaerobic clostridial and anaerobic clostridial infection.

Anaerobic clostridial disease INFECTION considered wartime. Indeed, the largest clinical material has been accumulated and summarized the experience of the Great Patriotic War, but now days when analyzing the results the Afghan war and large ecocatastrophe (earthquake in Armenia, Turkey, California). Floor "is originated from the fact that the implementation of clostridium, mainly in the soil which fall from the gastrointestinal tract of mammals requires certain conditions that in fact, occur at mass lesions:

- Large amounts of necrotic tissue and poorly oksehenovanyh;

- Significant damage muscles and bones;

- A deep wound channel;

- Presence in the wound closed cavities, "pockets" and "heats";

- Ischemic tissue damage due to major vessels or imposed on long plait.

Pathological-anatomical changes during anaerobic gas gangrene characterized by an acute inflammation of the serous-alternative, followed by progressive necrosis of tissues. In areas traumatic necrosis produced a large number of microbial exotoxins (hemoliziny, miotoksiny, neurotoxins) that cause progressive necrosis of muscle tissue. In Cases fascial swelling increases with subsequent stasis and thrombosis in the great vessels. As a result of exotoxins in the affected area develops hemolysis, which together with the decomposition products of muscle (myoglobin) prosyakaye fat and skin, causing the appearance of typical anaerobic gangrene brown bronze and blue spots.

Pretty typical for definite pathology phenomenon is gassing. Gas bubbles infiltrate klitkovynni tight spaces and cause expression of a number of symptoms.

In anaerobic clostridial infection quickly growing endotoxemia, accompanied by significant disturbance of water and electrolyte balance, depending on extremely large exudation in the area of ​​injury. Because progressive endotoxemia and dehydration quickly death occurs.

Classification.

For anatomical features:

surface forms - epifastsialni gangrene

deep forms - subfastsialnye gangrene.

In pathological anatomical features:

emphysematous, swelling and tkanynnolizuyuchi form.

Adrift:

lightning, rapidly progressive and torpid forms.

Fulminant form usually manifests within a few hours.

Rapidly progressive - during the day.

When torpid course Clinic can develop within 2-3 days.

I give very demonstrative example lightning clinical course of anaerobic gas gangrene, which was observed in our clinic: the patient appealed to the district hospital with complaints of intense pain in the area arching right hand, which was 2 hours after injury shovel at work in the garden. When viewed in the district hospital suspected anaerobic gas infection and the patient ambulance was sent to our clinic. In the receiving department was delivered in 25 minutes, stated that the swelling had spread to the upper third of the arm. After 15 minutes, the patient brought to the operating room and in the performance of metameric cuts limbs from fastsiotomiyeyu, literally at hand surgeons observed an intensive dissemination gas on the front and back surfaces of the chest, first with the affected side, and then on the opposite side. Despite surgery and started intensive therapy the patient died on the operating table.

Clinic and diagnostics.

Initially when anaerobic gas gangrene manifest local symptoms (Fig. 1, Fig. 2). Very characteristic is the complaint of pain arching nature, occurrence of edema, which quickly spread to proximal direction. If the wounds it has areaktyvnyy appearance with minor mucous secretions ihoroznym character with an unpleasant odor. The skin on the periphery of the wound cyanotic, pale, or cyanotic with bronze and blue spots. Quite often we can determine trombovani subcutaneous veins. Fiber swelling, soaked hemolyzed blood is "weak" look. Muscles as "cooked meat" swollen, grayish, protruding from a wound on the skin surface. When gassing in fluid bubbles last observed (Fig. 3).

On the periphery of the wound swelling increases in the volume of certain segments of the limbs or the entire limb. The skin konturuyutsya traces of superimposed bands. Progression of edema well detected by AV symptom Melnikov (ligature imposed on the limb at the most proximal level distribution of edema in 20-30 minutes crashes into the skin).

Palpation in the area of ​​swelling is determined crepitation, with shaving skin wounds on the periphery bugged high "metallic" sound - a symptom blade, or a symptom of "spatula" (metallic sound with percussion spatula).

Gas accumulation in the wound when removing a tampon from the cavity latter accompanied by typical hlopayuchym sound - champagne cork symptom.

When radiography of the affected limb konturuyutsya band enlightenment that defoliate muscles - Symptom Krause (Fig. 4).

Along with this, and sometimes even earlier than the local symptoms manifested severe clinical of intoxication. Patients complain of progressive general weakness, thirst, nausea, vomiting, lethargy, until he lost consciousness. On examination: the skin of patients with pale yellowish earthy shade, facial features sharp, dry tongue with massive gray-yellow layers. It is noted marked tachycardia, blood pressure falls, breathing rate to 40 for 1 min. It is noted oliguria.

In blood, usually hyperleukocytosis with a shift to the left, accelerated SHOYE in urine protein appears and cylinders. In biochemical analysis of blood - hypoproteinemia, the increase in urea and creatinine.

IMGA0527

Fig 1. Anaerobic clostridial abscess shoulder and chest.

 

IMGA0529

Fig 2. Anaerobic clostridial abscess leg.

 

IMGA0519

Fig. 3. Vesicles gas fluid under anaerobic clostridial infection.

 

IMGA0521

Fig. 4. Emphysema soft tissues in gas forming anaerobic infection (symptom Krause).

General principles of treatment.

Treatment Program anaerobic gas infection should include simultaneous execution of radical surgical treatment with powerful multicomponent intensive therapy and hyperbaric oxygenation.

Radical surgical treatment is determined by excision of all nonviable tissue, especially muscles, because this is the best substrate for vehetuvannya anaerobes and their distribution. The viability of muscle during surgical treatment can be identified macroscopically in appearance, the degree of bleeding, to reduce muscular fibers, and more precisely by determining the response to Electro stimulation.

All guidelines regarding gas gangrene recommended implementation lampasnyh cuts, but not always highlighted feature of these cuts. And it is this feature is extremely important and that cuts have to be not only very long but also include mandatory fastsiotomiyu. Unfortunately neglect this feature rarely leads to the fact that surgeons cut through only the skin and subcutaneous tissue, limited drainage of these substrates and anaerobic infection while progressively distributed in the muscles, which remain in a closed fascial pouch.

After fastsiotomiyi and determining the viability of muscle, if necessary, performed necrectomy, then washed the wounds antiseptic solutions (preferably oxidants) and drained shyrokoprosvitnymy tube drainage. This volume of surgical intervention may be radical in the early stages of gas gangrene (Fig. 5-7).

Often, when there is total destruction of the soft tissue extremity only way to save the patient's life is amputation.

IMGA0512

Fig. 5. Debridement anaerobic clostridial phlegmon.

 

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Fig. 6. View wounds after surgical treatment before grafting local tissues.

 

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Fig. 7. The appearance of the wound after plastic local tissues.

