1.1. Periostitis of jaw bones
Periostitis is an inflammatory process with focus of inflammation in the periosteum. Causes of the disease - teeth with chronic foci of inflammation in a pulp or periodontal, the suppuration of an odontogenic inflammatory cyst, difficult to teething both temporary and constant teeth, injury. According to the clinical flow and the pathological picture, the periostitis of acute (serous and munning) and chronic (simple and precisitive) are distinguished.
Acute serous periostitisit is manifested by the smoothness of the transitional fold, pronounced soreness during palpation. The mucous membrane over the inflamed periosity of the hyper-mirovan, edema. The process is localized in the area of \u200b\u200b"causal" tooth and one or two neighboring teeth, manifests itself more often from the vestibular surface of the alveolar process. In the adjacent soft tissues, peripocal changes in the form of collateral edema are noted.
For acute purulent periostitethe swelling of the transitional fold is determined by the formation of a substitute abscess, the symptom of fluctuations (in the destruction of the periosteum and the propagation of pus under the mucous membrane), the pathological mobility of the "causal" tooth. In the surrounding focus of inflammation of soft tissues, perifocal swelling is expressed, in the location of direct contact with the subperiodal-nym abscess, inflammatory infiltration of soft tissues with hyperemia of the skin is observed.
For chronic periostitethere is an increase in the bone due to the imposition of an excess of a young bone on the surface of the jaw in the form of layers with varying degrees of OSSI
fiking. The focus of chronic infection in the bone, injury is the source of additional pathological irritation of the periosteum, which in children and so is in a state of physiological irritation. With a simple chronic periphet, the newly formed bone after adequate treatment is subjected to reverse development, with a precipitating - the ossification of the bone is developing in the early stages and ends, as a rule, a hypero-stose. On radiographs of the lower jaw, a young bone tissue is determined in the form of a gentle strip outside the cortical bone layer. In the later stages of the disease, the latitude of the newly built bone is clearly pronounced. With an x-ray study of the upper jaw, it is rarely obtained a clear picture that helps the diagnosis.
1.2. Odontogenic osteomyelitis
Jewish bones
Acute osteomyelitis of jaw bones.Depending on the path of penetration of infection into the bone and the mechanism of development of the process, three forms of osteomyelitis of facial bones are distinguished: odontogenic, hematogenic and traumatic. Odontogenic osteomyelitis occurs in 80% of all cases, hematogenous - in 9%, traumatic - at 11%. In children under 3 years old (more often in the first year of life), it develops mainly hematogenous osteomyelitis, from 3 to 12 years - in 84% of odontogenic cases. The following forms of the disease are distinguished: acute osteomyelitis and chronic, divided depending on the clinical and radiological picture on 3 forms: destructive destructive and productive and productive.
Acute osteomyelitis- purulent infectious-inflammatory disease of the jaw bone (all of its structural components), accompanied by a bone lysis by purulent exudate, impaired its trophic and leading to osteonosis. For the clinic of acute osteomyelitis, general symptoms are manifest. The disease begins acutely, with lifting body temperature up to 38-39 ° C, accompanied by chills, general weakness, ailment. In children of younger and pubertal age, cramps, vomiting and disorder of the gastrointestinal tract function may appear when lifting the body temperature, which indicates the irritation of the CNS as a result of high general intoxication of the body. In odontogenic etiology, the disease is characterized by a spilled inflammation around the causal tooth, there is a pathological mobility of it and intact intact teeth. From the gum pockets may be released, subperiodal abscesses are formed, which, as a rule, are localized from both sides of the alveolar process and the jaw bone. Osteomyelitis is accompanied by severe inflammatory changes in soft fabrics of the face, inflammatory infiltration with hyperemia and skin swelling develops in the adjacent tissues. Regional lymphadenitis is always present. For acute osteomyelitis, the formation of abscesses or phlegmon is characterized, adenoflems are more often developed. In advanced cases, more older children, acute odontogenic osteomyelitis is complicated by the near-oolel phlegmon.
X-ray study in the first days of the disease does not identify signs of changes in jaw bones. By the end of the week there appears a spilled dice, which indicates its melting of purulent exudate. The bone becomes more transparent, the trabecular pattern disappears, it is thinned and the cortical layer is interrupted.
Acute odontogenic osteomyelitis of the upper jaw significantly becomes a chronic course compared with the processes in the lower jaw, since the anatomy-physiological features of its structure contribute to the rapid breakthrough of abscesses and the relief of the osteomyelitic process.
Chronic osteomyelitis- purulent or proliferative inflammation of bone tissue, characterized by the formation of sequesters or lack of trend towards recovery
and increasing destructive and productive changes in the bone and periosite. In case of chronic odontogenic osteomyelitis of jaw bones, the routines are involved in the process of constant teeth, which "behave" as sequesters and support inflammation. Depending on the severity of the processes of death or constructing a bone substance, three clinical and radiographic forms of chronic osteomyelitis are isolated: destructive, destructive and productive, productive. The lower jaw in children is amazed by odontogenic osteomyelitis much more often than the top.
Chronic forms of odontogenic osteomyelitis are most often the outcome of acute odontogenic osteomyelitis, and the chronization of the process in children occurs in a shorter period of time than in adults (to interpret the process as chronic in children already on the 3-4th week from the beginning of the disease). However, chronic osteomyelitis can develop without prior to a clinically pronounced acute stage, which determined its name as the primary-chronic (productive form of chronic odontogenic osteomyelitis).
