LESSON 5.
Surgical infection classification.
n– Acute suppurative ndisease of purulent tissues: abscess, furuncle, ncarbuncle, hydradenitis, mastitis, nerysipelas, lymphadenitis, lymphangitis, paraproctitis. Acute hematogenous nosteomyelitis.
n– The acute specific nsurgical infection. Gas gangrene. Tetanus. nDiphtheria of wounds. Anthrax.
n– Chronic specific nsurgical infection. Tuberculosis. Actinomycosis. Syphilis. The general purulent ninfection. SIRS. Sepsis.
Abscess n(abscessus) – Separated by a collection of pus in the different tissues and organs ndue to purulent fusion of tissues and the formation of cavities (unlike empyema nin which the accumulation occurs in the natural body cavities and hollow norgans).
Etiology and pathogenesis. Pathogens purulent infection is staphylococcus – nmonoculture or in association with other microbes (Escherichia coli, nstreptococcus, Bacteroides, and others.).
Pathogen infection usually enters from outside n(exogenous infection), although possible and endogenous infection – penetratiowith neighboring or distant organs, metastatic abscesses with sepsis. The cause nof the abscess can be input into the tissue kontsentrovannyh solutions of drugs n- 25% solution of magnesium sulfate, 24% solution kordiamin, 50% solution of naspirin and others. Purulent inflammation that develops, leading to melting of ntissues, and sometimes to the exclusion of necrosis and gangrenous ntissue-sequestration. Sequestration could face further enzymatic melting.
Abscess cavity can be as simple rounded and complex, nwith numerous pockets. The walls of the abscess initially covered with purulent nfibrinous layers and remnants of necrotic tissue. Then, on the periphery of the nabscess developing area of inflammation, which leads to the formation of pyogenic nmembrane, surrounded by connective tissue.
Formed as a result of purulent or aseptic inflammatioabscesses have different resolution: spontaneous dissection of breakthrough noutside (abscess subcutaneous fat, muscle abscess, mastitis, paraproctitis netc..) Perforation abscess in a closed cavity (peritoneal, pleural, in the njoint space and so on.) with the development of septic processes (peritonitis, npleurisy, pericarditis, arthritis, etc.). Possible ulcer perforation into the ncavity of communicating with the external environment (the cavity intestine, nbladder, etc.).. Abscess cavity, which freed, under favorable conditions, nreduced in size, and subjected spadayetsya scarring, with incomplete released, nthe process can go into with chronic fistula formation at the place of abscess.
Clinical nmanifestations and diagnosis. When superficial acute abscesses marked redness, nswelling, pain, local temperature increase, dysfunction, sometimes referred nfloktuatsiya. Inflammation may hold a different area. Character pus abscess (texture, ncolor, smell) contained in the cavity, determined by the type of agent: stinky nsmell, dirty-gray pus typical putrefactive flora thick yellow-green pus – for nstaph, blue-green color and sweet smell – for blue-purulent sticks etc.
Common clinical nmanifestations abscess: fever of sub-febrile to high, malaise, weakness, loss nof appetite, headache. In the peripheral blood – leukocytosis with a shift nneutrocytosis and leukocyte formula. ESR increased.
abscess of neck
Left thigh abscess in a patient with diabetes
SEVERE abscess dominated nphenomena of intoxication may be due as absorption of toxic products from the nlesion (purulent resorptive fever), and the development of sepsis (see Sepsis).
Abscess should be ndistinguished from the hematoma, cysts, tumors that fail. Of great importance nis the diagnostic puncture: a manure allows, in addition to establishing the ndiagnosis in doubtful cases to bacteriological examination – abjection and ndetermine its sensitivity to antibiotics.
If aerogenous flora in the noral abscess may form and accumulate gas – gas abscess. Percussion over the narea abscess appears timpanichesky sound, X-ray images of the abscess cavity ndefined by gas bubbles and horizontal fluid level below it (usually occurs whean abscess caused by septic infection).
Treatment nconsists iopening the abscess, drainage and emptying his mouth. Not subject to sectiocold abscesses of tuberculous etiology due to superinfection, which inevitably noccurs while hnoyeridnoyu microflora. A small abscess formed, with well-defined ncapsule removed completely.
For opening an abscess choose the shortest line access including nanatomical features and topography of the body. Often used method of opening nthe abscess by needle, first punktuyut abscess, then the needle cut through ntissue. The autopsy abscess possibly suited to its lower pole to create good nconditions for drainage.
In order to reduce infection operative field in the course sectioabscess surrounding tissue carefully isolated gauze napkins and making a small nhole in the wall of the abscess, remove manure electric pumps. Aspiruvavshy pus nincision expand, the abscess cavity examined finger, sharing existing bridge is nremoved sequesters tissue. Avoid rough manipulations that violate pyogenic nmembrane. Abscess cavity was washed with antiseptic solution, then draining one nor more rubber or PVC tubes or injected into her gauze swabs soaked solution of nproteolytic enzymes and antiseptics. With insufficient emptying of the abscess nthrough the main incision is made additional – counterpuncture. Treatment nabscess after opening conducted on the principle of treatment of purulent nwounds.
General treatment includes strengthening therapy, blood and plasma, nantibiotics considering the sensitivity of the microbial flora of specific ntherapy (staphylococcal toxoid immunization, the use of specific y-globulin, netc.)..
Phlegmon – acute ndiffuse purulent inflammation of adipose tissue, not prone to separation. nDepending on the location distinguish subcutaneous, intramuscular, retroperitoneal nphlegmon and others of its species. A sharp localizations are some special nnames: purulent mediastinitis paraproctitis, paranefryt, paraartykulyarna nabscess and others. A sharp that developed as a result of the transition of npurulent inflammation of lymph nodes, called adenoflehmonamy. A sharp prone to nspread klitkovynnyh spaces, vascular bed, fascial cases.
Phlegmoof the left tibia
Etiology and pathogenesis. Causative agent of the disease is different nhnoyeridni microorganisms (Gram-positive and Gram-negative, aerobic and nanaerobic), but more often – staphylococci, streptococci, enterobacteria, nProteus, E. coli. Microorganisms penetrate into the fatty tissue directly or nhematogenous routes. Possible formation of secondary abscess – spreading nsuppurative inflammation in adipose tissue with osteomyelitis (parakistkova nabscess), septic arthritis (paraartykulyarna abscess), pyelonephritis n(paranefryt) and others.
Development phlegmon begins with serous infilfatsyiyi subcutaneous fat. nFluid rapidly becomes purulent character, formed areas of necrosis, which are nthen merged. Necrosis and melting fat lead to abscess phlegmon.
Changes in the tissues under phlegmon depend on the nature of the npathogen: putrefactive anaerobic infection and lead to tissue necrosis with the nformation of bubbles of gases. When coccal microflora is purulent fusion of nfabrics. The inflammatory process in phlegmon has no tendency to limit, as nobserved by an abscess, and distributed in the intervals between klitkovynnyh nconnective tissue.
Inflammation in adipose tissue is certain stage of development, nstarting with serous edema, with subsequent formation of an inflammatory ninfiltrate with subsequent tissue necrosis.
Phlegmon tibia in a patient with abnormal nstreptococcal
Adenoflehmona right groin in a patient with diabetes
Clinical nmanifestations and diagnosis. Signs phlegmon are nthe same as the symptoms of inflammatory processes (fever, fatigue, malaise, nheadache). They determine complaints of patients who also noted pain and nswelling at the site of inflammation, pain with movement, change of body nposition.
Local manifestations subcutaneous phlegmocharacterized classical signs of inflammation. Swelling usually increases, the nskin over it red, shiny, then gradually fades and becomes a normal color. nPalpation determined painful compression without clear boundaries, real, hot to nthe touch. When abscess phlegmon can determine softening infiltrate symptom nfluctuations. Regional lymph nodes are enlarged, painful. In some cases around ninfilfatu defined mesh red stripes or bands (mesh or tubular, lymphangitis).
Active and passive movements of the limbs, head nturns, changes in body position caused a sharp increase in pain in the nphlegmon.
Whedeep-seated (intramuscular) phlegmon limbs, its volume increases as compared nwith the healthy. Measurement measuring tape can accurately determine volume nincrease limb. Sometimes there is a protrusion of tissue in the area of phlegmon. nPalpation defined deep, sharply painful infiltration. Movement of limbs sharply npainful, sometimes there is protective (painful) contractions of the muscles ithe form of involuntary limb position in which pain is expressed to a lesser nextent. Regional lymph nodes are enlarged and painful. Detection by puncture npus confirms the diagnosis of deep intermuscular phlegmon.
On the neck nwith mild clinical symptoms of purulent inflammation may be determined ninfiltrate woody texture with bluish color of the skin over it – woody nphlegmon. Infiltration malobolyuchyy, fused with the skin, fascia, aponeurosis, nabsolutely motionless, gradually increasing in size. Suppuration infiltrate nobserved rarely. Latent disease occurs, the body temperature low-grade, mild nsymptoms of intoxication.
Treatment phlegmooperative. Only in the initial stage, the expected serous ninflammation acceptable conservative treatment: bed rest, rest the affected nlimb, antibiotykoterapiya, UHF-therapy, electrophoresis of chymotrypsin. nEffective novocaine blockade packs with antibiotics Vishnevsky. Improve the ngeneral condition of patients, reducing local inflammation are favorable signs nthat indicate a separation or reverse the development process. If no effect nwithin 12-24 minutes or progression shown in operation.
In urgently operated patients admitted late with nsevere intoxication, progressive process, the presence of purulent ninflammation. Under anesthesia conducted autopsy cellulitis, manure removing nnecrotic tissue. Reveals swelling and pus pocket wound thoroughly washed with nantiseptic solutions, drain. To ensure good drainage sometimes make additional ncuts – counterpuncture. Treatment after surgery is performed on the basis of ntreatment of purulent wounds.
Localization of purulent processes in the skin and nsubcutaneous tissue (Fig).
1 – anthrax, 2 – hydradenitis 3 – boil, 4-erysipelas, n5 – abscess subcutaneous tissue.
n
Folliculitis – purulent inflammation of the hair follicle. nAvailable as single and multiple lesions. They are located in any area of the skin where there is a long, well-developed vellus nhair.
Etiology and pathogenesis. Development of folliculitis is caused mainly nStaphylococcus aureus. Penetration of bacteria in the hair sac in disturbed noutflow contents causes inflammation. Development folliculitis contribute nexhaustion, colds, vitamin deficiency, chronic diseases, metabolic disorders.
Clinical nmanifestations nand diagnosis. Folliculitis is a small cone-shaped pustules that appears on the nskin, in the center of which is hair. Pustules surrounded by a narrow strip of nflushing. Around the small pustules palpable infiltration. After reducing signs nof inflammation produced purulent crusts, which vidpadayuchy leaves little nmorning with red shiny surface. After epithelialization remains for awhile nstain bluish-pink. With the localization of follicles on the scalp are ndetermined inflammatory nodes that merge together. Rozm’yakshuyuchys, ninfiltrates leading to the formation of deep purulent moves. After recovery nstill infiltrates remain severe scarring.
Treatment. Excluded, nbaths and even moisture follicles. Recommended observance of safety measures. nThe skin around fires wipe 2% salicylic alcohol, hair short obstryhayut. nFollicles reveal a sterile needle and treated with iodine tincture, greediamond to form crust.
In chronic nfolliculitis being treated comorbidities, antibiotic therapy, immunotherapy, nvitamin correction metabolic (eg, diabetes). Use physiotherapy equipment – nUV-irradiation of the lesion, electrophoresis of staphylococcal phage or nantibiotics to the affected area, diadynamic lesion area and others.
Boil n(furunculus) – acute necrotic inflammation of the hair follicle, sebaceous gland and nsurrounding subcutaneous fat. The most frequent localization is boils back of nthe neck, forearms, back of the hand, hip. The appearance of 2 or more boils nshows abrasions. In the occurrence of boils play a role microtrauma, such nscratches skin in diseases involving itching.
Etiology and pathogenesis. The most common pathogen is Staphylococcus aureus nfurunculosis, at least – purulent other microbes. Favorable conditions for nfuruncle is a weakening of the body, metabolic disorders (often diabetes), nvitamin deficiency, skin diseases. Development boil begins with festering npustule formation: after distribution of micro hair follicle in the papillary nlayer of the skin there is an inflammatory infiltrate. The center infiltrate nformed foci of necrosis (necrotic core), around the accumulated manure. After nexclusion of pus and necrotic skin defect rod filled with the subsequent nformation of granulation tissue.
Patients with early disease complain of the appearance nof abscess (pustule) or painful compression in the thickness of the skin. With nan increasing inflammation align complaints malaise, fever, pain in the seal nincreases. The most severe pain is the localization boil on the skin are nclosely adjacent to neighboring tissues: on the scalp, neck, ear canal, dorsum nof fingers.
Furunculus nface under abscessed
Furunculus forearm, which was complicated by phlegmoforearm
Clinical nmanifestations and diagnosis. On examination of patients with early disease iinflammation is a small abscess (pustule) with hyperemia of the skin around. nLess can be found in the thick seal skin and flushing of skin thickening, nabscess while absent. As the boil formed infiltrate cone rises above the skin, nwith a diameter of 0.5-
Sometimes wheviewed on the site furuncle defined globular swelling, softening, slight npurulent discharge. This abscesses boil, formed as a result of complete nmeltdown purulent necrotic rod and violation of the outflow of pus.
Identified nduring the inspection of the skin of patients with red stripes running from the nboil, suggest joining lymphangitis, increased tenderness to palpation of nregional lymph nodes – to join lymphadenitis.