 

There are three types of amputations that are recommended to perform during anaerobic gas infection:

- Amputation without suturing (the usual method trohmomentnomu amputation by fascial Cases held drains stump remains open seams imposed in the absence of progression of infection in 24-48 hours);

- Guillotine amputation (flush overlapping skin, fat, fascia, m 'muscles and bones, supporters of the transaction believe that in this way we can stop the spread of infection, but experience shows that this method has no advantages, only further complicates treatment);

- Amputation stump with dissection (performed in cases where the surgeon is not completely convinced of the viability of the tissue stump, the latter is dissected medially and laterally, skin flap can be filed to the unchanged skin as a clutch, allowing greater aeration wound).

In cases of infection until the joint must perform disarticulation of limbs.

General principles of the treatment include:

a) the specific treatment that involves the application of polyvalent antyhanhrenoznoyi serum containing 50 thousand IU sera antiperfrinhens, antiseptikum, antiedematiyens, only 150 thousand IU. Since when intravenous infusion of sera rarely anaphylactic reactions occur, when they are introduced should follow these rules:

- Serum diluted with 300 ml of saline;

- Introduced slowly infusion rate of 20-40 drops per minute.;

- Solution must be heated to 36-380S;

- Infusion is performed under general anesthesia.

b) Nonspecific treatment includes powerful antibiotic therapy, preferably with the inclusion of a class of antibiotics imipinemiv (Tien) and imidazole (metrahil, flahil). The most expedient way of intravenous and intraarterial. Important place in the treatment of anaerobic infections should take detoxification therapy using detoxification solutions crystalloids (to 4-6 ml per day) and forced diuresis. A special place is occupied by extracorporeal detoxification methods (plazmoforez, plazmosorbtsiya, splenoksenosorbtsiya). A symptomatic adjustment of all systems of homeostasis, especially cardiovascular and respiratory. Some attention should be given enteral nutrition as oral, and, in some cases, enteral probe.

 Hyperbaric oxygenation.

 At the present level of medicine proper treatment anaerobic clostridial infection is impossible without the use of hyperbaric oxygenation (HBO).

Research and B.V.Petrovskoho S.N.Efuni determined that a high concentration of oxygen paralyzes the formation of alpha-toxin klostridiy further decreasing its concentration. In addition, increased oxygen tension in the tissues inhibits anaerobes livelihoods through oxidative inaktyvuvannyu bacterial cells.

Sessions hyperbaric oxygenation is carried out at the level of compression of 3.2 atm. Number of sessions - 5-7.

 

Anaerobic noclostridial infection.

The said pathology is considered independently of the early 80-y.

Many clinicians in this period was noted that in some patients the clinical course of septic processes, as m "tissue and internal organs, ran distorted. There was an extremely rapid progression of endotoxemia with minimal early signs of local inflammation. Common approaches to surgical treatment resulted in relief of the patient. Many patients on a background of growing signs of immunosuppression manifest sepsis and they died.

With the development of anaerobic microbiological techniques were found to be major pathogens. that caused the aforementioned infectious processes were gram-negative bacillus genus Bacteroides.

American scientist S. Finegold in a series of fundamental works (1977-1984.) Found that some groups of people who, because of various reasons, are immunosuppressive effects of exogenous or endogenous, are at increased risk of surgical infection caused asporogenous anaerobes. These include, besides the aforementioned Bacteroides, are gram-negative peptokokki. peptostreptokokki, fuzobakteriyi. These microorganisms usually inhabit the gastrointestinal tract of man, and most of them vegetate in the colon. Usually they are facultative vegetative bacteria. Only in immunosuppression run their pathogenic mechanism. By the above risk groups S. Finegold took: patients with malignant tumors, especially those that are cytostatic therapy, diabetics, drug addicts, alcoholics, people with AIDS.

Clinical picture.

For the diagnosis of clostridial anaerobic infections (ANI) is crucial correct interpretation of clinical signs. Locally emergence ANI preceding minor microscopic, abrasions, scratches sometimes surgery. The skin over the lesions, unlike the banal infections, not flushed, but rather cyanotic. Determined noticeable swelling on the periphery of the hearth (Fig. 8). Pain in the center more often than not determined, as stated around as a "rim." When puncture typical manure can not be obtained. In the context of a scalpel if falls into underlying tissues. The wound looks like a conglomerate of "dirty flap" gray-brown color with a small amount of grayish-yellow fluid with drops of fat and unpleasant odor that most medical calls coli-bacillary (Fig. 9-10). It should be noted that this odor is inherent Bacteroides and E. coli culture no odor. In the subsequent revision of the wound can establish that purulent necrotic process applies to the subcutaneous fascia basis and muscles, and the true distribution process is more extensive than its imaginary boundaries during the initial inspection and examination. Thus, we can diagnose clostridial anaerobic cellulitis, fasciitis, miozit. Any damage to the soft tissues often ascertained combined lesion of these substances

IMGA0490

Fig. 8. Distributed anaerobic clostridial abscess prostate space and peritoneal tissue after imposition epicystostomy.

 

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Fig. 9. View wounds with clostridial anaerobic phlegmon thighs (cellulite, fasciitis, myositis).

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Fig. 10. Droplets of fat in fluid under anaerobic clostridial infection (indicated by arrow).

 

With regard to changes in the general status, as already seen us, they appear much more intense than the banal aerobic infection. Rapidly growing temperature, common signs of intoxication, there is respiratory distress syndrome, showing signs of hepato-renal failure. Late and inadequate surgical treatment arises, as we have already noted, sepsis.

Verifikuvaty ANI can bacteriologically, with a special microbiological techniques, defining characteristic of this infection unsaturated volatile acids by chromatography and rapid method of staining of native material wounds Gram. The latter method gives a positive result in 75-85% of cases and draws its simplicity and speed, it is a significant step in building a treatment program ANI.

Principles of treatment.

As with any surgery, infection is a defining moment in treatment strategies ANI is radical debridement. It is different because the rate of invasion bakteroyidnoyi infection suggests that even small amounts of residue affected tissues leads to further progression. Therefore, in this situation, in any case can not follow the tenet of Hippocrates: "Where manure - it cut." The surgeon who performs a radical surgical treatment should be guided by the idea to completely carve affected tissue, and in any case the idea of ​​economical treatment for possible future closure of the wound. The latter point is solved by the elimination of signs of infection any plastic methods. Particular attention in the surgical treatment ANI should consider fasciitis, because the fascia is the least tolerant substance for bakteroyidnoyi infection and the process of "creeping" on them the fastest and furthest.

After radical surgical treatment of skin flap should turn out as clutches and hem them in unmodified skin. Thus, we increase the area of ​​aeration wounds. The latter must be processed pulsating jet antiseptics and loosely fill drains with osmotically active ointments. Optimal completion of surgical treatment is treatment in a controlled environment abacterial that enables access by sterile air to minimize the possibility of vegetation clostridial anaerobes. In these circumstances, a 3-4 day appear young finely-granular granulation, which creates the opportunity for further plastic wound closure (Fig. 11 - 14).

Principles of antibiotic therapy ANI is not particularly different from the above-mentioned principles of treatment of anaerobic infections in general. It should only be kept in mind that asporogenous anaerobes most susceptible group imidasoles (trihopol, tinidazol, metronidazole, metrogil, flahil) because these drugs in combination with tsyfalosporynamy III-IV generation and klindamitsinom most appropriate to apply for ANI. All other points detoxification immunocorrective and symptomatic therapy are similar to those used in the treatment of generalized infection.