Destructive shape of chronic osteomyelitisit is observed in children of younger, depleted, weakened by a common infectious disease, i.e. with reduced organism immuno-resistance. The symptoms of acute inflammation subsided, but the symptoms of general intoxication of the body remain pronounced and accompanied the entire period of the disease. Lymphatic nodes remain enlarged and painful. Internal and / or external fistulas with purulent separated and sputtering granulations appear. The delay in the outflow of the exudate can cause an aggravation of inflammation (the clinic of which is similar to acute osteomyelitis). At radiological examination, the areas of resorption of spongy and cortical substances are determined. The fracture of the bone leaks quickly and diffuse. The final boundaries of the lesion are set in a later date: by the end of the 2nd - the beginning of the 3rd month from the beginning of the disease. The destructive form is accompanied by the formation of large, total sequesters, pathological fractures. Periosal bone constructing in all stages of destructive form is expressed slightly, the endoral construction is radiologically not determined.
Destructive and productive form of chronic odontogenic osteomyelitisit is observed in children of 7-12 years old and is the most frequent outcome of acute odontogenic osteomyelitis. The clinic is similar to the clinic of the destructive form of chronic osteomyelitis. With a radiographic study, small foci of bone praises are determined, the formation of a plurality of small sequesters. In the periosite there is an active construction of a bone substance, which is determined on radiographs in the form (often layered) of the bone. Signs of endostal bone restructuring appear in a later date - the decrees are alternate with the areas of osteosclerosis, and the bone acquires a coarse drawing.
Productive (primary-chronic) form of odontogenic osteomyelitisit develops only in children and youthful age, it is more likely to have 12-15 years old. Of great importance in the occurrence of primary chronic forms have the body sensitization, reduction of its protective properties. The irrational use of antibiotics (small doses, short courses) is played, incorrect tactics of pulpitis and periodontitis treatment, etc. Since the beginning of the disease prior to its manifestation is held for a long time (4-6 months), the diagnosis is very difficult. In the oral cavity, there may be no "causal" temporary teeth, and peri-koronites (the frequent cause of the defeat) to the beginning of the process are already completed by the rubber of intact teeth. Usually productive (hyperplastic) osteomyelitis occurs unnoticed for the patient. Classic signs of osteomyelitis - fistula and sequesters - no. In a separate section of the jaw, strain appears, slightly painful when palpation. The deformation increases slowly and with time can spread to several jaw departments. The process can last for years and is accompanied by frequent (up to 6-8 times a year) exacerbations. During the period of exacerbation, infiltrates surrounding soft tissues, triumism, may appear. During the exacerbation period, regional lymph nodes are also increased, painful during palpation, but periathenites, abscesses and occasional phlegmons are rarely developed.
The radiographic picture is characterized by an increase in the volume of jaws due to the pronounced endosteal and periosal co-steering. The sequesters are not defined.
In the affected area, the alternation of foci of praise with fuzzy boundaries and osteosclerosis zones is noted. The bone acquires a motley, booby, so-called marble pattern. The cortical layer is not viewed and, depending on the prescription of the disease, it is merged with the precisted periosal layers, which are most often longitudinal lamination. For this form of osteomyelitis, the retrograde infection of the in-clock teeth is characterized in the lesion focus (ascending pulpits and periodontitis).
1.3. Hematogenous osteomyelitis
Jewish bones
Hematogenous osteomyelitis of the bone of the person in children is developing against the background of the septic state of the body and is one of the forms of septicopemia arising against the background of low resistance. The source of infection can be inflammatory diseases of the umbilical umbilical bodies, carpentry lesions of the child's skin, inflammatory complications of the postpartum period of the mother (mastitis, etc.). This disease is found in newborns and children of 1 month of life (77.4%), aged 1-3 years (15.2%) and from 3 to 12 years (7.36%) (Roginsky V.V., 1998) .
The hematogenous osteomyelitis of the facial bones is more often localized in the zilly and nose bones, the outer jaw is affected by zilly and abnormal processes, on the bottom - the mumane process.
In the acute phase of the disease, regardless of the localization of the primary focus of the defeat, the newborn and breast-age children develop an extremely difficult general condition and the most expressed general intoxication of the body. Despite the timely starting and actively conducted therapy, new purulent foci in various bones of the skeleton or other organs. With severe forms of the disease, bone defeat is accompanied by the development of phlegm. Many children have a disease accompanied by septic pneumonia. After the surgical opening of uluses or the formation of fistula, the overall condition of the child is not improved immediately. With intensive therapy, the threat to life disappears by the end of the 3-4th week from the beginning of the disease.
In the acute stage, the cure is possible in a few children. More often hematogenous osteomy
lita goes into a chronic form and proceeds with the formation of extensive sequesters, including the deceased incarnations of teeth. Recovery processes in the bone of weakly-fell.
Exodes depend on the clinical form of hematogenous osteomyelitis and the deadlines for the start of rational therapy. After transferred chronic hematogenous osteomyelitis, children remain defects and deformations of jaws associated with their underdevelopment or vast sequestration of bones. With osteomyelitis, the lower jaw is formed a defect or underdevelopment of a mumane process with a subsequent violation of the growth of the entire lower jaw or the development of primary-bone lesions of the ENCH (see ch. 4.1).
1.4. Lymphadenit
One of the first places in frequency among inflammatory processes occupies lymphadenitis.Lymphadenites in the maxillofacial region in children are extremely rarely primary diseases. They accompany odontogenic, hundred-coogenic diseases, diseases of ENT-organs, ORZ, ARVI, children's infectious diseases and in these cases are considered as one of the symptoms of the underlying disease. Lymphadenitis can be caused by supercooling, injury, planned vaccination.
The clinical flow is distinguished by acute lymphadenitis (serous, in the periathenitis, purulent) and chronic (hyperplastic, in the aggravation stage).