Whelocalization boil on the face (Fig. 97) – the upper lip, eyelids, eyebrow narches – patients sometimes complain of a severe headache, high body temperature, nwhich are signs of complications boil purulent thrombophlebitis facial veins. nThe latter is sometimes accompanied by a purulent meningitis due to the ntransition of inflammation in the veins of the face through a vein in the eye ncavernous sinus.
Joining such nsymptoms as intermittent fever, chills, excessive sweating, delirium, ndizziness, pale skin, indicating the occurrence of sepsis, and the appearance nof abscesses in other organs (metastatic abscesses) confirms the diagnosis nseptikopiemia.
Treatment of nfuruncle conservative. Patients should be warned about the potentially nserious complications of pressing boils, pustules a razor cutting, use warming ncompresses. At the onset of the disease is treated skin 70% ethanol, 2% nsalicylic alcohol, spend UHF therapy. After opening the boil make bandages with nproteolytic enzymes, hypertonic sodium chloride, used UVR. After removing the nrod impose ointment dressings with sintomitsinovoy emulsion metyluratsylovoyu nointment. When complications boil lymphangitis and lymphadenitis showantibiotic.
Patients with facial boils subject to nurgent hospitalization in the surgical ward, where the local and general ntreatment, including antibiotics. Patients nprescribed bedrest, pureed food.
When abscess nfuruncle conduct surgical treatment – opening the abscess.
In rare nrecurrent boils and abrasions require the examination of patients that cadetect metabolic disorders (diabetes, vitamin deficiency). In order to increase nresistance to infection transmitting staph staphylococcus toxoid immunization.
Carbuncle – acute diffuse necrotic inflammation of several hair nfollicles and sebaceous glands, accompanied by the formation of general ninfiltration and necrosis of the skin and subcutaneous tissue due to nthrombosis.
Etiology and pathogenesis. The most frequent pathogen anthrax, Staphylococcus naureus, at least – streptococcus, sometimes – mixed infection (staphylococcus nand streptococcus). Factors predisposing to the development of carbuncle is nweakening the overall resistance of the organism with debilitating diseases, nhypo-and avitaminosis, metabolic diseases (diabetes).
The main localization carbuncle – back of the neck, nneck, upper and lower lip, back, back.
The disease begins with the appearance of ninfiltration, covering multiple hair follicles and sebaceous glands. There ncirculatory disorders caused by local thrombosis with the formation of necrotic nskin, subcutaneous tissue, sometimes hlybsheroztashovanyh tissues. Together nwith necrosis occurs purulent fusion of fabrics and oozing pus through the nopenings of hair follicles. After rejection formed festering wound of deep ntissue defects which healing occurs by secondary intention.
Clinical nmanifestations and diagnosis. Patients complain of severe pain, the presence of npainful infiltrate, fever, chills, malaise, fatigue, weakness, loss of nappetite, headache. In compiling the history clarify the possible presence of ndiabetes, beriberi, depletion.
When examining npatients, but general signs of purulent inflammation (increased body ntemperature, increased heart rate), it turns blue and Scarlet swelling in the nback of the neck, back, lower back, face, at least – the extremities. At the nonset of the disease may be several infiltrations, which are then joined ntogether to form a pronounced swelling, which rises above the surface of the nskin. The skin over the infiltrate intense, brilliant, with intense blue-purple ncolor in the center to the periphery, it gradually fades. On the surface ninfiltration determined several purulent necrotic pustules that are in the ncenter merge together to form extensive skiecrosis. Thinned area of necrosis breaks nin several places to form holes (symptom “sieve”) who stands manure. nInfiltration dense, sharply painful around it – pronounced swelling of tissues. nRegional lymph nodes are enlarged and painful (lymphadenitis), rarely observed lymphangitis.
With nself-rejection tissues nekrosis, center infiltrate produce large cavity, ncovered with gray-greeecrotic tissue with abundant Department manure.
Carbuncle face
If the nobservation of the patient revealed an increase in tissue edema, progression of nnecrosis, and increased symptoms of intoxication (tachycardia, headache, nweakness), chills, excessive sweating, lymphangitis, lymphadenitis, nthrombophlebitis, it should be regarded as unfavorable carbuncle, the ndevelopment of cellulitis, sepsis.
Especially ndangerous is anthrax through face may develop meningitis.
Autopsy carbuncle (a) and amputation of necrotic ntissue (b)
Carbuncle should be differentiated from nsybirvyrazkovym anthrax, characterized by the presence of hemorrhagic blisters, nno purulent discharge, painless infiltration, pronounced swelling of tissues, nnecrotic tissue black, formed, and surrounded by small bubbles with hemorrhagic ncontent. In content bubbles are sybirkovu stick.
Treatment of ncarbuncles in early stages conservative. It includes the complete rest of the naffected organ. When carbuncles face patients required bed rest. They prohibit ntalking, prescribe a liquid diet. After processing carbuncle 70% ethanol impose naseptic bandage appoint UHF-therapy. Parenteral antibiotics administered orally n- sulfanilamidnye long-acting drugs. When carbuncles in patients with diabetes, nthe necessary correction of metabolic disorders, careful of insulin, which nreduces the development of the inflammatory infiltrate and necrosis.
Failure of conservative ntherapy within 2-3 days, increase necrosis, purulent intoxication are nindications for surgery, which is done under general anesthesia. Cut crosswise ncut through infiltration to cut off the fascia and necrotic tissue throughout, nseparating them from the fascia, skin, revealing purulent edema (Fig. 99). nBleeding with minor (vessels in the inflammatory infiltrate trombovani), it nstops when injected into the wound swabs with hypertonic saline or with nproteolytic enzymes.
Large carbuncle back, in a patient with newly ndiagnosed diabetes
On the face of anthrax reveal linear incision after nthe abscess. Postoperatively treatment carbuncle conducted on the principle of ntreatment of purulent wounds for removing necrotic tissue used proteolytic nenzymes.
When to start treatment promptly carbuncle prognosis nis favorable, but in depleted patients with severe diabetes, as well as anthrax nface does not exclude the possibility of a bad outcome.
Hidradenitis – purulent ninflammation apokrynes sweat glands.
Etiology and pathogenesis. Gidradenity caused mainly Staphylococcus aureus, nwhich penetrates through the excretory ducts of sweat glands. Precipitating nfactor for the development of the disease are non personal hygiene, excessive nsweating, skin contamination, skin diseases (dermatitis, eczema).
In sweat glands develop inflammatory infiltration of ntissues with subsequent purulent melting.
Clinical nmanifestations and diagnosis. An examination of patients is painful swelling – noften in the underarm, at least in the groin or perianal areas (locations napokrynovyh sweat glands). From history we can determine the presence of ntriggering factors: increased sweating, rules of hygiene, the use of ndepilatories, shaving hair in the armpits.
Disease begins nacutely, with the appearance of small painful nodule that increases in diameter nof 1-
On examination, nmarked swelling purplish-red color. In engaging in the process of the sweat nglands several nodes merge into dense infiltrate, which can hold all the narmpit. Single units are superficially fused with the skin. After 10-15 days ithe heart swelling appears softening, defined fluctuant with infiltration, ndisclosed, begins to stand creamy pus. After discharge of pus occurs with the nformation of scar healing. The disease can recur.
In engaging ithe process of surrounding subcutaneous fat may develop abscess, with ninvolvement of lymph nodes – lymphadenitis.
Unlike boil speaker infiltration has follicular npustules and necrotic center. For axillary lymphadenitis specific location deep ninfiltration, enlarged lymph nodes, lack of cohesion tumor lesion of the skin.
Purulent hydradenitis left axillarise area.
To treat ngidradenitis using antibiotics, long-acting nsulfonamides. Spend staphylococcal toxoid immunization. In the armpit shaved noff the hair, skin rubbed with alcohol, cologne, smeared 3% solution of nbrilliant green. Apply physiotherapy – UHF, UV-irradiation.
When abscess ngidradenitis conduct surgery, autopsy abscess nmanure. With prolonged unsuccessful treatment gidradenity and the threat of nsepsis divide all the fatty tissue in the armpit, as in anthrax.
Mastitis – inflammation of the parenchyma and ninterstitial tissue of the breast. Acute mastitis is mainly found in the first n2 weeks postpartum in women who are fed milk – postnatal (lactational) nmastitis, at least – in women who are not breast-feeding and very rare – ipregnant women. The incidence of puerperal mastitis ranges from 1.5 to 6% n(relative to the number of births). Occurrence of mastitis contributes to nchange the species composition of agents of purulent infection, their antigenic nproperties and resistance to antibiotic . Usually mastitis develops in one nbreast, bilateral mastitis is rare.
Classificatioof mastitis
I. Swollen form.
II. Infiltrative nform.
III. Suppurative ndestructive form.
1) abscesses nmastitis;
2) phlegmonous nmastitis;
3) gangrenous nmastitis.
Etiology and pathogenesis. Causative aureus mastitis is often in the form of monoculture and in associatiowith E. coli and streptococcus, at least – in the form of isolated E. coli or nStreptococcus, sometimes found Proteus, Pseudomonas aeruginosa, anaerobic nflora, fungi. There are also specific forms which are rare, mastitis – ntuberculous, syphilitic. The source of infection is bacteria carriers and npatients with sore forms purulent-inflammatory diseases that surround the npatient. Of primary importance in causing mastitis is nosocomial infections.
Purulent nlactation mastitis
Input Worth infection is often cracked nipples. Caalso intrakanalikulyarne of infection during breastfeeding or pumping milk, nrarely spread of infection is hematogenous and lymphogenous ways of endogenous nfoci of infection. The presence of pathogenic bacteria on the skin and nipple nof the mother, as well as in the mouth of the child does not always lead to nmastitis. Contributing points for disease development is the weakening of the nmother comorbidities, lower immunobiological reactivity, Running across a ndifficult childbirth (especially the first or large fruit), various ncomplications of childbirth and the postpartum period (bleeding, infection of nthe birth canal, and others.). A major factor predisposing disease, is a nviolation of the outflow of milk from the development of its stagnation, which noften occurs in childbirth due to lack of milk ducts, irregular structure nnipples and functional disorders of the breast. When ingested bacteria ienhanced milk ducts milk thickens, wall ducts swell, which increases ngalactostasia and if damaged ductal epithelium promotes penetration of microbes nin tissue cancer.
Features purulent process in glandular organs are mild nability to its differences and almost unlimited proliferation involving ninflammation is more glandular tissue. This distribution often does not stop at nopening fire and then created more new abscesses in the parenchyma of the ngland.
The inflammatory process in the gland may be limited nby inflammation of mammary ducts (halaktoforit), which is accompanied by milk, nwhether pus or inflammation of glands in the areola area (areolit). During the ntransition process in the tissue and its development can be consistently nobserved phase serous and purulent inflammation, often with marked destructive nchanges. In the phase of serous inflammation of the gland tissue soaked with nserous fluid around the vessels observed accumulation of leukocytes. With the nprogression of inflammation serous impregnation breast parenchyma changes ndiffuse purulent infiltration with small foci of purulent fusion, which later nmerged to form abscesses. Recent dramatic thinning due mizhchastochkovyh walls ncaused by inflammation and increased secretory apparatus during lactation may ncoalesce and burst into subcutaneous tissue or retromamarnyy space.
The most frequent localization of ulcers – intramamarna, nsubareolyarna. When the location of the abscess in pieces on the back of the ngland it can be opened in klitkovynnyy space behind it to form a rare form – nretromamarnoho abscess. Sometimes due to involvement in the inflammatory nprocess vessels and thrombosis following necrosis of individual sections of ncancer developing gangrenosum form of mastitis.
Underlying chronic suppurative mastitis is the formatioof small abscesses with marked induration of the surrounding tissues. He ndevelops as a result of improperly conducted the treatment of acute mastitis n(irrational antibiotic use by local re-entered them in the inflammatory ninfiltrate).
There are acute and chronic mastitis. Inflammatory nprocesses may wonder predominantly parenchyma (parenchymal mastitis) or breast ninterstitium (interstitial mastitis). However, the distinction between these nforms on the basis of clinical data is not practically possible, the more nfrequently they are combined with one another.
For practical purposes, is the most appropriate clinical nclassification of acute mastitis in view of inflammation: serous (initial nstage), acute infiltrative and destructive – abscesses, abscess, gangrenous. Ithe group of chronic mastitis distinguish purulent and purulent form.
Clinical nmanifestations and diagnosis. Early diagnosis of early forms of mastitis and npromptly started treatment in most cases to achieve the reverse of the process, nprevent its transition in purulent, destructive phase.
Acute ninflammation in the mammary gland must be differentiated from acute congestioof milk. In women after the first birth galactostasia meets 2 times more often. nPatients complain of heaviness and tension in the gland that gradually nincreases. Tumor formation corresponds contours lobules of the breast, it is nquite moving, with clear boundaries, uneven surface, painless. When you click non him milk secreted freely pumping painless. After racking comes relief. nOverall condition is deteriorating slightly, body temperature, clinical blood ntests often are normal. Acute galactostasia more often bilateral and develops nin 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 nstagnation is not always easy, so any swelling of the breast that occurs with nfever should be considered stage serous mastitis. This allows time to start ntreatment and prevent the transition process in purulent phase.
With the penetration of purulent microflora ngalactostasia 2-4 days becomes inflammation – phase serous mastitis. Disease nbegins acutely with chills, fever, sweating, weakness, weakness, sharp pain ithe gland. The gland is enlarged, painful on palpation, infiltration is defined nclearly. Pumping milk painful and brings relief. In blood leukocytosis to n10,0-12,0 – 109 / l ESR 20-
The inflammatory process leads to changes in the nacidity of milk toward increasing pH, which is associated with increased activity nof alkaline phosphatase. Microscopic examination of the cellular composition of nbreast secretions determined by a large number of leukocytes.