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Fig. 11. Anaerobic clostridial abscess anterior abdominal wall.

 

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Fig. 12. View wounds after radical surgical treatment.

 

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Fig. 13. Combined plastic wound by auto and ksenoskin.

 

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Fig. 14. The appearance of the wound on day 14 after plasty (skin patches fixed, marginal epithelization).

 

Tetanus (tetanus).

Epidemiology, etiology and pathogenesis. Causative agent of tetanus is tetanus bacillus (Vas.tetani), which has three characteristics: there are anaerobes, forms spores and release a toxin.

It is found in soil, and its spores are in the digestive tract of sheep, horses and other animals. In an environment coli comes from human and animal feces.

The causative agent of tetanus is very stable. He for one hour withstands heating to 80 ° C. In dried form can maintain its viability without light for 10 years. Tetanus spores are not always die after boiling for 30-60 min. In the external environment, they can be stored for a long time (years).

Gateway to tetanus bacillus are random wound mechanical and thermal surface skin damage, frostbite, burns. Tetanus bacillus may enter the body by criminal abortion, surgery of the colon, removal of foreign bodies, etc..

Contact with sticks in the wound does not necessarily lead to the development of tetanus. Sometimes wounds vysiyuyut tetanus bacillus without clinical signs of disease. To the presence of a microbe developed tetanus, required under its virulence, local favorable conditions, hypoxia, presence of hematoma, foreign bodies (crushed wound of necrotic tissue without oxygen) and lowered body resistance.

The incubation period for tetanus ranges from a few days to 3 months, often it is 10-14 days. What a shorter incubation period, the heavier the disease.

Once in the wound, tetanus bacillus begins to produce strong exotoxin that has two factions - tetanospazmin (causes convulsive muscle contractions) and tetanolizyn (causes hemolysis of red blood cells).

Tetanospazmin - a neurotoxin that affects the central nervous system. Concerning his actions there are several opinions. Some believe that the toxin from the wound axial cylinders of peripheral nerves (in the front, motor, roots) moves in the spinal cord, which affects the anterior horn cells. Part of the toxin enters the lymph and blood, and with them - at the end of motor nerves and further in anterior horn cells of the spinal cord and motor nuclei of the brain stem. From here formed cells arousal reflex affects the muscles, causing a typical symptom of tetanus - their rigidity.

According to other researchers, the toxin from the injury immediately into the blood and lymph and from there only affects motor centers and neuromuscular connections.

Toxin damage and some internal organs (heart muscle, liver, lungs). It affects higher autonomic centers of the brain stem, leading to tachycardia, hypotension, severe sweating.

Classification. In place of penetration of the pathogen into the body distinguished: wound, postinjection, post burning, postoperative tetanus and tetanus after frostbite, electrical. Separately isolated neonatal tetanus and mothers.

With the spread of it is classified as follows. Overall tetanus: the ascending form more often in animals, descending - often observed in humans. In this form first appear muscle tension head, neck, general stiffness. Later in the process involved all the muscles of the trunk and limbs, there are general clonic convulsions.

Mixed form characterized by uniform signs uplink and downlink tetanus.

There are still local (limited) tetanus, which is characterized by limited lesions muscles localized in the area of ​​injury.

Local tetanus is usually preceded by a general, but not promptly recognized.

The clinical course distinguish four forms of tetanus: a rapid, acute, subacute and chronic.

According to the severity of the process distinguish very severe, moderate and mild forms of tetanus.

Clinical picture. Overall tetanus begins with slightly expressed Prodrome: weakness, irritability, rapid onset of fatigue, headache, sweating, pain and slight twitching of muscles in the wound.

After the prodromal period, there is first a formidable sign of disease - muscle stiffness. With an upward revision it occurs first in the muscles near the wound, while descending - captures the chewing muscles (lockjaw - trismus). They are not antagonists, as previously frantically cut. The patient experiences difficulty during mouth opening, short-term cramps and pain in masticatory muscles ("locked jaw"). Signs of these steadily increasing.

Patients concerned about pulling pain and stiffness in the neck muscles, neck, back, lumbar region. Having difficulty while walking, heaviness in the back and lumbar region. Sometimes there are abdominal pain and muscle tension anterior abdominal wall, which may cause misdiagnosis of acute surgical pathology of the abdominal cavity. Tetanus often begins with swallowing difficulties and pain in the throat, which is the reason for the referral of patients to consult a otolaryngologist.

In connection with the reduction of facial muscles of the face of the patient acquires a characteristic appearance - "sardonic smile" (risusSardonicus).

All these phenomena are accompanied by a sense of fear, sleep disturbance, general weakness, and sometimes irritability, sweating, fever.

Subsequently tonic convulsions cover all the muscles of the trunk. Since the back muscles are stronger than muscles of the anterior surface of the body, while reducing their patient arch, lies on the heel and neck. The provisions of this was called Opisthotonus - opisthotonus (Fig. 15).

Limbs at this time bent at the elbow and hip joints.

Stiff intercostal muscles severely restricts breathing movements of the chest, which becomes inactive. When convulsive contractions of the diaphragm is covered, it may be sudden respiratory failure until asphyxia. Seizures occur under the influence of the smallest hearing or visual stimuli. A drop of water that falls from the tap, sunbeam, creaking beds - all of which can lead to their appearance. Originally seizures are rare, but if the disease progresses, they become more and more frequent, and there are already spontaneously.

Fig.15. Opisthotonus a patient with tetanus.

 

Duration minor court did not exceed 1-2 with intervals of several hours, medium - 2-5 sec intervals for 10-15 minutes. Seizures are accompanied by severe pain. They are sometimes so strong that lead to the breakdown of muscle and fracture.

Because tonic muscles perineum violated acts of defecation and urination.

In some cases, tonic (characterized by prolonged spasm) and clonic (muscle spasm alternates with their relaxation) may include muscle spasms only certain parts of the body (local form of tetanus).

Consciousness in tetanus preserved, making the patient's condition even more difficult. Reduces blood pressure, tachycardia and arrhythmia appear, decreased urine output (oliguria).

The clinical picture of severe tetanus increases downward to 2-3rd week. With favorable course all these phenomena gradually die down: the frequency and strength of the court reduced the body temperature decreases, decreases trismus, improves swallowing. Spasmodic muscle contractions disappear in the following sequence, which were: chewing, facial muscles, neck, trunk, and extremities.

Each of the clinical forms of tetanus has its own characteristics. Yes, lightning forms symptoms develop rapidly, within 12-24 hours. The disease runs hard, seizures occur, often accompanied by threatening asphyxia. Body temperature rises to 39-40 ° C, accelerated heartbeat. After 1 - 2 days dies.

In case of severe forms symptoms at ¬ hvoryuvannya develop within 24-48 hours. (All symptoms of diseases ¬ tion). Seizures court repeated several times an hour. Often within 4-5 days the patient dies.