Acute serous lymphadenitisstudently with a pronounced general reaction and local symptoms. Increases body temperature. Common signs of intoxication appear, stronger in young children (1-3 years). In the initial stage, local symptoms are characterized by a minor increase in lymph nodes, pain during palpation, the lymph node remains movable, dense, skin color is not changed. Then (2-3 days from the beginning of the disease) soft tissues are involved in the process, the inflammation extends beyond the limits of the lymph node capsule, which is interpreted as periatoenite. At the site of the lymph node, a dense, sharply painful infiltrate. Subsequently, the melting of the lymphatic node occurs
purulent exudate, which is clinically manifested by a softening with a symptom of fluctuations (acute purulent lymphadenitis). The lymphatic nodes of the side surface of the neck, the libochiness and nearby regions are affected more often.
Chronic hyperplastic lymphadenitisit is characterized by an increase in the lymphatic assembly - it is dense, movable, not connected with the surrounding fabrics, painless or light-oracked during palpation. More often the ethiology of this form of the Lymphajenitis is not uncommon-naya. In these cases, several regional lymph nodes are palpable.
Chronic abscessive lymphadenitisit is characterized by the appearance of the focus of hyperemia and skin thinning over an increased lymph node, palpatorically determined by the symptom of fluctuations, indicating the purulent melting of the node. The spontaneous opening of the abscess with the formation of a fistula is possible. The general condition of children in chronic formats of lymphadenitis does not change.
1.5. ABSCESS
Abscess- The focus of the accumulation of pus, resulting from the melting of the tissues to form the cavity in soft tissues. The abscess in the field of the face occurs due to damage or inflammation of the skin of the face, the mucous membrane of the oral cavity, lips, nose, eyelids. Less often abscesses in children arise due to the spread of infection from an odontogenic focus. The applened abscess represents a sputtering, domed, brightly hyperemic plot. Leather over it is thinned. Palpation is sharply painful, fluctuation is easily detected. The general condition is violated slightly. The abscesses located in the depths of the fabrics are more seriously proceeding, is obscalogling, paratrozillary, hatchable space, language. They are accompanied by pronounced intoxication, violation of the chewing, swallowing, breathing, triumph. In the focus of inflammation, infiltrate is formed, in the area of \u200b\u200bwhich the skin or mucosa is a hyper-mugged, tense. In the center of the infiltrate is determined by fluctuation. The boundaries of the altered tissues are clearly defined. Often, the skin or the mucous membrane in the abscess area sputs above the surface.
1.6. PHLEGMON
1.7. FURUNCLE
Phlegmon- acute purulent spilled inflammation of subcutaneous, intermushkin and interfaces-allen loose fatty fiber. In childhood of phlegmon, it is often developing as a complication of acute purulent lymphadenitis (ADE-Noflemmon) or accompanies odontogenic osteomyelitis (osteophmon). Adenoflemmon is observed in children from the very early age - from 2 months and older. The most frequent localization of the adenoflemmon - peel, over- and sub-mandibular, less often - the pre-arms and the near-wing-chewing area. The source of infection can serve as teeth, LOR-organs, traumatic damage, including post-reliections, due to violation of the aseptic rules. At phlegmon, there is an increase in the level of intoxication of the body in combination with a pronounced local symptomatomy - is determined by a spilled inflammatory infiltration propagating into several anatomical regions. In the center of inflammatory infiltrate, the foci of softening with fluctuation is determined. The skin of the affected area becomes a dense, tense, hyperemic bath. The speed of development of phlegmon in children contribute to the weak bond of dermis with the basal membrane and subcutaneous fat layer, good blood supply. These are the main causes of the development of purulent-necrotic processes of spilled nature in children. Immaturity of immunity also contributes to the development of inflammation and prevents the restriction of the focus.
Osteophmonit aggravates the course of acute odontogenic osteomyelitis and sharply enhances the general intoxication of the body. With osteo-phlegmon, the spread of the purulent inflammatory process occurs as a result of the melting of the periosteum and the breakthrough of purulent exudate into soft tissues.
In newborns and breast-age children, the formidable complication of hematogenous osteomyelitis of the upper jaw is the formation of phlegmons in the cavity of the orcap or retrobulbar space. With acute odontogenic osteomyelitis, surface phlegmon develops more often. Flegmons of deep intertensive spaces in childhood are rarely found (with long non-accomplished bone processes).
Furuncle- acute purulent-necrotic inflammation of the hair folnation and associated with it of a rider with its surrounding fiber, due to glorodic microbes - staphylococci. The development of a furuncle is promoted by skin injury with subsequent infection. The predisposing factors are the strengthened activity of sweat and sebaceous glands of the skin, vitamin failure, metabolic disorders, imminent immunity. The furuncle may occur on any skin area where hair has, more often in the neck, lips and wings of the nose.
The development of a furuncule begins with the appearance of a dense painful infiltrate with a diameter of 0.5-2 cm of bright red, towering over the skin in the form of a small cone. With a favorable course for the 3-4th day in the center, it is formed by a focus of softening, which can independently reveal with the advent of Mouth. At the point of autopsy, a section of necrotic cloth of greenish color is detected - the furuncular rod. In the future, along with the pus and blood, the rod is brazed. The defect of the skin tissues is replaced by granulations. After 2-3 days, healing comes to form a scar. With an uncomplicated current cycle, the furuncule development continues 8-10 days.
The furuncle in the field of lips and the wings of the nose, as a rule, is hard. Inflammatory edema extends to the surrounding fabrics. There is a strong irradiating pain. The body temperature is high. There is a possibility of developing such severe complications such as meningitis, mediovenitis, sepsis, so the treatment of children with furunculars of the person should be carried out in the hospital.
In weakened children, the disease can flow sluggishly, with a weak inflammatory response, and with excessive accumulation of pus, the melting of the necrotic rod may occur and the abscess (abscessive furuncle) may occur.