Go early forms of mastitis in purulent inflammatiophase characterized by increased general and local symptoms of inflammation. nBody temperature is constantly high or hectic nature. Infiltration in the gland nincreases, flushing of the skin increases, fluctuations appear in one of the nareas of cancer.
Critical condition of patients observed in the form of ngangrenous mastitis: the body temperature rises to 40-41 ° C, heart rate – up nto 120-130 per minute, sharply increased breast, skin swelling, with bubbles nfilled with hemorrhagic content, with areas of necrosis. Swelling spreads to nsurrounding tissues. In the blood – high leukocytosis with a shift to the left nand leukocyte toxic grit leukocytes, protein appears in the urine.
The course of mastitis may be complicated nlymphangitis, lymphadenitis and (rarely) sepsis. After opening the pustules, nespecially involuntary, can be formed mammary fistula, which closed itself over ntime.
Treatment of nearly forms of mastitis conservative, festering – operative. If signs of nstagnation of milk glands provide an elevated position by mobilizing bandages nor a bra that need support, but do not squeeze the gland. To drain the gland nsuck milk breast pumps, breast feeding does not stop, limit fluid intake, nprescribe oxy-totsyn and no-silos. In serous and infiltrative venerable used nantibiotics (semi penitsyllin, aminohlikozid, cephalosporins, macrolides), nsulfonamides (in combination with antibiotics), infusion therapy with the nintroduction blood substitutes liquids gemodez, protein preparations, saline, nused as means of improving the body’s defenses (γ-globulin, and others.). Mandatory regular pumping nmilk (to prevent stagnation in the gland). Reverse the development process ncontribute retromamarni novocaine blockade with antibiotics and proteolytic nenzymes: 70-80 ml of 0.5% solution of novocaine, 500 000 ED kanamycin and 10 mg nof trypsin or chymotrypsin. In serous and infiltrative forms of mastitis to naccelerate the development process used reverse electric field UHF, D, UV nirradiation of cancer. All procedures carried out after emptying cancer. Isevere mastitis recommend suppress lactation combination of estrogen from nandrogen.
When purulent nmastitis shows the operation, which is done under general anesthesia, only for nsmall surface-located abscess can use infiltration anesthesia, supplemented nretromamarnoyu novocaine blockade. Conduct broad and deep enough cuts breast, nremove all necrotic tissue and accumulation of pus. Intramamares ulcers reveal nradial slits. Manure is removed, the cavity ulcer examined finger, separating nbridge washed with a solution of hydrogen peroxide and dried. Then cut edges nthrow hooks and in good light inspect the abscess cavity, pushing the gland. If nyou find a connection with another abscess located deep abscess, the hole which nreceives manure, expanding forceps. Cuts and remove necrotic tissue associated nwith cancer tissue that hang in the cavity of the abscess. If there are multiple nabscesses intramamarise each one revealing a separate incision.
|
The cuts, which are used in mastitis: 1 – radial; 2 – Bardenheyera; 3 – paraareolarese
|
Ductal-aspiratio drainage retromamarese abscess. |
Retromamares nand deeply located abscesses intramamarni reveal semioval section of the lower ntransition crease. It peeled gland from the pectoralis muscle. Intramamarni nulcers reveal behind abscess cavity drain the wound stitched to drainages. This nmethod of opening the abscess avoids crossing intralobular mammary ducts, nproviding good conditions for the outflow discharge of pus and necrotic tissue ngives a good cosmetic result. In localized forms of acute mastitis, especially nin chronic mastitis possible cuts purulent focus within the healthy tissue and nblending “blind seam” with leaving small drainage for the nintroduction of antibiotics.
Treatment of wounds after opening the abscess spend nconsidering phases of wound healing process. The use of secondary sutures nreduces treatment time and improves the cosmetic surgery results.
Prevention of mastitis begin in antenatal long before nbirth. The basis for preventive measures is to increase the body’s resistance npregnant woman. An important place is occupied rehabilitation endogenous foci nof infection, studies of women, especially those in which the first birth, nbreast feeding rules, care for breast cancer, hardening of the body, nstaphylococcus toxoid immunization, UV irradiation of the body, etc. Particular nattention should be given to pregnant women with high risk of mastitis (with nmastitis, suppurative infections of different localization in history), as well nas mastopatiyey, abnormalities of the breast, nipple, with complications of pregnancy.
The complex of preventive measures include preventing ninjuries and hospital blood loss, anesthesia delivery, combating congestiomilk processing nipples before and after breastfeeding breastfeeding, nprevention and early treatment of cracked nipples. Given the importance of nnosocomial infection in the development of mastitis, an extremely important noutlet sanitary-epidemiological profile of hospitals to prevent npurulent-inflammatory diseases of infants and mothers. This is particularly ntimely identification and rehabilitation of bacteria, careful implementation of nsanitation requirements in the care of women in labor, regular wet cleaning, nventilation chambers using germicidal lamps etc.
Erysipelas – progressive nacute inflammation own skin, less mucous membranes.
Etiology and pathogenesis. Erysipelas caused by various forms of streptococcus nrefers to contagious diseases. As to the antiseptic period it was one of the nmajor complications of wounds in hospitals. Which can lead to nosocomial ndiseases significant contingent of wounded and sick.
Microflora penetrates the skin from the external nenvironment; lymphogenous, especially hematogenous, route of infection is nextremely rare.
In place of getting pathogenic streptococci growing nfocus serous inflammation localized in the reticular layer of the skin. Ifluid determined neutrophilic leukocytes, stasis in blood and lymphatic ncapillaries. Marked inflammatory changes extend the width, capturing all the nnew skin. Such changes are characteristic erythematous erysipelas.
As the process occurring epidermal desquamation, nexfoliation last inflammatory exudate to form blisters (bullous form of nerysipelas). Content bubbles are transparent yellowish fluid, sometimes there nis a collection of pus, rarely fluid in the bladder is hemorrhagic nature.
The progression of the inflammatory process in the nskin with purulent infiltration of tissues leads to the formation of nsubcutaneous tissue phlegmon (abscess form erysipelas).
Development of inflammation in the skin can lead to ncirculatory disorders, thrombosis with the formation of skiecrosis n(necrotizing form of erysipelas).
In the pathogenesis of erysipelas importance is nallergic factor. Erysipelas prone to relapses, which are based on the state of nsensitization of the organism. Relapses inflammation leads to sclerosis nsubcutaneous tissue and lymph flow disorders of development lymphostasis first nand then elephantiasis.
Erysipelas may develop as a result of primary ninfection with exogenous and endogenous sources. But erysipelas may develop as na manifestation of secondary process – as a result of complications of various ninflammatory diseases (furuncle, carbuncle, osteomyelitis, and others.).
Erythematous nerysipelas
Some forms of erysipelas, diagnosed on the basis of nclinical signs, in fact are the phases of the development process, the progress nof which can be terminated at any given stage.
Nodulus erythema left leg requires differential Erythematous erysipelas
diagnosis of erythematous nerysipelas
Clinical nmanifestations and diagnosis. The disease occurs with severe clinical nmanifestations; infringement general condition prior to the development of nlocal symptoms. A small group of patients experienced prodromal period ncharacterized by malaise, weakness, headache. The disease often begins acutely nwith stunning chills, severe headache. There are sharp tachycardia, rapid nbreathing, body temperature for a short period reaches 40-41 ° C. From the ngeneral symptoms of intoxication observed insomnia, decreased amount of urine, nit determined the protein, erythrocytes, leukocytes, hyaline and granular ncylinders.
In the blood – nmarked leukocytosis and neutrophilia, mild anemia, reduced the number of neosinophils, but the beginning of recovery decreases neutrophilia disappears neozynopeniya appears lymphocytosis. Sometimes it may be noted enlargement of nthe liver and spleen. In some cases, severe intoxication leads to changes ithe central nervous system with the emergence of agitation, severe headache, nsometimes delirium.
Local symptoms nerythematous erysipelas – a burning pain, feeling the heat in the affected narea, the appearance of a bright red with sharp, jagged like, outside. nErysipelas often localized on the face, head and lower extremities. For all ncircuits zone lesions similar to a map, areas of hyperemia resembling flames.
The skin in the narea of inflammation swelling, its ntemperature is increased, pain intensely expressed on the periphery, there is nobserved a more pronounced redness, whose intensity in the center of lesions ngradually decreases. In areas where the skin is inactive, tightly coupled with nthe appropriate tissues, redness usually breaks. For bullous form of nerysipelas, but signs of erythematous erysipelas, characteristic of bubbles of nvarious sizes, filled with serous, purulent or hemorrhagic exudate, which are nstreptococci; fluid is very contagious and can be a source of transmission of nerysipelas by contact. The duration of this form of the disease is usually 1-2 nweeks. By the end of the disease is critical body temperature falls with nconsiderable sweating. After calming down local inflammation remains strong nexfoliation of the epidermis, the skin on the scalp noted significant hair nloss.
Abscess erysipelas changes on the nsurface of the skin (redness, itching, pain) may be less pronounced, but the ncommon symptoms are stronger than in the erythematous and bullous beshysi. The ngeneral condition of the patient difficult: tachycardia, fever, chills. Iemaciated, frail and elderly patients with phlegmonous erysipelas form can go ninto necrotic, which is characterized by the appearance of skiecrosis – nblack limited painless dense areas in the field of severe congestion, edema, nblistering.
Localization erysipelatous inflammation defines some nfeatures of its flow. On the face of erysipelas characterized by its swelling. nPhlegmonous erysipelas of the scalp accompanied by plenty of pus, purulent nedema, exfoliation of skin.
In the trunk of erysipelas characterize active ndissemination process, accompanied by severe intoxication. This inflammatiocan move sequentially capturing all the new skin and even areas previously naffected (creeping erysipelas). Erysipelas may affect areas of the body surface nat a certain distance between them (erysipelas migrans). With the localizatioof erysipelas on the limbs mainly observed erythematous and bullous forms of nit, but clinically it runs hard, when expressed commonplace. This form is ofteaccompanied by lymphadenitis, phlebitis, thrombophlebitis.
In places where loose connective tissue erysipelas occurs nwith noticeable swelling of tissues, circulatory disorders and the development nof extensive skiecrosis (areas eyelids, scrotum).
Erysipelas mucous membranes characterized by the same ngeneral and local symptoms, as in skin lesions: clearly delineated redness, nswelling, pain in erytematoznoy phase, the development of blisters containing nserous fluid in bullous phase formation of necrosis with necrotic form of nerysipelas.
Erysipelas is distinguished by frequent relapses (i20-25% of cases), recurrence of disease in the extremities lymphostasis lead to nthe development of elephantiasis.
Erysipelas can spread from the skin to the surrounding ntissues to cause metastasis streptococcal infection with the development of nfoci of inflammation with severe toxemia. The inflammatory process iflehmonoznoy beshysi may apply to tendon sheath, joints, muscles.
In typical cases the diagnosis of erysipelas has no ncomplications. It is based on such manifestations as fever, a sharp increase ibody temperature in the presence of pronounced redness with clear boundaries, nswelling and hyperesthesia certain areas, abrasions, often located near scuffs, nscratches, wounds and so on. No redness observed in rapidly debilitated npatients (old and depleted patients), or disguise her scalp greatly complicate ndiagnosis. In these cases correctly diagnosed erysipelas allow the presence of nsevere intoxication, fever and detection on the periphery of the inflammatory nskin lesions summed shaft, featuring a sharp pain.
Differential diagnosis should be made with erysipelas nerythema, dermatitis, cellulitis, limfanhytom in some cases of anthrax.
Major complications occur in the differentiation of nerysipelas with ordinary phlegmon. When rose process is localized in the skiand more pronounced on the periphery of lesions, in contrast with phlegmoinflammation affects subcutaneous and intramuscular fat, skin changes n(swelling, redness) are secondary iature and amplified from the periphery to nthe center of the lesion. Maximum tenderness phlegmon also localized in the ncenter of swelling, but not in the periphery, as in beshysi. In addition, the nphlegmon in the area of skin lesions observed dense infiltrate in appropriate tissues, which is not nthe case with erythematous and bullous form of erysipelas.
Erythematous-bullous nform of erysipelas
When abscess beshysi process usually begins with a nskin lesion, while abscess – subcutaneous and intramuscular fat skin changes nconnected to other displays. Suspicion of bullous and gangrenous erysipelas, nespecially in severe general condition of the patient and contact with animals, nskins, wool, should be performed differentiation of cutaneous anthrax. For nanthrax is characterized by lesions in the central area nekrotyzo-bathroom ntissue with subsidiaries bubbles on the periphery and extensive soft tissue nedema (sybirkovyrazkovyy anthrax). In these cases, usually considerably nenlarged regional lymph nodes. Local changes in beshysi differ from described nthe clinical picture.
Result erysipelas depends on the severity of the nprocess and the patient, his immunological forces, the presence or absence of ncomorbidities on the timeliness and accuracy of treatment. The best results are nobserved in erythematous and bullous beshysi significantly worse prognosis iphlegmonous and gangrenous forms.
Treatment ihospital. Significant nprogress in the treatment of erysipelas was achieved after began to use UV nrays, especially combined therapy with antibacterials (sulfonamides, nantibiotics). When UV irradiation is usually used Erythemic or suberytemni ndose. When erythematous or bullous beshysi radiation dosing based localizatioprocess: on a limb – 4-5 biodoz on the face – 3 biodozy. If exposure started ithe first days of the disease, usually after 1-2 sessions is the body ntemperature drops, redness is reduced, improving the health of the patient, ie, nthe process terminates. When abscess beshysi exposure spend carefully because nit may lead to increased swelling and thrombosis of small vessels of the skin. nWhen gangrenous beshysi irradiation is contraindicated.