Slower growing clinic in case of an acute form (incubation period lasts 4-6 days). Expressed mild symptoms, seizures are rare, several times a day. Other symptomivvyrazhena moderately. Often the disease ends recovery.

Chronic tetanus is rare and is characterized by less severe. With him there is limited muscle damage localized in the area of ​​injury.

There are still late and recurrent tetanus. The first may develop several months or even years after getting sick injury. The reason it is the activation of latent infection under the influence of triggering factors: trauma, surgery (especially late removal of foreign body).

The cause of recurrent tetanus is also activation of latent infection.

When you have the classic triad of symptoms (trismus, dysphagia, neck stiffness), the diagnosis of tetanus is not complicated. The presence of only one component of the triad is the basis for the diagnosis of tetanus. Trismus may be a manifestation of dental disease, and isolated dysphagia or muscle stiffness in the neck - the result of nervous and mental disease.

During this period of treatment, begun at a typical clinical picture, we can consider late. It is important to establish the diagnosis in the early stages of the disease. The main feature is a symptom of increased reflex excitability. You can check with your fingertips lightly on the parotid region, accompanied by spasm of the facial muscles. Lorin and Epstein offered to investigate reflex masticatory muscles by tapping on the spatula assigned to the lower teeth. In patients with tetanus, in the absence of overt clinical signs observed apnea, prolonged contraction of masticatory muscles.

By the early signs of tetanus are also pulling pain and muscle twitching in the wound, excessive sweating, which does not correspond to body temperature, pain in the back.

The diagnosis is confirmed by detection tetanus in material necrotic tissue thin bacilli with similar disputes to drumsticks and detection tetanus toxin in cultures with tests "toxin - antitoxin" in mice.

Treatment of patients with tetanus aims to maximize pathogen destruction tetanus toxin neutralization that circulates in the blood, ensuring the free passage of respiratory depression reflex excitability of striated muscles and prevent complications.

Therefore, treatment of tetanus should be conducted in the following areas: 1) the specific therapy, and 2) anticonvulsant therapy, and 3) improve the overall condition, correction of protein, fluid and electrolyte balance and acid-base status, and 4) surgery, 5) aids.

Specific therapy involves the use of tetanus toxoid (PPS). Dose of serum for adults is 100 000-150 000 AO for children - 20 000-80 000 AO, Baby - 10 000-20 000 AO. Before the introduction of therapeutic doses spend intradermal and subcutaneous tests for Bezredkom. Originally administered 0.1 ml of diluted (1:100) serum intradermally in 20 minutes - 0.1 ml undiluted serum subcutaneously. A negative result (induration diameter less than 0.9 cm) heated serum remainder injected intramuscularly and intravenously. Half doses of serum injected intravenously (diluted in isotonic sodium chloride solution at a ratio of 1:10), the second half - one time intramuscularly.

Serum was administered 2-3 days in a row, gradually reducing the dose. Course dose serum - 200 000 - 350 000 AO. Today abroad some authors refuse administering serum because of the risk hypersensitivity, possible allergic reactions including anaphylaxis.

We must remember that whey is effective as a prophylactic because it neutralizes a toxin that circulates freely in the blood.

At fixed nervous tissue toxin none of the current medications is not valid. Therefore, the serum should be introduced in the first 2-3 days.

Specific therapy includes intravenous administration of not less than 10,000 OD of human tetanus immunoglobulin diluted isotonic sodium chloride solution.

The literature highlights the beneficial therapeutic effect of homologous antitoxin, ie serum obtained from immunized donors. Introduction antitoxin should be combined with antibiotic therapy (intramuscular or intravenous) and rectal introduction as suppositories metronidazole 1 g every 8 hours, destroying all living microorganisms and prevents future development of toxin.

Important role in treatment of tetanus is active anticonvulsant therapy. In milder forms of the disease incubation period of 2 weeks, occasional bouts of court a good therapeutic effect give input neuroleptics drugs, 25% magnesium sulfate solution (20-30 ml intramuscular) use hloralhidratovyh enemas. With neyroplehichnyh drugs used chlorpromazine, which produces a calming, anticonvulsant, analgesic effect (4 ml of 2.5% solution 4-5 times a day intramuscularly).

The average degree of severity of tetanus with frequent severe seizures, breathing disorders shows neuroleptics administration of high doses (50 mg aminazine after 6 h), antihistamines (diphenhydramine, suprastin) drugs in combination with hloralhidratis.

In case of heavy flow tetanus expressed breathing disorder that threatens asphyxia, often painful cramps used muscle relaxants and produce mechanical ventilation. Patient intubuyut, injected him muscle relaxants, connect the device to mechanical ventilation and exercise superficial anesthesia nitrous oxide. If you want to continue this therapy for a long time, perform tracheostomy. It uses muscle relaxants antydepolyaryzuyuchoyi action (tubaryn, tubocurarine). Artificial ventilation may be a long time (sometimes up to 14 days).

To correct protein, fluid and electrolyte balance and acid-base status conduct corrective infusion therapy.

Surgical treatment of tetanus is the wide opening wounds (especially blind wounded), excision of necrotic tissue, removal of foreign bodies (fragments, splinters of wood, scraps of clothing, etc.), providing good outflow of wound, locally administered antibiotics. The wound was thoroughly washed with hydrogen peroxide and loosely tamponuyut. For large lesions with massive limbs, crushed fabrics shown amputation.

A role in the treatment of tetanus play HBO and antibiotics. We must remember that most bakteroyidnyh microorganisms resistant to antibiotics, and planting often results should wait a few days. In this case, shows broad-spectrum antibiotics.

A patient with tetanus requires a special care. First of all, it should be placed in an isolated, quiet and darkened room to avoid any irritants to care for patients allocated special middle and junior medical staff that operates under the direction of a physician.

Great attention should be paid to patients' diet (food should be high, fortified with plenty of fluids). If patient to feed ridkok food through poyilnyk with rubber tip or via nasogastric tube.

In case of delay urinary catheterization demonstrated a soft catheter in case of constipation - cleansing enemas. The vessel must be rubber.

From the epidemiological point of view, patients with tetanus is not contagious and danger to the environment is not. The patient required daily laboratory and x-ray (for early diagnosis of lung atelectasis).

 

Preventive measures in tetanus pravtsya.Profilaktychni divided into nonspecific and specific.

Nonspecific prevention of tetanus is to conduct timely and complete debridement, cleaning it from foreign bodies, necrotic tissue, bacteria, blood clots, which is complemented by the introduction of antibiotics.

Specific prophylaxis of tetanus include active immunization regardless of injury and active-passive for suspected disease tetanus.

Active immunization is pertussis-diphtheria-tetanus (DPT) and adsorbed diphtheria-tetanus vaccines to all children under 1 year (1st and 2nd injections at intervals of 6.8 weeks, 3rd - 4-6 months), and tetanus toxoid popula ¬ around nude, living in areas with incidence of tetanus 1 or more per 100 000 population, all agricultural workers, builders, workers and employees of railway transport, water supply, sewage and water treatment facilities, peat 'wooden development and logging, laboratory workers who work with tetanus culture workers vivarium, athletes dopryzovnykam.