1.8. Inflammatory diseases of the salivary glands
1.8.1. Farm newborns
The disease is rare. Ethiology and pathogenesis of the disease are not sufficiently studied. It develops more often in premature or weakened children with concomitant somatic pathology. The reason for the development of the vapor can be the introduction of infection through the withdrawal duct of the salivary gland or hematogenic.
The disease develops sharply, more often at the 1st week of the child's life. It begins with the appearance of dense spilled inflammatory infiltrates of one or two parothes-chewing regions, is accompanied by a pronounced general intoxication of the body. After 2-3 days, purulent or purulent-necrotic melts of the gland occurs. It is possible to propagate in the region of the temporomandibular joint, which can lead to the death of growth zones on the lower jaw and as a result - to the ankylosis of the NEXC, underdevelopment of the lower jaw.
Anamnesis;
Palpation;
Radiography of facial bones;
Ultrasound research;
Blood tests and urine.
Farming newborn differentiates with:
Adenoflemonia.
1.8.2. PAROTITIS
The causative agent of epidemic vapotitis is the filtering virus Pneumophilus parotidis.The vapor virus is quickly inactivated when exposed to high temperature, ultraviolet irradiation, weak solutions of formalin, lizola, alcohol. The source of infection is a sick person. Transmission of infection occurs with airborne droplets, as well as through contaminated salivary sick items (dishes, toys). The virus is found in saliva at the end of the incubation period (18-20 days) and in the first 3-5 days of the disease, as well as in the blood. Perhaps primary damage to the virus of the cerebral shells, eggs and pancreas.
The disease is more often manifested between the ages of 5 and 15 years. Even before the appearance of distinct clinical signs, an increased content of amylase in serum and diastases in the urine, disappearing only after the 10th day of the disease, can be detected. The beginning of the disease is characterized by an increase in body temperature up to 38-39 ° C and the appearance of the octopicity of the parole salivary gland with one or both sides. It is also possible to involve into the process of subband and lifting and sub-speaking salivary glands, with extensive edema of the cervical fiber. The skin over the inflamed glands is stressful, shiny, but usually keeps normal color. The appearance of the swelling of the parotid gland is accompanied by pains, irradia, towards the ear or neck, amplifying during chewing and swallowing. The swelling of the affected glands is the first 3-5 days increases, then to the 8-10th day begins to decrease. Sometimes the oscillating of infiltrate is delayed for several weeks. Occasionally, the disease is accompanied by bradycardia, changing tachycardia. Often an increase in the spleen. EFA indicator is usually increased. It is often observed a damage to the nervous system (meningitis, encephalitis), sometimes with paralysis of cranial and spinal nerves; Sometimes accompanied by mental disorders.
Frequently complicated is the orchitis. Oforite with epidemic vapotitis is less common. It is also described mastitis, accompanied by swelling and soreness of the mammary glands.
The diagnosis is made on the basis of:
Complaints;
Epidemiological anamnesis;
Clinical inspection (palpation of salivary glands, pancreas, genital organs);
Visual survey of saliva;
Uzi salivary glands.
Epidemic vapotitis should be differentiated from:
Various types of salyagenit;
Chronic nonspecific parotitis in the aggravation stage;
Infectious mononucleosis;
An abscess of the cheek region;
Lymphadenitis;
Hematogenous osteomyelitis;
Lymphangioma in the stage of inflammation;
Adenoflemonia.
1.8.3. Chronic parenchymal pairotitis
The etiology of the disease is not clarified.
The process is characterized by primary chronic principle and hidden by flowing inflammation in the parole salivary glands.
The disease is more often manifested in children 3-8 years. The peculiarity of chronic nonspecific parenchymal vapotitis is the duration of the flow. Exceitings can occur 6-8 times a year. It is characteristic of the deterioration of the overall state, the appearance of pain and swelling in the field of the parotid glands from one or two sides. The appearance of hyperemia and tension of the skin.
With palpation of the near-wing-chewing area, an increased, painful (weakly heated), dense, buggy iron is tested. In case of mass production of the area of \u200b\u200bthe variety of salivary duct, a viscous jelly-like saliva is released with an admixture of pus or fibrin bunches.
In the occasional radiological stage, the initial, clinically pronounced and late. In each of the stages, the period of exacerbation and remission is distinguished, as well as active and inactive flow. With the active flow of the process, the disease is distinguished by a pronounced inflammatory response of the BC. The duration of exacerbation with active flow ranges from 2-3 weeks to 2 months, the number of exacerbations varies from 4 to 8 times a year.
With an inactive flow, the exacerbation of chronic parenchymal vapotitis flows without the pronounced local and general symptoms of inflammation with a smaller number of exacerbations per year (from 1 to 3).
The diagnosis is made on the basis of the following data:
Complaints;
Anamnesis;
Clinical inspection, including palpation of salivary gland;
Visual study of the secrets of the salivary gland;
Clinical analysis of blood and urine;
X-ray studies of the AU with preliminary contrasting of gland ducts with water-soluble contrasting substances: verte, urographic, Omnipak (sialography, orthopantomy-graphic);
Research of purulent separated from salivary gland on sensitivity to antibiotics (during the exacerbation);
Cytological studies of smears of saliva and Penage of the ARC during the remission;
Ultrasound.
Chronic parenchymal vapotitis should be differentiated with epidemic vapor, lymphadenitis, specific lymphadenitis in the near-speech-chewing area, with chronic osteomyelitis of the lower jaw, lymphangioma and cysts in the near-tree region, neoplasms.