Along with the radiation used antibiotics and nsulfanilamide preparations. With antibiotics being used penicillins, nsemisynthetic penicillins (the disappearance of redness and normalization of nbody temperature). Effective in these cases, the simultaneous use of nsulfonamides prolonged action. The earlier treatment is begun, the faster the nrecovery comes. In severe cases of erysipelas limbs used Endolymphatic nadministration of antibiotics.
Wet bandages, compresses, baths absolutely ncontraindicated. In bullous form of bladder after treatment with alcohol and nreveal a plot defeat bandage with sintomitsinovoy emulsion streptotsydnoyu nsuspension, tetracycline ointment, and others. In phlegmonous and gangrenous nforms other than the described treatment, conduct an autopsy accumulations of pus, ndrainage, removal of necrotic tissue.
Of great importance is the high calorie milk and nvegetable diet with a high content of vitamins. Required adherence asepsis, npatient better isolate in a separate ward.
Prophylactic treatment of erysipelas is to microtraumas, ncareful adherence to the rules of asepsis in surgical hospitals, implementatioof preventive measures.
Eryzepeloyid, pork measles nor swine erysipelas, erythema creeping – infectious disease, resulting iinflammation of all layers of the skin.
Etiology nand pathogenesis. The causative agent of the disease – swine erysipelas bacillus – ncrosses mikrotravmatychni skin damage when cutting meat infected animals. The nincubation period of 3-7 days. Most affected people directly associated with nthe processing of meat, fish, fowl, ie working meat, fish, canned and skiindustry, domestic housewives and others. The disease is not a rare but oftevisible or diagnosed as “erysipelas finger”, “dermatitis”, n”felon”, “lymphangitis”. In the skin develops serous ninflammation of all layers of the accession limfangita and tissue edema with ncongestion in the area of inflammation mast cells.
Eryzepeloyid finger of the right hand
Clinical manifestations. Most affected nfingers. On the 1st day of the disease on the dorsum of the thumb appears npainful stain pink-red, itchy, with clear boundaries, towering above the nsurrounding skin. After a few days of itching increases in 2-3 weeks decreases nswelling, itching stops, congestion persists, remains exfoliate the skin. nInflammation can spread to the back of the hand and fingers with the accessioof lymphangitis and lymphadenitis. Sometimes acute arthritis of interphalangeal njoints. The general condition of almost constant body temperature usually does nnot rise and only a mixed infection can be high.
When diagnosis nis necessary to bear in mind diseases such as erysipelas and acute nlymphangitis, but they are accompanied by more severe general symptoms of high nfever. From panaritiums erizipeloyid differs less acute course, the presence of nitching, lack of local pain. The disease can go into the chronic form, there is nalso a relapsing disease.
As treatment nused immobilization brush antibiotics by intramuscular injection, UV radiatioskin effective novocaine blockade packs with simultaneous administration of nantibiotics.
Prevention of the disease is to improve sanitary nconditions of work in the meat and fish industry, to protect hands from nmicro-traumas and infection.
Paraproctitis. Acute paraproctitis – purulent ninflammation pararectal fiber.
Etiology and pathogenesis. Pathogens paraproctitis often are Escherichia coli, nStaphylococcus and white staphylococci, anaerobes, and others. Usually ndefined mixed microflora.
Penetration of microorganisms in the perianal tissue ncontribute anal fissures, hemorrhoids inflammation, damage to the mucous nmembrane of the rectum and anal canal, inflammation of crypts, perineum nbruising, rozchuhy covers the anus, and others. A sharp navkolokyshkovoyi ntissue as possible complications of gunshot wounds, and tumors that splits. The ninflammatory process differs edema and purulent infiltration of loose nconnective tissue. Putrid infection rospovsyudzhuyuchys onavkolopryamokyshkoviy tissue or lymphatic tissue on the pelvis, often causes nnecrosis – the disintegration of tissue without the formation of abscesses n(suppurative necrotic paraproctitis). There are 5 forms of limited perianal nabscesses: subcutaneous, ishiorektalis, subcutaneus, pelviorektalis and nretrorektalis.
Ishiorektalis nparaproctitis left
Subcutaneous nparaproctitis localized under the skiear pozadoprohidnoho hole. Patients nfeel a sharp pain in the pozadoprohidnoho channel, especially during bowel nmovements. Increases body temperature. Clearly defined painful swelling of the nskin over her hyperemic. When it abscessed can determine symptom fluktuation.
Ishiorektalis nparaproctitis occurs with severe general symptoms. Process, capturing the ndeeper layers of tissue sciatic-rectal cavities, spreads behind the rectum to nthe other side to the prostate and, going up, grabs pelvic tissue. Patients nnoted throbbing pain in the rectum, high body temperature, sometimes chills.
Swelling, nredness of the skin at the general intoxication facilitate diagnosis ipatients with this form paraproctitis. However, in the early stages of the ndisease wheo external signs of it, we need a bimanual examination, nintroducing the finger of one hand into the rectum and placing a finger of the nother hand on the swelling out. It is possible to define a painful infiltration.
Submucosal nparaproctitis localized in submucosal layer of the rectum above pozadoprohidnyh npillars. With digital examination can determine the swelling and soreness ithe anus. Unlike subcutaneous abscesses pain pidslyzystiy form paraproctitis nless intense.
Pelviorektalis nparaproctitis – rare but most severe form pararectalis ulcers. An abscess is nformed above the pelvic floor, but may also be located low in front, behind, othe sides of the rectum. Disease at an early stage is characterized by the nabsence of any external signs of inflammation in the anus, ishyorektalnyh ndepressions. Later inflammations, punching muscle lifting anus descends dowbetween tendon reflex arc and fascia tissue in the gluteal-rectal cavity, while nhere there is abscess with characteristic clinical signs ishyorektalis abscess.
If pelviorektalis nabscesses are low on soft yazom, raising the anus, then the digital examinatioof the rectum can be determined relatively early swelling.
Retrorektalis nparaproctitis formed as a result of infection in the lymph nodes and differs nfrom pelviorektalis only that originally abscess located in the tissue behind nthe rectum, and may well go down in ishyorektalis fiber and cause it nphlegmonous inflammation.
Treatment. Ithe very early stage of the disease in the presence of a small infyltratu iperianal area used conservative treatment: sitting warm bath with a solution of npotassium permanganate, lumbar novocaine blockade radiators, UHF-therapy and nothers. All heat treatments combined with antibiotic therapy.
Cutting nabscess (at paraproctitis) and abscess.
a – nabscess at autopsy paraproctitis: 1 – the cut, 2 – cutting abscess b – opening nabscess: 1 – cuts used 2 – opening the abscess
Surgical treatment of acute paraproctitis includes early emergency surgery nby opening the abscess with removal of manure and nekrosis tissue abscess cavity examination finger separatiobridges and drainage cavity.
Locatioulcers in acute paraproctitis. Lumbar (a) and sagittal (b) sections.
1 – nsubcutaneous, 2 – ishiorektalis 3 – pelviorektalis 4 – submucosa, 5 – nretrorektalis
Apply radial, venous, cross sections, the most comfortable with them – nvenous and radial. They provide an open wound and outflow of purulent exudate, nand less traumatic. After surgery, the purpose of delay stool for 3-4 days npatients prescribed tincture of opium (5-6 drops 3 times a day). Requires nstrict bed rest. When reflex urinary retention patients put a heating pad othe area of the bladder or nintravenously injected 5.10 ml 40% solution of hexamine.
When putrefactive necrotic paraproctitis during surgery is performed ncomplete excision of tissue that numb within healthy tissue, and do this 2-3 nmore cuts skin and subcutaneous tissue for drainage.
The nincisions used in
acute paraproctitis
1 – perianal nabscess;
2 – retrorectalis;
3 – ishiorektalis
Surgical approach used in
ishiorektalis (1) and npelviorektalis (2) abscesses
Lymphangitis – inflammation of the lymphatic nvessels, complicating inflammatory disease. Penetration of bacteria in the ninterstitial spaces and lymph vessels there always, with any disease, but nclinical manifestations are possible only when the inflammatory changes iblood vessels.
Etiology and pathogenesis. The most common pathogen is Staphylococcus limfangita, other pus germs are nrare.
Lymphangitis – disease secondary. It complicates the ncourse of this disease, as abrasions, karbunkuloz, abscesses, cellulitis, nfelons, nahnyvayuchi wounds etc.
Inflammatory process affects both surface and deep lymphatic nvessels. In the wall of the lymphatic vessels and surrounding tissue edema, ntissue infiltration by lymphocytes with phenomena perylymfanhitis.
Clinical nmanifestations and diagnosis. Joining acute lymphangitis with varying purulent process indicates the nprogression of the underlying disease and increases the severity of its noccurrence. Typically, the body temperature rises to 39 – 40 ° C, accompanied nby chills, headache, increased sweating, weakness, high leukocytosis. Whereticular lymphangitis there is a pronounced hyperemia of the skin, similar to nerysipelatous, but without clear boundaries, sometimes you can define mesh ndrawing in a zone of intense redness. When stem (trunkulyarnomu) lymphangitis ncongestion has some kind of bands, ranging from inflammation to the area of regional lymph nodes – to the naxillary fossa or groin folds, skin swelling. Palpation perceptible painful nconsolidation in the form of strands along the lymph vessels. Regional lymph nnodes are enlarged, thick, painful on palpation. In engaging in the process of ndeep lymphatic vessels dermahemia absent, defined pain in extremity, swelling, ntenderness on deep palpation and early appearance lymphadenitis.
When perylymfanhitis defined areas induration along nthe lymph vessels.
Infected wound of forearm, complicated truncus lymfanhitis nforearm and shoulder
Treatment is directed primarily at neliminating the primary lesion: an autopsy abscess, cellulitis, purulent nswelling, drainage of abscesses. Antibiotic therapy prescribed by the nature of nthe microbial flora and its drug resistance. Important creating calm, elevated nposition affected organ, for this purpose, using immobilization of the limb.
Prevention lymfangitis reduced to a thorough and ntimely primary surgical treatment of wounds, limb immobilization, timely nincision and drainage of purulent foci, regional antibacterial therapy.
Lymphadenitis – inflammation of the lymph nnodes. Arises as a complication of various purulent-inflammatory diseases n(festering wounds, furuncle and carbuncle, felon, erysipelas, osteomyelitis, nthrombophlebitis, venous ulcers, and others.) And specific infections n(tuberculosis, plague, actinomycosis).
Etiology and pathogenesis. Pathogens are disease festering germs penetrating nthe lymph nodes in the lymphatic vessels. Extremely rare microorganisms npenetrate the nodes hematogenous route. Possible contact spread of infection.
The inflammatory process starts with serous edema n(simple catarrhal lymphadenitis), which can go into festering and purulent ninflammation in the surrounding tissue develops adenoflehmon.
Cervical nlymphadenitis left without abscess Purulent lymphadenitis neck nleft
Clinical nmanifestations and diagnosis. Acute lymphadenitis begins with pain and swollelymph nodes, headache, weakness, malaise, fever. Often, the disease occurs nsimultaneously with lymphangitis. When catarrhal lymphadenitis general ncondition of patients suffering enough. They note a dull pain in the area of regional lymph nnodes, the latter enlarged, tight and painful on palpation, not soldered to the nsurrounding tissues, the skin over them is not changed.
When purulent nlymphadenitis pain is sharp. The skin over the nodes hyperemic, painful npalpation sites previously lymph nodes, clearly palpable and merge with each nother and surrounding tissues become immobile. When adenoflehmoni determined ndiffuse hyperemia of the skin, tight, without clear boundaries infiltrate with nfoci of softening. Body temperature is high, there are chills, tachycardia, nheadache, severe weakness. When putrid phlegmon palpation reveal crepitus ithe lesion. Purulent lymphadenitis may lead to the spread of purulent process ntissue spaces (for peritoneal spaces, mediastinum, and others.) And sepsis.
Treatment of early forms nof lymphadenitis conservative: the creation of peace to the affected organ, nUHF-therapy, active treatment of the underlying source of infection (timely nopening of abscesses, phlegmon, efficient drainage of abscess, incisiopurulent edema) antibiotic therapy. Purulent lymphadenitis treated with nsurgical method: reveal abscesses, adenoflehmon, remove pus, wound drain. nFurther treatment is carried out according to the principles of treatment of npurulent wounds.
Osteomyelitis
The term “osteomyelitis” was introduced in 1831 Reynaud.
Osteomyelitis – an acute purulent ninflammation of the bone marrow with involvement in the actual process of bone nnadkistnytsi and often characterized by the generalization process.
Classificatioof osteomyelitis.
According to the International nClassification of Diseases Injuries and Causes of Death osteomyelitis nclassified:
1. Monoculture (staphylococcus, nstreptococcus);
2. Mixed or associated culture n(double, triple Association);
3. The causative agent is not nknown.
II. Clinical
1. Acute hematogenous nosteomyelitis
na) generalized form;
b) local (focal) form.
2. Posttraumatic osteomyelitis:
a) after fracture;
nb) firearm;
nc) post radiative.
3. Atypical forms of nosteomyelitis:
a) Brodie abscess ( intraosseous nabscess);
Brodie abscess .
No specific complaints and characteristics of nthe disease. The disease begins in early childhood and is manifested in many nyears. Appearance – slight tenderness to percussion bones.
Notable changes in the blood were detected.
The X-ray is a hotbed of enlightenment in the nmetaphysis or epiphysis femoral, tibial.
Shape rounded pockets, clear sclerotic border, nempty cavity, bone tissue along not changed peryostal reaction is absent.