Tetanus toxoid introducing 0.5 mL (2 vaccinated and 2 booster).

From the completeness active immunization depends on further active and passive immunization in case of injury (Emergency Prevention). It is open for all injuries, burns, frostbite, gangrene and tissue necrosis, animal bites, criminal abortion, birth, which took place not in a hospital, abscesses, penetrating wounds of the digestive system, removing foreign bodies.

Active immunization spend tetanus toxoid and human tetanus immunoglobulin, at least - of tetanus toxoid.

Scheme emergency specific prevention of tetanus depending on the conditions and situations contained in the special instructions.

Weather in tetanus depends on the duration of the incubation period (it is shorter, the heavier the disease), the clinical forms of tetanus, reactivity, specific and nonspecific timely prevention, complete treatment.

 

ANTHRAX.

It is an acute infectious disease that belongs to zooantropogenous and occurs in the form of skin, lung and septic forms. Note that not all scientists recognized intestinal and pulmonary form of anthrax. Professor V.N.Nikiforov argues that there are only two forms of human anthrax: cutaneous and septic. Anthrax outdoor K. times in 1850, but the name was given Vas.antracis F.Konom. Vas.antracis-gram-positive bacillus, motionless, with large obrublenymy ends. In humans and animals exist in vegetative form, beyond the body-forms spores. Vegetative forms are very sensitive to chlorine, mercuric chloride and formaldehyde. Disputes stable in the environment for decades and remain viable in the soil for a long time - in the skins of animals not killed by salting m "meat resistant to disinfectants means. Under certain conditions, they can grow and accumulate in the soil, maintaining focus. Spreading germs is based on preserving the soil resistant spores.

Source of infection, large and small cattle, horses, pigs, deer, antelope, buffalo. Sick as a dog, mink. Of transmission to man occurs in the processing of carcasses of animals that died in the use of food as well as in contact with water, soil, skins, hutryanyanymy products contaminated with spores. Infection, mainly, is professional in nature. Atrium is damage to the skin and mucous membranes con "conjunctiva, gastrointestinal tract, respiratory tract. At present the doctrine of anthrax intestinal and pulmonary lesions interpreted as a manifestation sybirovyrazkovoho sepsis.

Incubation period not exceeding 12 days, usually 2-3 days, with a massive infection, several hours. The most common form of skin that has practical implications for surgeons. Cutaneous form develops as a carbuncle. In place of the entrance gate of the infection "is stain red. In the near future it becomes a papule copper-red color with a purple tinge, itchy. During the first day papule becomes a vesicle filled with serous, and hemorrhagic content. Combing pustules frustrated, rarely burst independently and in their place quickly formed blackish scab. Characteristically for sybirovyrazkovyh skin lesions develop secondary pustules, which are located around the primary focus. They undergo the same phase of development. As a result, formed a large black-brown crust round with infiltration underneath and around in a purple shaft that rises above the surrounding tissues. Formed typical of this clinical form of infection trohkolorovyy transition: black scab in the center, around-narrow zhovtuvatohniynyy whisk, then wide-purple shaft. (Fig. 1). Characteristic of this ulcer is the lack of purulent discharge and pain in the affected area. Can develop regional lymphadenitis. By the end of the first day, little disturbed general condition deteriorates sharply raises the temperature of the "is a headache, tachycardia, fatigue develops. With favorable motion of the disease after 5-6 days the temperature drops, more critically, improving overall decreases swelling, limfanhoit and lymphadenitis fade, scab disappears, the wound heals with scar formation. In cases nespyyatlyvoho disease develops secondary sepsis with repeated fever, significant deterioration of general condition, gain headache, tachycardia increase, the emergence of secondary pustules on the skin and other skin changes character haematogenously-metablastychnoho origin. Perhaps the development endokardita may be bloody vomiting and diarrhea. The patient's condition progressively worsened. Probable lethal consequence caused by pulmonary edema, coma.

 

Fig.1. The distinctive appearance of anthrax.

 

In the intestinal form, essentially elementary sybirovyrazkovomu sepsis, toxemia develops from the first minutes of the disease. There hyperpyrexia, malaise, abdominal pain, vomiting, bloody diarrhea rarely. The skin may be secondary rash. Fast-paced dyspnea, cyanosis. Perhaps the development of meningoencephalitis. Patients dying with an increase in cardiac weakness after 3-4 days of onset, sometimes 1-2 th day.

Pulmonary form of anthrax infected in the processing of wool, hair or animal skins. The disease develops rapidly: malaise, fever, pain and sensation in the chest, coughing up foamy phlegm that recalls after the collapse of raspberry jelly, the growing phenomenon of intoxication, respiratory failure, disorders of the cardiovascular system. Clinically and radiographically defined pneumonia and pleurisy hemorrhagic effusion. Death comes for 2-3 days due to pulmonary edema and collapse.

Septicemic form occurs rapidly, with multiple hemorrhagic manifestations and ends in death within 1-2 days.

Diagnosis is based on epidemiological, clinical and laboratory data.

To identify patients defense of those who have had allergic disease using intradermal test with antraxinum. Evaluation tests conducted in 24-48 hours. Considered positive when infiltrate and flushing more than 0.8 mm in diameter.

Treatment anthrax carbuncle conservative: rest, immobilization. Surgical intervention is contraindicated, as results in the generalization process. Patients with mild disease (no trend to a rapid increase in the size of skin necrosis was expressed phenomena ailments) only prescribe antibiotics - penicillin preference from 5 ml to 20 ml units per day during 5-7 days. In second place are the preparations of tetracycline.

In moderate and severe forms of the course of anthrax antibiotic treatment combined with pathogenic (aimed at restoring hemodynamic disturbances) and specific treatment - putting antianthrax globulin. It is administered in an amount of 40-50 ml / intramuscular once. With increased sensitivity, he introduced the background to / venous infusion of 90-120 ml prednisolone.

Prevention for diseases anthrax regulated by official instructions and guidance. Preventive immunization people made a living dry vaccine CTI twice with an interval of 21 days, revaccination - a year later. Emergency prevention spend antibiotics for 5 days. All patients, regardless of disease with suspected anthrax immediately hospitalized in the infectious department, in the absence thereof - in a separate ward. Provided a separate staff. All patient selection dezinfection.

Patients with cutaneous discharged after wound epithelialization in place scab. Dressing material (cotton, gauze, swabs and others) burn. In carrying out disinfection should remember that the patient is not a source of infection.

 

Diphtheria wounds

In recent years, marked increase disease incidence of diphtheria in the population. Diphtheria wounds develops when injected into the wound stick Leffler. In doantyseptychnyy time wound diphtheria was quite frequent "guests" surgical clinics., Especially in children.