1.8.4. Cytomegaly
Cytomegalia is a viral disease that affects salivary glands predominantly newborn and infants under the age of 6 months. The causative agent is Cytomegalovirus Hominis (Cytomegalovirus Hominis), relating to the family of herpes viruses. Sources of infection: Virosters and patients. The virus is highlighted with saliva, breast milk. Cytomegalovirus can penetrate the placenta and cause intrauterine defeat of the fetus at any stage of its development. Infection in the first weeks of pregnancy can be the cause of spontaneous abortion or the formation of congenital defects (for example, lips and nose cleft). Infection in a later date can lead to damage to the central nervous system, liver, gastrointestinal tract. Future infection can happen when passing through the generic paths of an infected woman. The primary fixation site of the virus is salivary glands. Older glands are amazed more often than lifting glands and regional lymph nodes and regional lymph nodes.
In the salivary gland, the narrowing is determined and even the blockage of small salivary ducts by giant epithelial cells protruding in their lumen. In the kernel and the cytoplasm of these cells are distinctly notable inclusions. Such giant cells in cytomegaly are in saliva, urine and feces.
With the local course of cytomegaly, the salivary glands swell due to inflammation and the formation of small cyst. In generalized the course of the disease, light, kidneys, pancreas, brain and other organs may affect the pathological process. After transferred cytomegaly
children can occur congenital vices of heart and large vessels, skin angiomes, myocardits.
In childhood children, in rare cases, there is a lesion of the skin in the form of a large-perch peeling, a long-term existing diarmity or non-healing ulcer. In some cases, the disease can occur as sepsis.
The forecast was previously considered completely unfavorable. Currently, light shapes are diagnosed, proven virologically, with a favorable outcome.
The diagnosis is made on the basis of:
Parents' complaints;
Anamnesis;
Clinical inspection;
Clinical analysis of blood and urine;
PCR and serological diagnostics. CMV infection of salivary glands in children should be differentiated from:
Herpetic infection;
Fungal inflammation (actinomycosis, candidiasis);
Echinococcal infection;
HIV infection;
Hemolytic disease of newborns;
Toxoplasmolysis.
1.8.5. Slutnokamnaya diseases of the subband salivary glands in children
The mechanism for the formation of concrections is not fully found. In the occurrence of salivinal disease, a violation of calcium metabolism is of great importance, sometimes injury or foreign bodies in the outlines of the salivary glands are noted.
The main diagnostic symptom is the detection of the concrete, the pain that occurs when taking food associated with a violation of the outflow of saliva. Siiaodochitis and sialogenis are accompanying symptoms. Listed symptoms increase with the child's age.
The diagnosis is made on the basis of general clinical methods of surveys (complaints, anamnesis, inspection of the child, the palpation of the gland, the visual study of the secret, clinical analysis of blood and urine, the x-ray study of the subband salivary glands, ultrasound).
Slyunokamnaya disease of the puzzleless saline glands is differentiated from the retention of the pylon-free salivary gland, the hemangioma and lymphangioma of the sub-surround region, sialodochitis, with an abscess of the maxillo-tongue groove.
Fig. 1.1.Baby 3 years old. Aggravation of chronic Fig. 1.2.Baby 5 years. Exacerbation of chronic periodontitis tooth 84, acute periodontitis of the tooth 54, acute purulent purulent periostitis of the lower jaw on the right periostitis of the upper jaw on the right
Fig. 1.3.Increased panoramic radiograph of the lower jaw of the child is 9 years old. Chronic precision periostitis of the lower jaw on the right in the area of \u200b\u200bthe teeth 46, 47
Fig. 1.4.Baby 6 years old. The aggravation of chronic periodontitis of the tooth 64, acute serous periostitis of the upper jaw on the left
Fig. 1.5.Baby 5 years. The aggravation of chronic periodontitis of the tooth 75, acute serous periostitis of the lower jaw on the left
Fig. 1.6.Baby 6 years old. The aggravation of chronic periodontitis of the tooth 75, acute purulent periosteit of the lower jaw on the left: but -condition in the oral cavity; b.- orthopantomogram
Fig. 1.7.Child 13 years old. Chronic destructive productive osteomyelitis of the lower jaw on the right: but- the appearance of the child; b.- orthopantomogram. Definitions of bone tissue destruction in the field of branches, angle and body of the lower jaw on the right; in -view of the body of the lower jaw on the right at the stage of operation
Fig. 1.8.Child 13 years old. Chronic productive osteomyelitis of the lower jaw on the right. Illness of the disease is 6 months: but- the appearance of the child; b.- Overview radiograph of bones of the facial skeleton in direct projection
Fig. 1.9.Child 15 years old. Chronic productive osteomyelitis of the lower jaw on the left. The longitude of the disease is 2 years: orthopan-tomogram. Sesteosclerosis sites are noted due to a previously repeated inflammatory process without signs of sequestration. The cortical plate is not clearly traced. Characteristic marble dice
Fig. 1.10.Chronic destructive osteomyelitis of the lower jaw in the sequestration stage. Dental volumetric tomogram of a child of 16 years. The bone tissue of the lower jaw in the field of missing teeth is 45-48 has an inhomogeneous structure. In the projection of the missing tooth 46, the focus of the destruction of bone tissue of an irregular shape of up to 5.5 x 4.5 x 3.5 mm is determined, in the cavity of which is visualized by an additional seal of bone tissue (bone sequestrel). The cortical plate of the lower jaw in the area 46 is not traced all over. On the vestibular and gear surfaces of the lower jaw in the region 45-48, pronounced linear periosal layers are noted
Fig. 1.11.Chronic destructive productive osteomyelitis of the lower jaw. Dental volumetric tomogram of a child of 12 years. There is a change in the bone structure (against the background of osteosclerosis of the lower jaw on the right, multiple foci of degradation of various sizes and shapes are detected) and layered periosal layers
Fig. 1.12.Chronic destructive productive osteomyelitis of the lower jaw. Multispiral computer tomogram of a child of 17 years (a, b.- axial projection; in- 3D reconstruction). In the body of the lower jaw, multiple foci of bone destruction of 2.5 to 9.8 mm is visualized. In the pagan and vestibular surfaces, there are linear and fringe periosal layers, more expressed in the body of the lower jaw in the projection of missing teeth 36-46, there are areas of a sharp seal (from 173 to 769 units) of soft tissues, right up to their sightseeing
Fig. 1.13.Chronic destructive productive osteomyelitis of the lower and upper jaws. Multispiral computer tomograms of a child 9 years old: but- axial slice; b.- MPR in a coronary projection; in- MPR in a sagittal projection; g.- 3D reconstruction. The bone structure of the entire lower jaw, the upper jaw, the main bone, both zoomy bones and zicky arcs is pronounced due to the presence of solubular foci and focus of vacuum and osteosclerosis, with uneven, fuzzy contours, practically inconspicated from unchanged surrounding bone tissue, violating the integrity of the cortical plates . The volume of the above bones is increased (more in the lower jaw), the ratios are not changed. In both ENCH, the relations are not violated, the joint heads of the swollen, the integrity of the contours is broken by places. In the left maxillary sine and the lattice labyrinth cells, the soft content of the density is about 16. N.