Treatment – Surgery: trepanation bone ncurettage inner wall of the cavity, with muscle plastic.
Fig. 12. Brodie abscess.
b) Sclerosing nGarre;
Starts subacute, with pain in extremity, there is ndysfunction, mild fever.
General effects pass quickly and prevailing local nfeatures:
1) nswelling
2) ninfiltration soft tissue
3) nsometimes intermuscles phlegmon, fistula.
Course of long-term with remissions and exacerbations.
X-rays pronounced fusiform thickening of the ndiaphysis with areas thinning and small sequestra. Channel completely obliteration (hard bone, with small ncavities and sequestration).
Treatment: 1) conservative – Antibiotic
2) surgery – removal of small lesions osteomyelitis
Fig n13. Sclerosing Garre;
c) albuminous osteomyelitis Ol ‘are;
d) antibiotic osteomyelitis.
III. Stages nand forms of osteomyelitis:
1. Acute nphase:
a) nintramedullary phase;
b) nextramedullary phase.
2. Subacute nphase:
a) phase recovery;
b) phase continue.
3. Chronic nphase:
a) acute nphase;
b) the phase nof remission;
c) phase recovery.
IV. For nlocalization process:
1. nOsteomyelitis of long bones:
a) epiphyseal;
b) metaphyseal;
c) diaphyseal;
d) total.
2. nOsteomyelitis flat bones
a) Pelvic;
b) blade;
c) iliac;
d) skull.
V. morphological nforms:
1. Diffuse;
2. Alopecia.
VI. nComplications:
1. Local:
a) npathological fracture;
b) pathologic dislocation;
c) false joints;
d) ncontracture;
e) ankylosis.
2. General:
a) namyloidosis;
b) destructive pneumonia.
Hematogenous osteomyelitis.
Statistical data.
Seasonality – winter – summer – about 28%, Fall – nSpring – 72%.
Localization.
Most affected thigh and shin, namely the Department of bones that more nis involved in the growth in length (distal metaphysis of the femur and nproximal tibia metaphysis). They account for 2/3 of all cases of osteomyelitis.
Variants of nacute hematogenous osteomyelitis.
1. Breakwire (49%) – nvyzdorovlennya occurs within 2-3 months of onset.
2. Protracted (36%) – nvyzdorovlennya after 6-8 months of treatment.
3. Lightning (2%) – usually fatal nand happens when toxic and septic forms.
4. Chronic (13%) – formed nsequesters, voles, broken limb function, marked by periodic worsening in terms nof more than 6 months.
Etiology.
The main causative agent is Staphylococcus aureus (61%). Less is nstreptococcus, pneumococcus, intestinal bacterium, Proteus, Pseudomonas nbacterium. 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 nreactivity ohanizm and accompanied by a violation of homeostasis.
Theories of pathogenesis.
1. Vascular (embolic). Founder – nA.A.Bobrov (1888). In children, bone vessels depart at an acute angle in the nmetaphysis forming an extensive network and end blindly. This contributes to a nsharp slowdown in blood flow and sedimentation of bacteria in the blood nvessels.
2.Alergic (S.M.Derezhanov, 1940). nOsteomyelitis developed on the basis of sensitization of the organism. There is na fireplace aseptic inflammation of vasoconstriction and impaired blood supply.
3. Neuro-reflex (N.N.Yelanskyy, n1954). Reflex vasospasm due to external stimuli leads to impaired blood flow.
The author does not exclude the nrole of sensitization and the presence of covert infection .
4.M.V. Green (80th years of the ntwentieth century.) Believes that the MGO based osteonecrosis is not nintra-vascular circulatory disorders (embolism) and external compression of nvascular inflammatory infiltrate.
Patients MGO significantly depressed cellular immunity.
None taken separately theory caot explain the overall pathogenesis of nthe disease and its versatility.
MGO develops on the background of nonspecific resistance, previous sensitizatiowhen exposed to an infectious agent.
Predisposing factors.
1. Endogenous focus i”Running across yalo infection.
2. Sensitization body.
3. Nonspecific stimuli (trauma, nhypothermia, exhaustion, illness, weaken the body).
Pathological Anatomy.
By the 5th day of onset observed reactive inflammation (hyperemia, nvasodilatation, blood stasis using formennyh elements intercellular ninfiltration).
Up to 15 day – marked bone marrow necrosis, focal hemorrhage, naccumulation 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 nstarts in metaphysis bone marrow inflammation. Increases pressure in the closed nspace marrowy channel. Disturbed microcirculation (blood stasis, nthrombophlebitis shallow vessels). Developed intramedullary abscess with nsubsequent formation subperiosteum and intermuscular phlegmon.
With the development osteomiyelitis phlegmon in the process of nsequestration of bone.
Sequestration – a fragment of the affected bone pathological process nthat separated from the parent base. They are divided into:
cortical (outer) intracavitary (side endosteum), penetrating (the entire nthickness of the bone in a segment) pervasive (across the circle diaphysis).
Fig.14. nDevelopment osteomiyelitis nphlegmon
Fig.15. 1 cortical.
2.Central.
3. npenetrating
4. ntotal
The formation of sequestra from 4 weeks to 4 months.
Clinic MGO.
The clinic depends on:
virulence of microorganisms, nreactivity and localization process, the patient’s age, presence of ncomplications.
The local (focal) form of the ndisease is characterized mainly by local suppurative inflammatory changes.
Pain is constant. After 2-3 days nof the “edema is soft tissue (density, intensity). At the end of the week ninfiltrate captures all tissues.
Acute onset after triggering nfactors (trauma, hypothermia). Prodromal period – 1-2 days. Increases body ntemperature to 38.5-
Generalized form.
1. Toxic (lightning) form a very nserious infection, complicated toksytchnym shock.
Getting rough with hyperthermia nand fever. Muscular pain, agitation, delirium, seizures, a symptom of severe nintoxication. Leather gray, cold, collaptoid condition oliguria. Manifestations ntrombohemorahic syndrome. Local signs do not have time to develop, or are nminimal. Often death occurs in the coming hours or days.
2.Septykopiemia form. Getting nsharp. Fast-paced intoxication. The emergence of other purulent lesions ibones (multiple osteomyelitis), in other organs. Body temperature is a constant n39-
On “objectively: swelling, palpatio- severe pain. Possible appearance of complications – pneumonia, pleurisy, nmeningitis, pielonephritis.
Diagnosis.
1.General blood (hyperleukocytosis, nshift to the left, toxic granularity neyrofililes, erythrocyte sedimentatiorate).
2. Biochemical analysis of blood n(hypoproteinemia by reducing fine factions, hypokalemia, hyponatremia, nhypercalcemia).
3. Radiography (swelling soft tissue, nperyostitis, availability sequestration).
4. Puncture bones (search nand evacuation of pus, measuring intraosseous pressure, it is possible aincreased to 200-
5. Rheovasography (increased nvascular tone, spasm and contraction of tissue edema).
6. Ultrasonic echolocatio(presence osteomiyelitis fire)).
7. Skin thermometry (body ntemperature over the fire at 2-
8. Thermography (increase the nintensity and duration of infrared radiation).
9. Cytological method n(accumulation of neutrophilic leukocytes in bone marrow punctate).
10. Computer “tomography n(serial sections).
11. Densitometry (determining the ndegree of bone demineralization).
12.Osteomedulohrafiya (Normally ncontrast resolves after 10-30 min. When osteomyelitis – more slowly).
13. Radionuclide nimaging.
Figure 16. Osteomyelitis of the tubular bones:
1. subperiosteum abscess.
2. metaphyseal focus
3. Purulent fistula
4. diaphyseal fireplace
5. nepiphyseal center
6. sequestration
Treatment.
I. Effect on Macro-organism.
II. Effect on microorganism.
III. Treatment of local focus.
I. Effect non Macro-organism.
1. Detoxification therapy;
2. Reducing or eliminating dysfunction of vital norgans;
3. Increasing the body’s defenses.
Intensive care.
1. Correction of homeostasis.
2. Therapy dysfunction of vital organs.
3. Increasing imunorezystance and maintain energy nbalance:
a) non-specific immunotherapy (adjuvants);
b) specific immunotherapy (impact on active immunity, nthe 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 iinflammation (intraarterial administration).
4. Duration of antibiotic therapy in optimal doses (up nto 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 nthe onset).
2. Surgical treatment – in advanced cases, phlegmon:
a) nosteoperforation (application holes in the bone with the production of drainage ntubes for flow irrigation and the introduction of antibiotics);
b) disclosure subperiosteum and intermuscular phlegmowith active and running catchment.
Fig. 17. nSurgical 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 nosteomyelitis).
Prehid MGO in chronic occurs from 3 weeks to 4 months. The process of nsequestration lasts months and sometimes years. Sequestration become infected nstranger body. Formed long healing fistula (tens of years). The ongoing changes nin parenchymatous organs (liver, kidney failure, amyloidosis).
Clinic.
Characterized by mild symptoms – aching pain at the site of the fire, npurulent fistulas, severe postoperative scarring.
At aggravations – pronounced pain, fever to
Diagnosis.
The main importance is radiography. The X-ray observed:
thickening of the bone, the presence of cavities in it and nsequestration; osteosclerosis, narrowing marrowy channel; thickened periosteum.
With modern methods of ndiagnosis using computer “tomography.
Treating complex.
Radical surgery, targeted antibiotic therapy, detoxification therapy, nactivating the body’s immune.
Radical surgery is the excision of fistulas after previous coloring them ntrepanation bone sequestrectomy the removal of granulation and pus to normal nbone flowing drainage of suturing wounds.
With a large cavity in the bone using plastic muscular flap on the nmiddle leg bone or plastic (own bone or canned demineralized bone).
nTotal purulent infection (sepsis). Endogenous nintoxication in acute surgical infection.
The word “sepsis” Greek norigin, means decay, decomposition and is associated with illness and death. nAfter the discovery of the role of microbes in putrefactive processes, sepsis nhas become synonymous with heavy, deseminovanoyi infection, n”poisoning” of blood. For a long time considered the pathogenesis of nsepsis according to the classical definition of N. Schottmuller (1914): n”On the sepsis can say when the body is the focus of infection from which ncontinuously or periodically enter the bloodstream bacteria, and as a result, nthere are both subjective and objective ‘objectively symptoms. ” This ndefinition, which many clinicians have not given up and now, almost reflecting nthe clinical situation, and thus appear as clinical and medical errors that nlead to late diagnosis and inadequate treatment of pain. Despite the fact that nthe problem of sepsis remains very relevant for many decades, in terms of nterminology and understanding of the essence of sepsis still remains unclear nand much disputed.
Despite the use of new antibiotics, nthe introduction of new methods of medical and surgical treatment, the nincidence of sepsis and its complications is reduced. In Germany from sepsis ndie each year 75,000 patients (the same patients and dies from acute myocardial ninfarction). Overall in Europe, nearly half a million cases of sepsis, a ncondition diagnosed in one patient in a thousand hospitalized. In the United nStates registered 300 thousand cases of gram-negative sepsis.
Evidence of the complexity and the nmany unresolved fundamental issues pathogenesis of sepsis and its terminology nis holding 5 of the World Congress on the issue of sepsis, shock and ninflammation, held in Munich from 1988 to 2000, the Organization of the Academy nof multiple organ failure in Trieste (Italy).
In Soviet literature for a long ntime used the terminology and classification of sepsis suggested M.I.Kuzinym nand BM Kostyuchenko (1981).
Determining driven them talk about nthe difficulties of this controversial problem. On the one hand, sepsis should nbe considered as a consistent link in the development of surgical infection as na result of generalized infection that initially localisation in the primary focus, with the rest, “sepsis – a heavy nonspecific ninfectious process occurring against the backdrop of changes ireactivity.” Classification MI Kuzin and BM Kostyuchenko contains a number nof provisions which do not have proliferated like “purulent resorptive nfever”, on certain terms, such as “chronic sepsis,” the authors nthemselves refused.
MI Kuzin and BM Kostyucheno (1990) nfind that from a practical point of view can be guided by the following time nparameters:
1) fulminant septicemia – clinical npicture unfolds within 1-2 days (2% of patients);
2) acute sepsis occurs within 5-7 ndays (39-40% of patients);
3) subacute sepsis lasts 7-14 days n(50-60%);
On the development of clinical ndisease after infection infestations should, according to M. Kuzin and BM nKostyuchenko (1990), to provide:
– Early sepsis arising in terms of n3 weeks after injury, when the role of the primary lesion is undeniable;
– Late sepsis, such as that ndeveloped after a month or more similar conditions when the primary focus is nlosing its clinical significance, which often leads to misconceptions about nacute cryptogenic sepsis.
In addition, based on the phase ncharacter of biological responses that sometimes is not related to temporary nfactors, the authors consider clinically reasonable to provide 3 phase sepsis:
– Tension;
– Catabolic disorders;
– Anabolic.
In everyday clinical npractice to classify sepsis by type of microbe-agent:
– Staphylococcal
– Kolibacillus
– Pseudomonas etc.
Since the species of microbe has a nsignificant impact on hospital sepsis, this division has a certain practical nsignificance for physician directs for the most rational antibiotic therapy. As nyou know, microflora in monoculture occurs in less than half of the patients. nSpecies composition of its stake in the blood is ofteot the same as in the ntreatment process quickly changing. Clinical course of sepsis is determined not nonly the kind of pathogen and its “dose”, but pretty much the nature nof reactions to the infection, as well as a number of other factors, such as nprimary and secondary septic foci, concomitant diseases, age of patients and nothers.
Depending on the nlocation of the primary vohnyscharozriznyayut:
– Odontogenic
– Otogenic
– Obstetric and gynecological
– Urological
– Surgical and other types of nsepsis.