Clinical signs initially not typical. The general condition of patients do not suffer. However, granulation become flabby and become gray and yellow. Appears tendency to form a scab. The surrounding tissues are blue and red, with is infiltration. In severe cases the wound diphtheria is characterized by thick gray-green layers on vitreous granulation. Rushes into the eyes of progressive proliferation of blue-red color perifocal. When abscess forms these changes extend to the depth of wounds. In the opinion of diphtheria wounds suggests the characteristic decay infiltrated edges (Fig. 1). If it is a wound after tracheostomy in patients laryngeal diphtheria, the suspicion of this complication, according occurs sooner. Up to 40% of diphtheria bacteria are found on infected wounds after frostbite. Flow flabby, slow. The risk of wound diphtheria is not only in severe disorders healing of wounds, but the possibility that due to constant propagation diphtheria may be entering the bloodstream. In addition, the diphtheria toxin can be caught in the blood.

Fig.1. Diphtheria wounds.

Treatment of diphtheria wounds should be directed to the removal of her agent by imposing bandages with serum, local antiseptics, ultraviolet irradiation.

 

 

TUBERCULOSIS

 

It includes a variety of localization of the disease to be surgical treatment (tuberculosis of bones and joints, urinary tract, lymph nodes, peritoneum, etc.)..

 

Due to the widespread use of antibiotic treatment and surgery advancements used surgical treatments for various localizations of tuberculosis, including in previously inaccessible surgery.

On the other hand, treatment of TB patients has always been complex, the main component of which is the use of specific antibiotics and general firming agents.

Tuberculosis is caused by mycobacteria, which opened in 1882, Koch. The infection is transmitted from patients with open pulmonary tuberculosis, which is batsylonosiyamy.

Mycobacterium tuberculosis enters the body primarily through the respiratory tract, at least - through the digestive tract while taking food (milk, meat) containing Mycobacterium tuberculosis, and rarely - through damaged mucous membranes and skin.

Primary tuberculosis infection occurs in 80-90% of people ill with TB but only 1-2%. Most TB affects the lungs (60-65%), the remaining patients appear extrapulmonary (tuberculosis of bones and joints, urinary tract, peritoneum, lymph nodes, skin, etc.)..

After the recess of Mycobacterium tuberculosis in tissues of developing tuberculosis inflammation. In inflammation processes of alteration (restructuring), tissue edema and exudation. As a result of proliferation occurs tuberculous tubercle, consisting of epithelioid and giant cells, which are located around the Mycobacterium tuberculosis and lymphoid cells in the periphery. Tuberculosis tubercles in congenial scars, they deposited calcium salts.

With the progression of the disease produced tuberculous infiltrates necrotising tubercles, caseous decay occurs with the formation of caseous masses. Breakup TB tubercles leads to the formation of cavities fistulnyh moves wandering abscesses.

Total body reaction in tuberculosis characterized by general malaise, fever, accelerated heart rate, sweating, reduced regeneration processes, change immunobiological condition.

For tuberculosis is characterized by a chronic course with frequent exacerbations and prone to generalization disease.

Tuberculosis of lymph nodes. Tuberculous lymphadenitis usually observed in children and adolescents. Tuberculosis usually affects the bronchial, mesenteric and cervical lymph nodes.

 

In surgery usually have to deal with cervical tuberculous lymphadenitis. Affected lymph nodes in the submandibular, supraclavicular areas and the progress hrudynnoklyuchychnososkovoho muscle. Lymph nodes are enlarged, often bumpy spayuyutsya in dense conglomerates. With the progression of tuberculosis as a result of the collapse of cheesy formed fistula that long to heal.

 

Treatment. Apply conservative treatment - antimicrobials (streptomycin, sodium paraaminosalitsylat, ftivazid et al.). Locally administered ultraviolet irradiation. Recommended restorative treatment.

 

Osteoarticular tuberculosis. Tuberculosis of bones and joints observed in approximately 7 patients with extrapulmonary tuberculosis. Affected mostly the spine (Fig 1.) Hip (Fig 2.) And knee joints (Fig. 3)., Accounting for 70-80% of all cases. Defeat other bones and joints is less common (Fig. 4, 5.).

Fig.1. Tuberkulosis spondylitis X, XI thoracic vertebrae. Visible deformity of the vertebrae and abscess

Fig.3. Tuberculosis honitis with fire in                                      Fig.2. Tuberculosis koksytis

                                                                                                                            femoral epiphysis

 

    

Fig.4. Tuberculosis of the shoulder joint            Fig. 5. Tuberculosis of the elbow joint

 

Ill mostly children and teenagers, because of the peculiarities of the child's body, including increased growth and increased blood supply of bone.

Osteoarticular tuberculosis is a secondary disease. Mycobacterium tuberculosis penetrate through hematogenous other tubercular lesions, often with the lungs.

Occurrence of the disease contribute to virulence and massive tuberculosis infection, trauma, intercurrent disease, malnutrition and poor sanitary conditions.

Originally affects bone metaepiphysis develops by PG Kornev, primary osteitis. Bone is resorbed (rerafikatsiya) and formed cavity (cavity) with cheesy collapse and small sequestra. This phase is called peredartrytychnoyu or initial phase of osteitis.

Lokalizuyuchys near the joint, tubercular process gradually extended to him, affects synovial membrane, and then the bones that form the joint (arthritic phase) occurs tuberculous arthritis.

Postartrytychna phase is characterized by remission process and the development of secondary deformities of the joints.

 

Clinic. Symptoms - fatigue, pallor, sweating, low-grade fever, weight loss and fatigue. Patients complain of local pain and difficulty during movement. Prominent local features of tuberculosis is muscle atrophy and thickening of skin folds (symptom Alexandrov).

Muscle atrophy leads to a decrease in volume of the limb. In connection with the joint lesions disrupted its function, limb gets forced position contracture develops it. Affected joints increases in volume, its contours are smoothed. The destruction of articular ends it deforms. Movements in the joint sharply painful, characterized by the absence of redness.

In exudative are dry forms of tuberculous arthritis that occur, such as damage to the shoulder joint.

In the study of blood marked anemia, leukocytosis and increased ESR.

Great value for the diagnosis of a specific tuberculin Mantoux test, and radiographic studies. In X-ray showing bone defect in a fire clarification of sequestration, atrophy and poroznist surrounding bone (osteoporosis). Any damage to joints observed different degrees of osteoporosis and bone fracture, expansion joint space, and when joined bones in postartrytychniy phase develops joint ankylosis.

Wandering abscess often complicate the course of tuberculous spondylitis. As a result of the spread of tuberculosis boil on neighboring tissue formed sinter abscesses surrounded by dense fibrous tissue. They are accompanied by a local inflammatory response, despite a considerable amount of manure that is why they are called cold abscesses.

Wandering abscess gradually spread along fascial spaces down at large distance from the primary lesion (eg, hip tuberculosis lumbar vertebrae) and defined as malobolisnoho, elastic puhlynovydnoho formation, often palpation observed fluctuation.

With breakthrough tubercular abscesses formed outside fistulni moves that have long chronic and difficult to treat. For tubercular fistulas are characterized as slight sero-purulent discharge, bluish color and thinning of the skin around the fistula.

 

Treatment of osteo-articular tuberculosis complex. It includes antibiotic therapy, the effect on the local focus of infection and a general therapeutic measures.