Fig. 1.14.Child 4 years old. Acute serous lymphadenitis of the left subsidiary: but- the appearance of the child; b.- ultrasound, in-mode: lymphatic node reduced echo gene, bark is thickened; in- Ultrasound, CDC mode: strengthening the vascular pattern in the projection of the lemph node
Fig. 1.15.Ultrasound, CDC mode: a lymphatic unit of a rounded form, reduced echogenicity, inhomogeneous structure, by periphery - hypo echogenic rim (edema zone). Acute lymphadenitis in the stage of periatoenitis
Fig. 1.16.Baby 6 years old. Acute purulent lyumfajenitis of the right subband
Fig. 1.17.Baby 5 years. Acute purulent lymphadenitis of the left puzzle-luxury region
Fig. 1.18.Child 15 years old. Chronic hyperplastic lymphadenitis of the predatory region
Fig. 1.19.Child 1.5 years. Absoing lymphadenitis of the left subband after transferred by ORVI: but -appearance; b.- ultrasound, in mode: the echogenicity of the lymph node is reduced, the projection is determined by the liquid portion (abscess zone); in- Ultrasound, CDK mode: In the projection of the lymph node, the vascular drawing is marked, the abscess zone is avascular
Fig. 1.20.Absoing lyufajenitis with the right sub-luxury area with the development of adenoflems. Ultrasound, CDC mode: the capsule of the lymph node is intermittent, liquid areas are determined in the surrounding tissues
Fig. 1.21.Child 15 years old. Specific lymphadenitis (actinomyo-tichetic) of the right subsidiary
Fig. 1.22.Child 4 years old. The abscess of the left subsepsy region after the bite of an insect
Fig. 1.23.Baby 14 years old. Abscess side surface of the neck on the right: but- the appearance of the child; b.- ultrasound, in-mode: the zone of reduced echogenicity with uneven contours is determined, in the projection - liquid sections
Fig. 1.24.Baby 14 years old. Abscess lower lips: a, b -the appearance of the child; in- ultrasound, in mode: the formation of reduced echogenicity with the presence of a liquid section is determined
Fig. 1.25.Child 16 years old. Abscess of the right subsidiary
Fig. 1.26.Child 10 years old. Odontogenic phlegmon by the right subsidiary: a, b.- the appearance of the child; in- orthopantomogram
Fig. 1.27.Child is 7 years old. Furunculus of the left subagree
Fig. 1.28.Infiltrate of the left cheat area with abstract signs. Ultrasound, in-mode: the zone of reduced echogenicity is determined with the presence of a liquid sector
Fig. 1.29.Child 16 years old. Absoing furuncle with the right zilly region
Fig. 1.30.Baby 6 years old. Exacerbation of chronic parenchymal left-sided parotitis
Fig. 1.31.Child 13 years old. Aggravation of chronic left-sided parenchymal vapor
Fig. 1.32.Chronic left-sided parenchymal vapor, initial clinical and radiological stage. Orthopantomalogram baby 9 years
Fig. 1.33.Chronic bilateral parenchymal vapor, initial clinical radiological stage. Orthopantomalogram baby 6 years
Fig. 1.34.Chronic double-sided parenchymal vapotitis, pronounced clinical and radiological stage. Ortho-pantomosialogram baby 7 years
Fig. 1.35.Chronic right-sided parenchymal vapor, pronounced clinical and radiological stage. Orthopantomalogram baby 15 years
Fig. 1.36.Chronic bilateral nonspecific vapotitis, remission. Ultrasound, CDC mode: salivary iron is increased in sizes, reduced echogenicity with the presence of small cyst; Vascularization is not changed
Fig. 1.37.Chronic bilateral nonspecific vapotitis, aggravation. Ultrasound, CDC mode: in the projection of parenchyma gland vascularization is amplified.
Fig. 1.38.Slutnocameal disease of the left puzzle-luxury salivary gland. Radiograph of a child of 10 years (axial projection)
Fig. 1.39.Slyonokamnaya Disease of the right puzzle-luisny salivary gland. Radiograph of the child 11 years old (axial projection)
Fig. 1.40.Slutnocamean disease of the left subband salivary gland. Ultrasound, in-mode: Breast duct is extended, the consolidation is determined in it.