The feasibility of such a divisiois due to the fact that the course and outcome of sepsis is largely determined nby the success of treatment of the primary lesion, and how his treatment is nvery different: obstetric and gynecological sepsis should be treated with ngynecologists and surgery – surgeons, etc.
The concept of surgical sepsis nusually include sepsis that developed as a result of acute and chronic nsuppurative surgical diseases (furuncle, carbuncle, abscess, cellulitis, nosteomyelitis, peritonitis, and others.) And required local surgical operatioand general intensive treatment. Very close to the surgical wound sepsis that ndevelops against the backdrop of various, mainly severe gunshot wounds and ntraumatic. This also should include cases of sepsis that developed after nsurgery, intensive care and diagnostic procedures, intravascular manipulation, netc. This type of sepsis called nosocomial (hospital acquired within the ninstitution).
Modern terminology and the idea of Sepsis
Insight sepsis goes along with the ndesire to give a clear definition of this pathology. The literature continues nto debate on modern terminology and understanding of the essence of sepsis.
Complexity of the problem stems nfrom the fact that patients with clinical proyavamysepsysu only 45 – 48% of ncases can be detected bakteriyemiyu. It appeared that a large array of damaged ntissue (necrotizing pancreatitis, polytrauma, abdominal aortic rupture, burns) nmay be replaced as bacteria trigger a generalized response.
Exceptional achievements itheoretical and practical point of view, that changed the whole concept of nsepsis was the opening number of endogenous mediators of systemic inflammatory nresponse. At present, the common view that sepsis caot be the result of ndirect action of microorganisms on Macro-organism as a result of significant ndisturbances in the immune system that are in its development over the state of nactivation (“phase hiperzapalennya”) to the state of immunodeficiency n(“phase imunoparalisis” ). The body, therefore, is nan active member autodestruktyvnoho process. Septic “autokanibalizm” n- a concept that was introduced to describe the metabolism of the patient with nsepsis. Nowadays the leading role played by gram-negative flora (Escherichia ncoli, Bacillus blue-green pus, Klebsiella, Proteus).
One of the most powerful agents of nstarting sepsis is lipopolysaccharide membrane of gram-negative bacteria, ndesignated as endotoxin. Note especially spending antibiotic that endotoxin is nreleased in the process of microorganisms, and because their death under the ninfluence of antibiotics, and the degree of unequal allocation of endotoxin by nthe action of different antibiotics.
In order to eliminate differences nin terminology and in accordance with modern ideas about inflammatioconciliation conference the American College of Physicians and Thoracic nAssociation for the treatment of patients who are in critical conditio(American Colledge of Chest Physicians / Society of Critical Care Medecine Consensus nConferens, 1992), decided to standardize the terminology used in assessing the nseverity of the inflammatory response and diagnosis of complications that neliminate existing ambiguities.
At the suggestion of the nconciliation conference, severe body’s response to inflammation caused by ninfection, severe trauma, burns, acute destructive pancreatitis and other ntissue damaging factors recommended called syndrome of systemic response n(reaction) on inflammation – Systemic Inflammatory Response Syndrome – SIRS.
But we should celebrate this nconcept as “systemic inflammation”. This term in general pathology nthere. Inflammation is a local, protective, controlled immune system reactioto the above damaging factors. The response to inflammation depending on the nseverity of the latter may be primarily a local or systemic, total, such, naccompanied by dysfunction of several organs and systems. It should be nemphasized that SIRS is a set of symptoms rather than a diagnosis, and his npresence should make the doctor find the cause of this symptom, which does not nidentify a specific disease and is the basis for a treatment.
Definition of sepsis nadopted North American consensus yesamym reasonable, though not disclose all nthe features of the pathogenesis of this condition. Sepsis – a systemic nresponse to infection. To put this diagnosis must be at least two of the nfollowing four characteristics and the presence of foci of infection:
– Body temperature> 38 ° C or n<36 ° C;
– Heart rate>
– The number of breaths> 20 min., nOr pCO2 <32 mmHg;
– WBC> 12000/ml or <4000/ml, nmore than 10% immature neutrophils.
n
n
Tab. 1 The terminology adopted by the North American Conference of nReconciliation, 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 orga 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 ca stabilize blood pressure, but hypoperfusion remains. |
|
Arterial hypotension |
Systolic blood pressure < |
|
The syndrome of multiple orga failure |
The presence of acute lesions function of organs and systems, while the body without the aid caot alone stabilize homeostasis. |
The severity of the syndrome is determined by the nnumber of available evidence of dysfunction in this patient. If two signs nsyndrome assessed as moderate (mild) severity, 3 – as medium severity, 4 – as nheavy. At 3 and 4 signs of the syndrome of systemic responses to inflammatioof the risk of disease progress, the development of organ failure, sepsis and ndeath increases dramatically.
Obviously, the criteria for severity of systemic nreactions are more objective than subjective opinion of the patient’s conditioas satisfactory, moderate, heavy. Assessment of severity of the patient may be nsupplemented by a number of other criteria (impairment of mental status, npresence of oliguria, metabolic acidosis, increased bilirubin and ntransaminase), counting the number of points on a scale SOFA (Sepsis related nOrgan Failure Assesment) adopted by the European Society of Intensive Care i1994 for evaluation of organ failure associated with the presence of sepsis or nAPACHE-II, which takes into account not tilkyhostri violation of physiological nfunctions, but also the patient’s age, the presence of aggravating chronic ndiseases.
In recent years, in connection with the study of the nrole of different cytokines in the pathogenesis of sepsis gaining, with SIRS, nanother concept, as proposed by RC Bone – CARS (compensatory antiinfammatory nresponse syndrome). This well-connected phase winding, anti-inflammatory nresponses, early and late multiple organ dysfunction and nosocomial infection.
Fig. 1. Relationship SIRS and CARS (no RC Bone et al., n1996)
n
Statistically S. Wade et al. n(1998), the incidence of SIRS in ICU patients in the surgical clinic reaches n51.1%: 335 of 656 patients, in 65 (19.4%) of 335 patients with blood isolated nmicrobial culture and diagnosed with sepsis, in 47 of 65 patients sepsis ndeveloped septic shock mortality 53.2%. Cooperative research covers several nmedical centers in the
There are several options for assessment septic state. Clinical ninterpretation depends on microbiological data (or is no invasive infection, npositive blood culture) and the presence of these or other signs of systemic ninflammatory response (Table 2). Certain clinical and tactical assistance caprovide 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 ninvasive infection (no blood culture), but there are clinical signs of SIRS, we ncan assume that either it SIRS infectious nature (eg, traumatic) or this – nculturally negative sepsis.
Etiology SEPSIS
Difficulties of early diagnosis of sepsis associated noften with insufficient ob’yektyvnoyuotsinkoyu changes occurring in the wound – nthe local focus of infection, which under certain circumstances becomes primary nseptic foci that late, and then develops generalization process.
Complexity of the problem stems from the fact that npatients with clinical proyavamysepsysu, only 21-48% of cases can be detected nbakteriyemiyu. It appeared that a large array of damaged tissue (necrotizing npancreatitis, polytrauma, burns, positional compression syndrome, and others.) nCan be replaced as bacteria trigger systemic inflammatory response. Iaddition, the presence of membrane potential and heterogeneity of the surface nof blood cells leads to the microorganisms penetrate into the bloodstream, is nsoon fixed on the membranes of blood cells. Granulomas and lymphocytes can get nrid of foreign elements adsorbed by phagocytosis and other factors of cellular nand humoral immunity. Only red blood cells is to be inferior to cleanse itself nand so become carriers of infection in sepsis. It is on their membranes n”dormant” organisms.
“Entrance gate” in sepsis
The most common cause of sepsis is acute purulent ndiseases of soft tissues that make up the structure sepsis 44.3% – 52% – of the nso-called “Wound sepsis.”
Second in frequency cause of sepsis are patients with npurulent peritonitis as a complication of inflammatory processes in the nabdominal cavity.
Something specific group of patients with clostridial ninfection. Overall clinical presentation of this infection is so bright that ncomes to the fore and obscures the role of primary site of infection.
Reasons ngeneralization of infection
1) Wrong surgical ntactics and inadequate volume of surgery;
2) The wrong nchoice of size and antibacterial components, dezintoksykatsiynoyii symptomatic ntherapy;
3) Reduced or ndistorted imunnoreaktyvnist microorganism;
4) presence of nsevere comorbidities (diabetes, alimentary dystrophy, and others.)
5) Wide ndissemination of antibiotic-resistant strains of bacteria;
6) Change the netiological structure of pathogens of purulent surgical infection.
Hospital sepsis
Problem nazokomialnoyi (nosocomial) infection for surgery nis of particular importance. According to statistical studies, the incidence nnazokomialnoyiinfektsiyi in surgery an average of 6 – 8% with variations depending non the nature of the surgery. The frequency of wound infection complications ivarious fields of surgery in the 80 years ranged from 1 to 14%, 42% lethal nrezultativpislya operations was due to purulent-septic complications.
The highest level of infectious complications that have nno connection with the transaction, was in the surgical intensive care unit n(VAIT). The average rate of infection iazokomialnoyi VAIT is 25% and is ndirectly related to the duration of stay of patients in the department.
Sources nnazokomialnoyi infection causing factors pathogenesis
There are two main sources of nosocomial infectiohirurhichnohohvoroho – exogenous and endogenous. Any external sources (air, nfood, water, contact with staff and visitors, invasive medical diagnostic nprocedures) may lead to colonization of the patient with podalshymrozvytkom ninfection.
In modern hospitals, which built and operated nwithcompliance all sanitary-epidemiological and health requirements, external nsources of infection persists reliably. However, in such offices, patients ndevelop nazokomialni infectious complications and deaths appear related to nseptic multiple organ failure, and external infection with careful analysis nexcluded.
Many bacteria live in the gastrointestinal tract of nhealthy humans – both anaerobic and aerobic. Normally they get along just fine nwith each other, but also support adequate motor, secretory and metabolic nfunctions of the gastrointestinal tract. However, under the influence of nsurgical stress, shock, protein deficiency, massive antibacterial such a state nof “biological comfort” is broken and there are conditions for the ntranslocation of toxins, cytokines not only in the portal system, but also ndirectly through the intestinal wall. This release of endogenous bacteria or ntheir toxins can cause septic and non-specific organ damage. In these cases, it nis the intestine, figuratively speaking, “motor” that runs and nsupports multiple organ failure (MOF). Therefore, the gastrointestinal tract, nusually first damaged by surgical stress.
There is a condition that clinicians still treated as a nmysterious “sepsis without primary focus” and is called “sepsis nintestinal origin”.
New perspective on organ failure is the evaluation of nmesenteric nodes as a link betweeon-functioning intestine and MOF. nExperimental studies have shown that mesenteric lymph nodes play an important nrole in the occurrence of acute phase inflammatory response, as a link betweethe intestine and damaged internal organs. Lymph containing activated lymphocytes, nneutrophils, cytokines enters the lungs, which in this case are between the nintestine and the liver on the one hand and the systemic circulation from the nother and take the first hit itself, being the primary filter.
Etiological nand nosological structure nazokomialnoyi infection
With more than 400 species of bacteria that live in the nhuman body, only about 15 play an essential role in the etiology nazokomialnyh ninfectious complications. Gram-negative enteric bacteria, Pseudomonas naeruginosa, staphylococci, enterococci, some anaerobes – that’s almost the nentire range of pathogens obligatory complications in abdominal, cardiovascular nand other major fields of surgery.
Recently, most authors are more common with epidermal nstaphylococcus as an etiological factor catheterization complications vascular nand endovascular cardiac surgery. And it is not only microbiological phenomenoor a consequence of poor asepsis.
As nosological structure nazokomialnoyi infection, it is nin surgery differentiates its widest range; any organ and anatomic area may be nincluded in the scope of surgical infection, even regardless of the locatioand nature of the surgery.
The main pathogen was Staphylococcus aureus osteomyelitis n- 83.4% of crops. When crops bile in patients with acute cholecystitis was nobtained nehatyvnyyrezultat in 69.3% of cases, and the growth of flora found i30.3%. With the positive response in 47.8% detected E.coli, and in 26% – nKlebsiella pneumonia.
Thus, we can assume that a significant proportion of n”negative” results of crops may be associated with the presence of nanaerobic microorganisms, which are available at our disposal methods are nunable to detect.
To date, a number of isolated components of microbial ncells that can directly cause the formation of so-called nprozapalnyhtsytokiniv-IL-1, IL-6, tumor necrosis factor, and run SIRS.
Dive proteins (Fig. 1), which are localized in the cell nmembrane of gram-negative bacteria, and proteins villi also have high enough nresolution to induce proinflammatory cytokines.
Fig. 1. Simplified diagram of nthe structure of the cell membrane of gram-negative bacteria (by Brooks GF, et nal., 1994).
The outer membrane, which is a lipid bilayer is in Gram-negative but not nGram-positive bacteria. It permeated Plunge – special proteins that provide npenetration of hydrophilic substances to the membrane cytoplasm. nPeptydohlikanovyy layer inherent only bacteria and is thinner in gram-positive norganisms than in gram. The outer membrane with peptydohlykanovym layer is the ncell wall.
Lipoprotyeyiny, glycoproteins, lipids, peptydohlykany is igram-negative and gram-positive bacteria in. All of them – the components of nthe cell wall. Specific surface proteins found only in gram-positive bacteria.
Obviously, the potential for ninduction of proinflammatory cytokines in gram-positive microorganisms is much nlower. For example, the concentration teyhoyevyh acids needed to trigger the ninduction of tumor necrosis factor is 1000 ng / ml.