 

Patients admitted to the special sanatoriums, where the health-orthopedic treatment that includes immobilization of the affected parts, solar and aerotherapy. Prolonged exposure to fresh air, heliotherapy or irradiation with ultraviolet rays, nutrition increases the body's resistance and contribute to the stabilization of the local process.

Immobilization shall first cast, then, as the remission process - corsets, zhelatynoformalinovymy removable devices.

Antibacterial treatment is of great importance for the speedy elimination of aggravation and generalization prevent tuberculosis. Patients prescribed intramuscular injection of streptomycin into sodium para-aminosalitsylat, ftivazid. Early use of antibiotic therapy enables cure process and restore the function of the affected joint.

Surgical treatments are as economical resection of joints, removing isolated pockets and corrective operations in vicious, wrong position of the limb. With a very long-standing forms of osteo-articular tuberculosis, septic symptoms, limb amputuyut.

Cold abscesses treated with punctures. After the maximum manure is injected into the cavity of the abscess 0.5 - 1 g streptomycin dissolved in 3.5 ml of 0.5% solution of novocaine.

 

Surgical treatment of pulmonary tuberculosis. In recent years, the surgical treatment of pulmonary tuberculosis achieved great success, which is largely due to the use of specific antibiotic therapy and the development of modern anesthesiology.

Major achievements in the development of surgical treatment of pulmonary tuberculosis include Soviet surgeons MG Stoica, L. K-Bogush, Amosov and I. Kolesnikov.

As a result of combined treatment with antibiotics, timely anesthesia, blood transfusions, etc. applicability of various surgical tuberculosis increased significantly. Have become widespread different types of lung resection.

 

Surgical treatment of subject patients with pulmonary tuberculosis in satisfactory general condition, without signs of decompensation of cardiac activity, if there is no express respiratory disorders and irreversible disorder parenchymal organs.

It is recommended to resort to surgery in the remission phase compensation and tuberculosis. When urgent indications (pulmonary hemorrhage, pneumothorax busy, etc.). Stage of the process should not be a contraindication to eliminate life-threatening symptoms of surgical procedure.

The main indication for surgical treatment is the presence of cavities and other purulent necrotic processes in the lung and pleura, are not amenable to medications and other special treatments.

 

Surgical intervention is indicated when common bilateral cavernous and disseminated process. Subject to surgical treatment tuberkulomah (kazeomy) lung melt or without insulated cavity with severe capsule hipoventylyatsiynyy partial atelectasis of decay Lobito with sluggish flow or unilateral, total lung, and partial stenosis of the main bronchus, armor pleurisy, tuberculous empyema, recurrent caseous lymphadenitis with abscess formation and a tendency to break.

The role of the surgical treatment of patients with tuberculosis belongs antibacterial drugs, particularly streptomycin, kanamycin and cycloserine.

 

Antibiotic therapy often allows you to change the nature of the process, translating it from infiltrative phase in the phase of remission and consolidation, withdraw symptoms of intoxication, promote resorption lesions bronchogenic dissemination. Thus, in some cases it is possible to transfer patients neopera-condition steadily in operabilnyy.

With significant achievement surgical treatment of pulmonary tuberculosis is now possible in many cases even cure patients from those previously considered hopeless. Especially effective in this partial lung resection with limited processes.

 

In chronic fibro-cavernous pulmonary tuberculosis using different surgical intervention until pulmonek-volume, and combining the various operations performed individually depending on the changes found in patients.

Choosing the operation and its timely enable to achieve cure the patient, make it abatsylyarnym and workable.

 

Palliative surgery (thorakoplastyk, kavernotomy, extrapleural pnevmolyze etc.). Done in cases where radical surgery is not indicated.

 

In connection with the expansion of surgical care for patients with pulmonary tuberculosis applying artificial pneumothorax limited.

 

 

Actinomycosis

 

The disease is caused by a luminous fungi (actinomycetes) are distributed in nature. There are two main types of them - aerobic and anaerobic. Very often actinomycetes contained in the oral cavity, carious teeth, tartar, gingival pockets.

 

Burying actinomycetes in the body occurs in different ways aerogenic, hematogenous, limfohenym and contact.

 

Actinomycosis affects mostly neck-jaw area, lungs and abdominal organs. Actinomycosis of the lungs are mostly secondary phenomenon.

 

Damaging the mouth, esophagus, colon, actinomycosis in further secondary spread to the mediastinum and lung tissue, rarely observed aerobic infection.

 

When actinomycosis form specific granulomas composed of granulation tissue with round-epithelioid and giant cells we. Characteristic is the presence of fat-rich, so-called ksantomnyh cells.

 

The center-specific granulomas around Druze radiant fungus develops suppuration, the periphery is formed fibrous connective tissue. This fibroskleroz tissue to form rocky density infiltrates along with the steady spread of the pathological process by contact is the hallmark of actinomycosis.

 

First place on the incidence of cervical-ranked facial actinomycosis (Fig. 6.), Where there are dense fixed infiltrates, which gradually softened with the formation of fistulas. Isolation fistulnyh moves slightly, has the character of stringy pus containing drusen as dense grains of yellowish serous color size of millet seeds and less. The skin in the area of ​​infiltration dark red or purplish-bluish color with a purple hue.

 

 

Fig.6. Cervico-facial actinomycosis

 

The disease is usually chronic, less acute suprovodyachys high temperature (38-39 ° C).

 

Actinomycosis of the lungs characterized by severe destruction of lung tissue with subsequent formation of large air-sclerotic, scarring, leading to severe and destructive and functional disorders of the respiratory, cardiovascular and parenchymal organs (pulmonary heart amyloidosis internal organs).

 

Clinic Pulmonary actinomycosis depends on the spread of the pathological process, complications and accompanying diseases.

 

There are primary, lung (which resembles a picture of chronic suppuration of the lungs), perytrahealnu, prefistuloznu, pulmonary and pleural fistuloznu forms of actinomycosis of the lungs.

 

Most actinomycosis has chronic, long-term damaging basal lung. For actinomycosis is characterized by severe neuralgic pain, lasting cough with phlegm release small amounts and no "drum your fingers." Sputum is mucopurulent character mixed with blood, containing drusen and thin strands of mycelium characteristic of actinomycosis.

 

When X-ray in patients with pulmonary actinomycosis depending on the stage and spread of the disease are varying degrees pnevmosklerotychni changes with obliteration of the external sinus massive plevrokostalnymy and phrenic seam. It is noted sharp compression mediastinal pleura and lung root.

 

In the development process in the abdominal cavity is formed specific aktynomikotychnyy infiltrate woody consistency, which affects colon and spreads to nearby organs. Infiltration painful, with little softening and formation of characteristic fistulas with little selection. The skin in the area fistulnyh turns a dark purple color.

 

Unlike tuberculosis aktynomikotychnyy infiltration has strict localization and can develop in the basal parts of the lung in the axillary, subclavian and navkololopatkoviy areas.