Fig. 1.41.Slyunokamnaya Disease of the right subband salivary gland. Sialiam child 8 years old. Determined by the expansion of the duct, the concretion in the mouth of the duct
Fig. 1.42.Slutnocamean disease of the left subband salivary gland. Multispiral computer tomogram of a child of 16 years (A - MPR in a sagittal projection; b.- axial projection; in- 30 reconstruction). In the soft tissues of the oral cavity along the gear surface of the lower jaw in the front of the front group of the teeth and in the angle region, the calculations are visualized with dimensions of 2.5 and 8.5 mm, with clear wavy circuits, 1826 density. N.
Of the patients incoming to dental hospitals, 42.2% are patients with inflammatory diseases of the maxillofacial region, among them - 29.1% of people over 60 years old. In recent years, along with increasing the number of dental patients, some of them also marks the weighting of the clinical course of these processes. The cause of the death of patients is heavy complications: mediastinite, sepsis, brain abscess.
The main reasons for an increase in inflammatory diseases are insufficient cavity care and its sanitation, untimely diagnostics and hospitalization of patients, their early extract from the hospital and the irrational use of antibacterial agents. The processes arising in the body as a result of its aging during inflammatory diseases of the maxillofacial region.
In the elderly and old people, the source of infection, which is the cause of the phlegmon of the maxillofacial region, is most often not periodontitis, but colds, infectious diseases and pathological seashest pockets with periodontitis. The beginning of the disease can be caused by an injury of the oral mucosa during food, cleaning teeth, their treatment and preparation for prosthetics. The appearance of phlegmon can also be preceded by an inflammatory process of the oral mucosa.
With increasing age, the patients decreases the immunological reactivity of the body, the inflammatory process flows sluggishly, with a slight increase in temperature. The wound, through the day after the opening, is usually covered with fibrinous raid, separated, as a rule, moderate, liquid. Cleansing the wound from necrotic tissues occurs slowly, and the emerging granulations are atrophic. Sometimes there are exacerbations of inflammatory phenomena, which is associated with the delay of purulent separated or with the exhaustion of compensatory capabilities of the patient's body. The poorly pronounced local tissue reaction with the overall serious condition of the patient is a sign of a reduced organism resistance in general. The forecast at the same time becomes dubious.
Clinic. In some patients, the disease begins violently, with a significant rise in temperature, fever, is accompanied by chills, insomnia. The purulent-inflammatory process quickly applies to neighboring cellulums and in vital organs.
Ondogenic inflammatory processes of soft fabrics of the face have their own characteristics that need to be taken into account when diagnosing and treatment, especially in senior patients.
1. The possibility of rapid propagation of a purulent-inflammatory process from the primary hearth to neighboring anatomical areas is one of the differences in odontogenic phlegmon and abscesses. The basis of this is the topographic-anatomical features of the face and neck, in particular, the presence in the maxillofacial region of a significant amount of chewing and mimic muscles, a well-developed network of blood vessels, nerves, fat lumps Bisha. This creates the risk of penetration of the infectious-inflammatory process into neighboring anatomical areas, to the base of the skull, deep cellular spaces of the neck and mediastinum.
The propagation of pus occurs primarily within the limits of the interfassal space in which the hoping process originated. When making any wall of this formation, the process goes into adjacent cellular spaces. Often, in the odontogenic inflammatory processes of soft fabrics, the pus is spreading along the fiber located in interfascial and intermuscular spaces surrounding the vessels, nerves, salivary glands with their ducts, Kemki Bisha processes.
The spread of a purulent-inflammatory process to neighboring cellulum spaces, vital organs are accompanied by pronounced intoxication and the general response of the body. The patient's condition becomes heavy, pain in the field of wound increases, weakness increases, there is a bad sleep and appetite. For the purulent-inflammatory process of soft fabrics, the face is characterized by patenity of skin, anemia, elevated body temperature and other symptoms of intoxication.
In such cases, it is necessary to widely reveal the wound, reveal purulent chapels and "pockets", remove necrotized tissues, create conditions for permanent outflow of separated from the Russian Academy of Sciences.
2. Later, the appearance of fluctuations is one of the features of odontogenic phlegmon, which is associated with the localization of the pathological process of Knutri from powerful muscle formations (deep phlegmon of the temporal area, inflammation in the oss, picker, tidy and wonder-jaw areas, the day of the oral cavity). At the same time, a dense painful infiltrate is detected without clear boundaries and signs of fluctuations. The skin first the pale, movable, then hyperemia and swelling appear. This feature explains the need for an early opening of an ulcer. At the same time, a sleepless night is an absolute indication for surgery. The late opening of the inflammatory focus can lead to the spread of infection on the blood and lymphatic vessels.
Metastasation and formation of female foci occur mainly by hematogenic. The lymphogenic path of metastasis is also possible. Pi-demic foci is most often in the form of abscesses of various sizes, phlegmont infiltrates. CO The side of the internal organs during sepsis is found mainly severe degenerative-necrobiotic and inflammatory phenomena, swelling. In the elderly, the excretory function of the kidneys is most noticeable, as a result of which one of the most important links of the body's protective mechanism is disturbed - evacuation with urine toxins of bacteria and products of impaired metabolism of the inflammatory hearth. This circumstance largely determines the general condition of the patient and the course of the disease.
Sowing blood during sepsis na give growth, if a small amount is taken (up to 2 ml). Blood on the study must be taken at the moment of starting daily lifting temperature.
3. The proximity of vital organs (brain, upper respiratory tract, mediastinum, vision body) to the maxillofacial region leads to severe complications. At the same time, the inflammatory process extends from the focus of inflammation in various directions of lymphogenic and hematogenic means, by fascia and cellulum spaces.