Microorganism adapted to in order nto develop a pathological reaction in the human body, and between the humabody and the microbe is a constant dialogue. Of course, ongoing dialogue is nmainly due to surface structures. These proteins bind to immunoglobulins, and a nlarge group of proteins that recognize the extracellular matrix, ie those nproteins that allow microorganisms to attach to the extracellular matrix, nintercellular spaces in the human body. By surface structures include a number nof surface enzymes.
One of the main conditions for nthe successful treatment of purulent-septic patients is effective isuppressing these microbial pathogen that feasible only after his nidentification. Guess the character pathogen in some cases can be features oclinical manifestations of his life in the wound (general view of the wound, nthe nature of the discharge, smell them, and others.), But the final nvysnovokrobytsya according to bacteriological examination.
PATHOGENESIS OF SEPSIS
The pathogenesis of sepsis play nan important role not only pathogens but also the reaction of the immune system nthat is caused by bacterial toxins or products of inflammation (necrosis), npasses in its development path from excessive activation state (phase nhiperzapalennya) to a state of immunodeficiency (phase imunoparalichu) ( fig. n3). The body is an active member of the destructive process, rather nautodestruktyvnoho process, or as it is called, “autokanibalizmu.”
The main factor initiating SIRS nis endotoxin, which is lipopolisaharydnoyu substance (LPS), the toxic effect of nwhich is due to lipid A, which is included in its composition. Isolation of nendotoxin observed during the destruction of microbial cells, especially under nthe influence of antibiotic therapy. Value is how “aggressive” nantybyotykoterapiya, leading to a cascade of receipt of endotoxin into the nbloodstream from the destroyed microbes and use subterapevtychnyh doses of nantibiotics used prophylactically. This is because most antibiotics nsubterapevtychnyh doses have high affinity for protein PSB-3, causing ninhibition of bacterial cell separation, sharing with the formation of long nthreadlike structures – filaments. Consequently, the observed increase ibiomass production and endotoxin. A special role is played by the functional nreserves of the spleen, which provides not only general detoxification, but nalso the appropriate level of antibodies to LPS.
Endotoxin, which separated, activates multiple biological systems: nkinin, coagulation system, contact, complement, peripheral blood cells – nneutrophils, eosinophils, monocytes, macrophages, and endothelial cells from ninitiating the release of many neurotransmitters which vividly called n”metabolic anarchy.” Metabolic anarchy accompanying Spohn and found nincreased levels of lactate, total liposaharydiv, prostacyclin, zrostannyamaktyvnosti ncyclooxygenase, coagulopathy, low levels of circulating antibodies, reflecting nexcessive uncontrolled activation моноцитмакрофагальнихцитокінов, lack of control which is the nbasis for SIRS in critically different etiologies.
Toxic effects nLPS is a complex of disorders caused by simultaneous damage as cells ncirculating in the bloodstream and endothelial. Damage to endothelial cells nacquires special importance in the development Spohn, as opposed to npre-existing views on the endothelium as a passive barrier, now known for its nessential role in the regulation mikrotsyrkulyatsiyishlyahom impact on the nbalance of relaxation and reduction of vascular permeability (Fig. 4).
Among the many nmetabolic breakdown of particular note is the so-called oksyradykalnyy stress nthat forms autoposhkodzhennya in sepsis and SIRS. Free radicals and hipohlorna nacid damage endothelial cells of various organs as a result of lipid nperoxidation layer membranes, which leads to the formation syndrome VET (Spohn) nin patients with hypertension, liver failure, diabetes, and atherosclerosis. nThis is due to the normal flow, which is not provided due to the instantaneous nand complementing each other disorders of lipid prostacyclin PGJ2, supportive nand tromborezystentnist protyzhortannya and free-N0, which provides a nvasodilator effect.
Under the ninfluence of lipid A endotoxin disrupted the integrity of the membrane of red nblood cells, eosinophils, neutrophils, macrophages, polymorphonuclear nleukocytes, resulting in the release into the bloodstream a number of nbiologically active agents – cytokines such as TNF-a and TNF-p, interleuki(IL) 1-6 and others. TNF – tumor necrosis factor – the initiator release nphospholipases, violations products N0, inhibition of angiotensin II, which nleads to damage of systolic and diastolic function of the left ventricle, ninhibition of the contractile ability of the myocardium and arterial nhypotension.
Excessive nsystemic cytokine activation monotsytmakrofahalnyh is very harmful because it nstimulates the synthesis of additional natural inflammatory mediators such as nleukotrienes (LTC4, LTD4, LTE4), eicosanoids, interleukins, thromboxane, nbradykinin, microcirculation involved in the destruction, permeability and nedema formation by increase in hydrostatic capillary pressure and activatiovasodilation. At the same time changing the activity of cellular calcium and nprotein metabolism in skeletal muscle, increased breakdown of glucose increases nacidosis, increases the concentration of acute phase proteins.
Most cytokines – nis endogenous pyrogens that are responsible for the development of a model for nsepsis and SIRS hyperthermic syndrome. Thus, the activation of monocytes in the nblood enters the IL-1, which penetrate the blood-brain barrier to neurons of nthe hypothalamus, stimulates heat and breaks behavioral processes.
Although the nexact mechanism of destruction of hepatocytes and sinusoidal liver cells under nthe influence of cytokine unknown, found that TNF in combination with IL-6 nshows a direct hepatotoxic effect. The basic mechanism of endothelial damage nrenal tubules influenced TMF leukotrienes and LPS microbes consider local changes nfibrinolytic activity and endothelial damage withsubsequent intracellular nedema, increase in the number of lysosomes that attack membrane deposition of nfibrin.
Since the maipoint of impact of endotoxin and TNF is endothelial cell activation leads to the nrelease of prostacyclin (PGS2), allocation of elastase, toxic oxygemetabolites, platelet activating factor and complement with the release of nanafilaktoheniv as S3A, S4a, S5a, a terminal complement, bradykinin followed by nthe formation of a syndrome of increased capillary permeability. The release of nsubendothelial collagen accompanied kininohenu action against platelet adhesioby von Willebrand factor and the presence of thrombin. It promotes the release nof thromboxane Ah, strengthens capillary hydrostatic pressure increases nswelling and permeability in the presence of leukotrienes (LTC4, LTD4, LTE4) nand bradykinin.
Thus, the nseverity of disturbance of microcirculation and the formation of multiple orgafailure in sepsis and SIRS depends on the combined damage under the influence nof cytokines hemostatic system and immunity.
Coagulatiodisorders accompanied by thrombocytopenia, the advent of fibrinogen degradatioproducts, and fibronectin – a key modulator of the immune response that nprovides the bacterial invasion and activation of T-lymphocytes, activated nclotting protein depletion with anticoagulants, increased levels of binding nprotein. Damaged endothelium is able to produce platelet activating factor – a nstrong stimulant of aggregation, thromboxane Ah, serotonin, fibronectin. In the npresence of thromboplastin entering the bloodstream from damaged tissues and ncells against endothelial function affected both by coagulation forming block ncapillary circulation – the basis SPON.
Immuno paralysis – response to infection and extreme action. It is ncalled the phenomenon of change in the ratio of cells of the immune response, nunnatural increase in complement activation and lymphocytes. This is the T-cell ndysfunction – defective proliferation to the stimulus, until the stage of deep nstress by two cytokines – IL-2 and interferon-g, because of their inadequate nproduct. Along with this excessive systemic hyperactivatiomonotsytmakrofahovyh cytokines harmful, as it stimulates the synthesis of nadditional natural inflammatory mediators, such as eicosanoids, IL-8 and nothers.
Endotoxin is very immunogenic and stimulates nB-lymphocytes, enhances helper function, stimulates plasma cells and the nformation of immunocytes. In this process, endothelial cells are involved, highlighting ninfluenced cytokine activation of tissue compatibility antigens class II, which ncan be a source of cytokine stimulation, leading to disruption of nleukocyte-endothelial interactions.
If normal nonspecific natural immune mechanisms nprovide adequate protection against local infection, localized inflammation, nlimit excessive production of inflammatory mediators, prevent the development nof severe general (systemic) reactions vital organs in response to ninflammation, in terms of SIRS, – a massive inflammatory reaction, resulting ithe release of cytokines, leading to multiple organ failure.
Inflammatory reaction rid of the pathogenic factors ndistinguished “foreign” from “his”, what promotes recovery.
The most nstudied natural defense mechanisms include:
1) reaction of nthe central nervous system, the sympathetic and neuroendocrine systems that nregulate hemodynamic and metabolic disturbances in the body in response to ninflammation, trauma, presence of nonviable tissue in the body;
2) natural nnonspecific immune responses, such as chemotaxis, opsonizatsiya, phagocytosis, nactivation of complement, immunoglobulins, produce histamine, serotonin, nprostaglandins, and others;
3) inflammatory nmediators produced by cells (cytokines), discovered recently thanks to the nsuccess of molecular biology and molecular genetics.
Clinical npicture and diagnosis of sepsis
Sepsis is a clinical syndrome is difficult to define. nThe above mechanisms of inflammation suggest that SIRS is clearly delineated npathophysiological settings. SIRS, which develops due vazhkoyiinfektsiyi, no ndifferent from a syndrome that occurs in response to other damaging factors nbecause of their pathophysiological mechanisms involved in the same ninflammatory mediators. The syndrome of systemic inflammatory response caot nconsideredas sepsis, because to some extent, damage to the immune system, it nessentially means the only useful defensive response against infection and nother harmful factors. It becomes dangerous to the patient’s life in cases nwhere excessive production of cytokines and other mediators of inflammation and nan imbalance between pro-and anti-inflammatory mediators damage control nfunction of the immune system. In these circumstances, SIRS may be complicated nby the development of sepsis, septic shock, multiple organ failure.
Clinic SIRS varies depending on four stages, isolated nin the course of the syndrome.
Phase A, which is a normal response to stress after nmajor surgeries, injuries and diseases, is characterized by a moderate decrease nin systemic vascular resistance and a corresponding increase in cardiac output. nOxygen consumption that increases are hipermetabolichna response to stress, the nconcentration of lactate remains withiormal limits. This is a normal nreaction, which can be observed in each patient after major surgery and severe ntrauma. Assuming that the attendant complications missing transient SIRS, which nreflects the systemic effects of generalized inflammatory response solved as nthe patient return to normal physiological state.
Phase B is excessive stressful response. Loss of nsystemic vascular resistance becomes excessive. When supported by adequate npreload by increasing intravascular volume and at normal physiological reserve nleft ventricular cardiac output increased significantly to meet the needs ncreated by a significant decrease in load due to systemic vasodilatation. nCombination vasodilation of blood vessels and a significant expansion of nextracellular volume due to systemic edema creates the need for large volumes nof additional preload for patients in stage B. If achieving adequate preload n(preferably crystalloid solutions) fails, it can lead to hypotension, even ipatients with parameters this stage of SIRS.
Phase B is also characterized by a significant ndecrease in arteriovenous difference of oxygen.
This is the stage in the beginning to show the ndevelopment of multiple organ dysfunction syndrome. With increasing excess nlactate in the peripheral blood appears decrease arterial blood oxygesaturation. The level of serum bilirubin begins to rise. In the absence of nmeasures to prevent the development of acute gastric ulcers and erosions, these nsymptoms appear complications. Serum creatinine level greater than
Phase C is decompensated SIRS response to stress. Loss nof systemic vascular resistance pronounced. Physiological reserves left nventricle caot maintain pressure because of the very pronounced decrease nstress. Cardiac output is normal or slightly elevated, so we can assume n”normal” physiological state of the patient, but irezultatinadmirnoho reduce the load pressure caot be supported adequately. nDowngraded BP is maintained even in conditions of adequate preload. This ncondition hypotension traditionally attributed to septic shock or shock that occurs nwhen the “natural” development of sepsis. Clinically, these patients nhave a paradoxical combination of hypotension and warm skin.
Combination of bacterial infection and other potential nactivators of the inflammatory response may play synerhytycheskuyu role in the ndevelopment of septic shock. Shock (clinical stage I) is a set of effects of nall potential activators of inflammation, often bacterial nature. Not nsurprisingly, the combination effects of peripheral oxygen utilization and nhumble blood pressure leads to severe laktatatsidoza. Patients with septic nshock really (Stage With SIRS) require aggressive and rapid treatment.
Phase D is preterminalnoyu stage of SIRS. Available nhypodynamic circulation with low cardiac output, which seemingly caused by self nvasoconstrictor effect. Systemic vascular resistance increased sharply above nthe norm. Stage D, perhaps, is the superimposition of heart failure expressed nSIRS. The total oxygen consumption extremely low utilization due to violatioof the periphery, inadequate cardiac output and peripheral vasoconstriction. nLactate concentration significantly increased. Death at this stage likely imost patients.
It is important to recognize this syndrome in the nearly, early stages of development when there is only 2-3 signs in order to ndetermine the cause of its origin, to take measures to stop its progress and nprescribe adequate treatment to the development of severe systemic dysfunctioof organs and systems.
Markers of sepsis. As soon as identified mediators of sepsis, there were proposals to use nsome of them as markers of sepsis. Raising the level of many cytokines, nincluding tumor necrosis factor, interleukin – 6 -8, -10, indeed observed imany septic patients and some of them are associated with a poor outcome. Ofteused as a marker of sepsis IL-6. However, increased cytokines varies and, iaddition, there may be other conditions that cause an inflammatory response.
Among other biological markers known and widely used C n- reactive protein. This acute phase protein, increased in parallel vmistyakoho ngrowth cytokines. Several authors considers this figure as sensitive for ninfections than the number of white blood cells or temperature.