 

Actinomycosis of the foot (Fig 7.) (Maduromatoz, madurska foot):

- On the bottom one or several dense nodes

- The skin over them purple or red-brown

- Increasing the number of nodes

- Deformation of foot

- Voles with purulent secretions

- The process of moving the muscles, tendons, bones

 

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Fig.7. Actinomycosis foot

 

         Treatment of actinomycosis combined, it includes immunotherapy, the introduction of penicillin and blood transfusions.

 

Founders immunotherapy is Soviet scientists SF Dmitriev and G. Subtyeyev. SF Dmitriev in 1934 opened the spontaneous lysis in aerobic actinomycetes and used to treat actinomycosis aktynolizat. Do 20 - 25 injections. Aktynolizat injected intramuscularly in 3 ml 2 times a week or intradermally in the flexor surfaces of the forearm area after 2-3 days in increasing doses - 0.5 - 0.7-0.9 ml, then increase the dose of 0.1 ml. After a break after 2-month 21I2 repeat the treatment. Treatment of actinomycosis long, consisting of 3-5 courses aktynolizatoterapiyi combined with systematic blood transfusion and penitsylinoterapiyeyu.

 

For the successful treatment of a patient with actinomycosis should 000-12 8000 000 000 OD of penicillin. In combination with aktynolizatoterapiyeyu penicillin administered on 100 000 Unit 2 times a day for a course of treatment - to 4000 000-6 000 000 OD. It is recommended to combine treatment with penicillin, sulfanilamides and ftivazid (0.3 g 3 times a day).

 

Blood is made within 7-10 days 100 - 200 ml to stimulate the body. In some cases it is necessary to appoint additional radiotherapy and iodine preparations.

 

Surgical treatment is very limited evidence in connection with a significant spread of infiltration. Conducted small operation - cuts abscesses, encysted pleurisy and others.

 

 

SYPHILIS

 

Syphilis - a chronic systemic sexually transmitted infection that affects the skin, mucous membrane, internal organs, bone, nervous system. The disease has a succession of stages. Called bacterial pathogens - pale treponema (Treponema pallidum). According to the Ministry, the incidence of syphilis in Ukraine has a clear downward trend. The symptoms of syphilis are very diverse. Any manifestations such as selection or an unusual rash, especially in the groin area is a signal for immediate examination by a doctor. The symptoms of syphilis vary depending on the stage of the disease. There are three stages:

 

• Initial period - its main manifestation of a chancre, I cue formed in place of introduction pale treponem and is a dense, red, painless erosion formation (Fig 1.).

 

Fig.1. Chancre on the lip

 

• Secondary period - in this stage may experience skin rash and mucous membranes (Fig. 2);

 

Fig.2. Syphilis rash on the back (secondary period)

 

Third period - characterized by the appearance of infectious granulomas - clusters of cells in various tissues.

 

Third syphilis

• affects many superficially placed bones (forearm, leg, bones, nose, palate)

• Develops years after infection

• Serological reactions in half of the cases negative

• The nature of injury - gummy, developing periosteal layers that quickly ossification to form gummy osteoperyostitis

• Liquid damage vertebral joints

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Currently, the main way syphilis doctors determine sex; cases of domestic infection (using common utensils, cigarettes, pipes) are rare. Spirochetes isolated from open sores or skin rashes sick person and penetrate into the body of their new offerings through the mucous membranes of the genitals, mouth and anus, or through broken skin of other body parts. If syphilis is ill pregnant woman, she can infect her child in utero. Note: 1. Syphilis is transmitted mainly through sexual contact. Infection occurs through small defects in mucosal genital tract, mouth, rectum, 2. Occasionally, infection can occur in close household contact, except for items items 3. Infection of the fetus can occur in utero or during birth.

 

        

              Congenital syphilis.                             

Specific areas of bone destruction syphylisis (Fig. 3, 4)

- Epiphyseal cartilage discs that provide bone growth in length

- Cambial layer of the periosteum, which provides bone growth in thickness

Thus, specific changes in bone syphilis is osteochondritis in the epiphysis of long bones and syphilitic peryostyt in diaphysis

 

 

 

 

 

 

 

 

 

 

 

Fig.3. Syphilitic peryostyt                  Fig.4. syphilitic osteochondritis

 

The most commonly syphilis record in men and women aged 18 to 29 years old. Syphilis - can provide diverse picture displays and has a difficult course. The disease may be asymptomatic. This danger it! Treatment of syphilis is a complex task that requires an individual approach. If untreated, the possible lethal consequences. Doctors state, the best way to avoid infection is limited by sex, especially casual.

 

The course of syphilis

 

In the mucosa of genital syphilis pathogen - Treponema pallidum - enhanced multiply and spread to nearby areas of the body. From 4 to 5 weeks after infection lasts incubation period, symptoms while not detected. Then on the spot settlement spirochete appears ulcer or chancre round with a shiny surface and hardening at the base. A few days after onset of ulcers sharply with nearest lymph nodes. This - the initial period of syphilis. It lasts about a month, and as syphilitic ulcers and swollen lymph nodes are not accompanied by pain, the patient with syphilis may not notice signs of illness and seek timely medical help. Consequently, there is a need, as often as possible to see a doctor.

 

Pallidum rapidly multiply, spread in the body. They appear in all its organs and tissues, blood and lymph. In this secondary period of syphilis observed symptoms of intoxication (poisoning) body toxins spirochetes. There is no any specific grounds on which to accurately determine the incidence of syphilis, a common weakness, headache, malaise, pain in muscles, joints and bones, mild fever. Sometimes all it regards as ill flu. The only characteristic feature of the secondary period of syphilis - pinkish-red spots all over the body, they are not always easily detected, and if the patient sees them and then usually considers this an allergy to a certain food. In the secondary period of syphilis sore is very contagious to others. In the tertiary period of syphilis spirochetes in places where very affected tissue initially fabric strongly swells and then decays mertviye and in its place created a deep scar, characteristic only for syphilis. Such tissue damage (rubber) can appear on any part of the body. The appearance of rubber in the area palate causes destruction of bone in this location and appearance characteristic of syphilis huhnyavosti. Rubber in the area nasal bone breaks nose, leading to his "provalyuvannya." Damage to different parts of the body distort a person and make it invalid.

 

When syphilis is very affected vessels, especially the aorta, the wall of which is losing its high strength, elasticity and blood pressure gradually stretched and can break. Breaking aorta leads to almost instant death. Syphilitic vascular lesions and spinal cord tissues cause of severe neurological complications, in which disturbed the sensitivity of different parts of the body, there are persistent or recurrent severe borings or "shooting" pains. As a result of syphilitic lesions of the nervous system is disturbed coordination, gait becomes unstable, loss of balance, a person pohytuyetsya, are typical of speech disorders, loss of memory disorder counting, writing, reading, the gradual development of dementia. Patients are extremely irritating, inflammatory, or conversely, lethargic and apathetic.

 

Specific treatment of syphilis; antibiotics, including penicillin drugs. Early forms of syphilis, primary and secondary, to differentiate from the banal ulcers, lymphadenitis, simple warts around the anus, on the other surface inflammatory and degenerative processes. Destructive changes in bones treated plastic-surgery and orthopedic means.

 

 

Authores – doc. L.Yu.Ivashchuk