Prokaltsytonin, the precursor of calcitonin, is also noffered as a marker of sepsis. Origin and its function in sepsis are not clear, nbut the level rises several hundred times in patients with severe sepsis and nits use to differentiate infection from other causes of inflammation, as well nas a marker of severity of infection. Potential markers of sepsis include nneopterin, elastase, phospholipase-2.
The syndrome of systemic reactions may last only a few ndays at a favorable course of the disease, but can exist for a longer time. nSymptoms can go gradually to decline, in these cases the danger of ncomplications decreases sharply and you can expect to recover. In severe nsyndrome (3-4 signs and more) excessive production of cytokines and other nmediators of inflammation may disrupt immunological control the development of ninflammation. Pro-and anti-inflammatory mediators may reinforce each other, ncreating a growing immunological dissonance. There is a direct correlatiobetween the content tsytokinivv blood and severity of the syndrome and its ncomplications.
Conciliation Commission U.S. physicians defines sepsis nas very vazhkuformu SIRS in patients with primary site of infection, confirmed nby blood cultures. T and Blackwell et al. (1996) define sepsis as clinical nsigns and symptoms that occur as a result of excessive systemic inflammatory nresponse to the introduction of infection. However, in the 20 – 30% of patients nzsepsysom blood cultures may be negative. Perhaps this is due to insufficient npersistent search bakteriyemiyi or defects in the transportation and ncultivation made by the material. If the source of infection and severe SIRS nblood for culture should be taken at least 3 times a day, and in severe cases – nvprodovzh3 – 7 days. With this persistent search bakteriyemiyi it can be ndetected in sepsis more often.
Do not forget about the possibility of translocatioof intestinal bacteria in the blood. In such cases, the intestine is the source nof infection, which is not considered when searching for the cause of nbacteremia. Translocation of bacteria and endotoxin in the bloodstream becomes npossible with violating the barrier function of the intestinal mucosa because nof ischemia of its walls with peritonitis, acute intestinal obstruction, shock nand other factors. Under these conditions, the intestine becomes like “undrenaging npurulent cavity.” According to A. Pollock (1996), sepsis and septic shock ncan occur without infection or after the elimination of infection with nantibiotics. The mechanism responsible for this phenomenon carefully studied, nbut still caot determine when infection sepsis becomes noninfectious SIRS. nWe only know that they are the same frequency deaths. MI Kuzin (2000) nrepeatedly observed patients successfully cured of widespread purulent nperitonitis but died of sepsis (peritonitis at autopsy evidence they were nfound).
For the doctor nis important to identify early symptoms of sepsis according to the criteria of nthe conciliation conference.
Fever – the most common clinical finding in sepsis and nit is main symptom for the diagnosis of sepsis. Increase body temperature due nto the influence of pyrogenic cytokines, including interleukin-1 (direct and nindirect, especially prostaglandin E2) in the hypothalamus, although other nendogenous molecules may lead to the development of hyperthermia. By itself, nthe fever can be a favorable sign, judging by the results of the disease: nhigher mortality noted in the absence of feverish reactions in patients with nsepsis. The difference in mortality forces show evidence to prescribing, nlowering the temperature in sepsis.
In sepsis, and, rarely, with SIRS, often in elderly npatients with disorders of thermoregulation, hypothermia can occur.
Respiratory disorders in the early stages of sepsis noccur hyperventilation, which leads to respiratory alkalosis and respiratory nmuscle fatigue.
Dysfunction of the cardiovascular system can carry ndiverse nature. In the initial stage there is a decrease in peripheral vascular nresistance and hypotension on the increase in cardiac output. Further, under nreduced vascular resistance, although it can occur and peripheral spasm, ndecreased cardiac output and blood pressure remains low.
In the later stages of sepsis associated failure nfunctioyrokz azotemia and oliguria, when liver damage occurs nhyperbilirubinemia, the syndrome of disseminated intravascular coagulation. It nis also possible central nervous system dysfunction in violation of nconsciousness (disorientation, agitation, psychosis). In typical cases, the nsymptoms associated with the presence of the primary source of infection, nalthough the systemic inflammatory response center caot be determined. With nthe progress of pathological states show signs of failure, such as nhyperlactatemia, hypoxemia, oliguria, impaired consciousness. In laboratory nstudies revealed leukocytosis or leukopenia, thrombocytopenia and reduction of nother factors in the blood hemostasis.
Coordinated concept of sepsis requires a systems nassessment of severity of the patients, which will give the ability to nobjectively assess the severity of the patients, the effectiveness of the ntherapy, to predict the level of mortality and length of intensive care.
The systems proposed for assessing the severity of the patients can be ndivided into 3 groups:
♦ methods based on the collection of objective clinical and nlaboratory 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 nnumber and complexity of research methods and treatment necessary for its nmaintenance – the system TISS.
Studies have shown statistical significance and the importance of these nsystems and no significant difference in criteria such as sensitivity, nspecificity, and overall correctness of the method.
METHODS OF INTENSIVE CARE
Most of the patients with sepsis requires prompt readjustment npurulent-inflammatory foci, which lays the foundation for the effect of nintensive therapy. All methods of intensive therapy used in the treatment of nsepsis, the degree of priority can be classified into two groups:
• methods, efficacy demonstrated broad clinical practice (the preferred nmethod);
• methods, which use appropriate from the standpoint of pathogenesis, nbut their effectiveness is not recognized or proven only experimentally n(Supplementary Methods).
This separation is useful from a practical point of view, because it nallows to concentrate efforts on the most important areas of treatment, without nthe realization that you caot count on the effect of the other, especially nin terms of time and shortage of medicines.
Tab. Treatment of patients with severe SIRS and septic shock.
|
Control of septic focus |
Includes resection, plikatsiyu, eksteryryzatsyya firmware or perforation of hollow organs, drainage and necrosectomy iecrotizing 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 maintai 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- |
|
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 i this case you need to use vazodylyatatorov due to the pronounced increase i afterload due to peripheral vascular spasm. |
|
kidneys |
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. |
n
Primary methods of intensive care
Antibiotic ntherapy (ABT)
Despite the emergence of new, fundamental understanding nof the nature and systemic organ damage in sepsis, antibiotics continue to play na critical role in treatment.
Selection of ABT “first day” (before the nresults of bacteriological examination) is dependent on the location of the nsource of infection on the basis of known options domination of microorganisms nand their sensitivity to antibiotics, and the severity of the immune status of nthe patient, pharmacokinetics, potential side effects and cost.
TERMS nABT sepsis:
1. For empirical antibiotic ABT choose a nwide range of bactericidal action type or combination of drugs that have nactivity against potentially possible in this clinical situation pathogens.
The lack of protection mechanisms antiinfection sepsis nrequires reaching perhaps more complete eradication of microorganisms and thus nantibiotic with bactericidal action type (b-lactams, aminoglycosides, nfluoroquinolones).
In recent years, increased the number of observations nthat show high efficacy of monotherapy of severe sepsis carbapenems (imipenem, meropenem). nThis fact is connected with ultra range of products, low-acquired resistance, nthe ability to use in patients with multiple organ dysfunction.
Prediction result of septic process is largely ndetermined by the severity of homeostatic disorders before treatment. There is na direct correlation between the number of organ dysfunction syndrome severity nand probability pon fatal. For example, in sepsis with MOF 2-3 systems, septic nshock, mortality ranges from 35 to 75%. In this regard, the choice of optimal nstarting circuit ABT should be carried out taking into account the risk of ndeath: the higher the likelihood of an unfavorable outcome, the greater are the narguments in favor of the appointment of agents with the highest activity and nlowest ability to increase the content of endotoxin in the blood. In these ncategories of patients justifiably use carbapenems as the primary scheme ABT. nSimilar tactics are justified and in postoperative abdominal sepsis.
Dyskutabelnym remains the question of the admissibility nof monotherapy with carbapenems Escherichia infection. Perhaps this should be ndiscussed on a case-by-case basis, based on the severity of the patient’s level nof resistance of microorganisms. In severe angiogenic sepsis associated with ncentral venous catheterization when there is a high risk of the presence of nstaphylococci metytsylinorezystentnyh should begin therapy with vancomycin.
2. Intravenous route of administration of nantimicrobial agents is mandatory in patients with sepsis.
3. Selection of dose and multiplicity of nadministration depend on the type and availability of bactericidal antibiotic neffect and sensitivity of microorganisms.
Before antibiotics are bactericidal concentratiodependent, include aminoglycosides and fluoroquinolones. Therefore, they should nbe given the maximum allowable dose for a particular patient. For naminoglycoside antibiotic characterized by a long effect. In this regard, nrational bolus aminoglycosides, which creates a short-term high concentrations nof drug in the blood and tissues.
Detection of antibiotic in the aminoglycoside nantibiotics led to a number of one-time (1 per day) entering all the daily dose nof gentamicin, netilmicin, amikacin. Results of multicenter studies demonstrate nat least as clinical efficacy and reduced toxicity. However, you need to very nthorough approach to calculating creatinine clearance, especially in syndrome nMOF.
Bactericidal b-lactams time-dependent effects. nIncreasing concentrations not accompanied by accelerated destruction of nmicrobes. It is believed that one should strive to maintain a constant nconcentration of the IPC, which exceed in 2-5 times. To use this dosing ninfusion device. Precisely the pharmacodynamics b-lactams in many clinical nsituations do not apply to the maximum dose.
Yes, there were conclusive studies that demonstrate nthe same clinical efficacy medium (1.5-
4. After clarifying the nature of the nmicroflora and its sensitivity if necessary, make adjustments to treatment: a ntransition to monotherapy, narrower spectrum drugs or less expensive (eg, noxacillin instead of vancomycin in detecting metytsylinochutlyvoho S. aureus).
In most situations, except for infective endocarditis nshould not be long-term (> 7 days) used aminoglycosides. The use of ngentamicin as a component of combination empirically ABT possible only with ncommunity-acquired sepsis origin. With hospital infections preferred amikacior netilmicin.
Infusiotherapy
Fluid therapy in sepsis promotes restoration of nadequate tissue perfusion, correction of homeostatic disorders, reducing the nconcentration of toxic substances and mediators of septic cascade.
Heart failure is the reason for adding dobutamine ninfusion 5-7,5 mg / kg / min dopamine or 5.10 CIM / kg / mhv. With the ndevelopment of septic shock choice sympathomimetics determined by specific nhemodynamic situation.
All infusion environments have both their advantages nand disadvantages. Given those that have to date, there is no reason to prefer nany of infusion medium.
Respiratory nSupport
Adequate and timely respiratory support – one of the nhighlights of the treatment of sepsis. In recent years, along with well-knowarguments in its favor (support oxygen transport, reducing the work of nbreathing) was obtained by another: in hypoxic conditions dramatically nincreases the reaction rate of septic cascade.
Restoratioof organ and tissue perfusion
Restoration of adequate tissue and organ perfusion may ncontribute to the use of low molecular weight dextran plasma substitutes from nstarch, heparin 10-20 ths. / D / v, dopamine 0.5-3 mcg / kg / min, dobutamine n2.5-5 mg / kg / min and others.
Nutritional nsupport
The development of sepsis syndrome pon usually accompanied nby manifestations hipermetabolizmu. In this situation, covering energy demand nis due to destruction of their cellular structures (autokanibalizm), which nexacerbates existing organ dysfunction and enhances endotoxemia. Because of nartificial nutritional support is a very important component of treatment.
The optimal value of the daily calorie – 40-50 kcal / nkg. Emphasis should be put on enteral nutrition special blends (Izokal, nNutrilan, Nutrizon et al.). These mixes are balanced by major nutritional components, nhigh-calorie containing supplements of trace elements and vitamins. In enteral npath must be brought to 80% kalorazh entered.
Correctioof immune disorders
In severe sepsis, there is the development of nsecondary immunodeficiency. His appearance is most typical for surgical ninfection. Extensive festering wounds with high bacterial invasion leads to nintensive use of factors of cellular and humoral immunity. The basic principle nimunokorektsiyipry sepsis – filling in the missing parts of the immune defense. nHowever, its adequacy in surgical sepsis, primarily depends on the radical nreorganization of purulent lesions. In the acute phase of pathological process nshown passive (replacement) therapy immunoglobulins intended for intravenous nadministration: intraglobin (IGG) 2-5 ml / kg for 2-3 days pentahlobin (IGG and nIGM), 5 ml / kg / day three times.
Additional nmethods of intensive care
Extracorporeal ndetoxification
After performing a radical reorganization foci of ninfection, elimination of hypovolemia, recovery of peripheral microcirculation, neliminate hypoxia ensure optimum ABT, caloric support, immunotherapy and in the nabsence of gross disturbances in the hemostatic system in the treatment of nsepsis with MOF can be used extracorporeal detoxification methods: nhemofiltration and plasmapheresis.
Glucocorticoids
Glucocorticoids are used in the treatment of septic nshock, since the 50-ies. But in 1987 after the publication of the results of ntwo multicenter studies concerning evaluation of the application of npharmacological doses of methylprednisolone (30 mg / kg or more), much of the nresuscitation of using glucocorticoids refused. Their effectiveness could prove nonly with meningococcal.
In deciphering the mechanisms controlling the nsynthesis and secretion of cytokines new arguments in favor of their use, but nin very moderate doses of 60-120 mg prednisone or hydrocortisone 200 mg per nday.
Inhibitors of free radicals
Their purpose is shown in sepsis through activatioprocesses of free radical oxidation and the development of an imbalance in the nlipid peroxidation, which increases structural organ damage. The most dramatic nincrease in the rate of free radical oxidation observed in sepsis, combined nwith respiratory distress syndrome. To increase the antioxidant capacity of the npossible use of vitamin C, tocopherol.