According to the lymphatic vessels of the mandibular and maxillary nerves, the infection can be through the oval and round hole to penetrate the brain shell. The thrombophlebitis of the front facial, and then the angular and top of the orphanage also leads to the affix of the brain, and the phlegmon of the orbit occurs. The proximity of the larynx and the trachea causes the danger of asphyxia, which is significant at the phlegmon bottom of the oral cavity, neck, abscesses of the root of the tongue.
Mediastinites are developing as a result of the propagation of pus in the course of the vascular-nerve neck beam, as well as by the accumulatory and pretracy tissue. Mediastinites may occur lightning, to flow simultaneously with the phlegmon bottom of the oral cavity and neck, so the diagnosis is not always simple.
4. Anaerobic infection is often present in purulent-inflammatory foci of odontogenic etiology. Microorganisms represent a very extensive group, including both Kokkli and a wrecker flora. For their development, aerobic or anaerobic conditions are needed. The occurrence of the purulent process is based on the damaging effect of microorganism and compensatory priority reactions of the patient.
Along with staphylococci, streptococci, protemat, intestinal and blue sticks, in each third study, microflora are also determined by anaerobes: bacteroids, clostridia, anaerobic gram-positive coils, sticks. They are representatives of the normal microflora of a person. Anaerobes are on the mucous membranes of the oral cavity, sweat glands, lower intestinal deposits.
Bondnate anaerobes are very sensitive to oxygen. To their growth, a very low redox potential of the medium is needed: they can hardly stand out from clinical material. To a certain extent, the sterility of the point in the study of the pno from inflammatory foci indicates the presence of anaerobic infection.
The role of microflora as the etiological factor of the purulent-inflammatory process is very complex and cannot be reduced to the simple relationship of macroorganism with a microorganism. Often the simultaneous detection of aerobic and anaerobic flora with these processes is not accidental. The emergence of an anaerobic inflammatory process is prepared by aerobians, which penetrate the pathological center and "prepare the fabrics in a certain way" to develop an anaerobic purulent infection. In turn, the aerobic microflora present in the association and absorbing oxygen creates conditions for the growth of strict anaerobes and the development of anaerobic infection.
To influence the anaerobic infection, especially caused by bacteroids, the metronidazole and metragil are prescribed. From antibiotics, levomycetin, tetracycline, cefatoxins, which are used only in cases where traditional therapy is ineffective and the wound is covered with gray films.
5. Increased regenerative ability of facial tissues is due to good blood supply and innervation of the maxillofacial region, as well as the presence of low-differentiated cellular elements with high potency to regeneration. This may lead to the healing of the roughs of the oral mucosa in the earlier duration than the inflammatory process in soft tissues is fixed. Therefore, extensive cuts are expedient (with phlegmons at least 6 cm) with careful drainage.
6. Inflammatory contractures arise as a result of a reflex-painful reduction of chewing muscles or its defeat by an odontogenic inflammatory process. Inflammatory contractures are observed in odontogenic abscesses and phlegmons, which are localized in the field of muscles raising the lower jaw, and also noted with periostites, osteomyelitis of the lower jaw. A long-term inflammatory contracture as a result of destructive-degenerative processes in muscles leads to a scar contract. Inflammatory contractures make it difficult to inspect the oral cavity, the local diagnosis of the inflammatory process. In addition, chewing and swallowing functions are disturbed, which can lead to the depletion of patients. During the contract, you need a thorough special care for the oral cavity.
7. The need to special care for the oral cavity is determined by the fact that with the inflammatory process of the maxillofacial region, the process of self-purification of the oral cavity is broken. The character of microflora varies sharply due to the reproduction of concrete microbes, which causes the characteristic malicious smell. Care of the oral cavity patient performs independently or is carried out by medical personnel. The care of these events largely determines the result of patients treatment.
Treatment. As a result of a decrease in inflammatory and other reactions in patients with elderly and senile ages, indications of surgical interference with acute purulent inflammatory processes of soft fabrics and neck, HE should be waiting for the appearance of skin hyperemia above the focus of inflammation and fluctuations, since the purulent exudate can spread to neighboring areas. The indication to the opening of the inflammatory focus is palpatorically determined dense, sometimes painful infiltrate of soft tissues.
When choosing a type of anesthesia in elderly patients, not only reduced compensatory capabilities of respiration organs, blood circulation, endocrine apparatus, but also the fact that 70-80% of patients with this category are observed by concomitant diseases, often heavier than the main one. The cardiovascular system is most often suffering. It is often disturbed by coronary blood circulation, the reduction of the heart muscle is reduced, the minute volume of blood decreases. Frequently rises blood pressure. Pulse is usually cut.
As a result of atrophically, the respiratory surface of the lungs is reduced by about 25%. Due to the ossification of the rib cartilage and sclerotic changes, the lungs are fixed in the inspiratory position. In a state of rest, such a person is in equilibrium (heart rate and breathing in its norm), but a sufficiently small physical or nervous tension (excitement, excitement before the operation, etc.) and hypoxia can come, which will immediately affect the state of the heart muscle function.
When choosing an anesthetic method, the overall condition of the patient accompanying diseases and the amount of operational intervention is taken into account.
Sick elderly and senile ages need a systematic observation of the therapist, re-conducting ECG, blood tests and urine. Since the recovery of such patients is often delayed, the question of their fogging in the clinic must be solved in conjunction with the therapist.
Possible complications in acute odontogenic inflammatory processes of the maxillofacial region.
The complications of acute odontogenic inflammatory diseases include:
Mediastinit
Thrombophlebitis facial veins. Come sinus thrombosis.
Intracranial complications
A. Primary rhinogenic hydrocephalus
B. Basal Arachnoiditis
V. purulent meningitis
Meningoencephalitis
1. Mediastinit
The purulent mediastinite, as the complication of infectious-inflammatory processes of the maxillofacial region, is more often developing in patients with phlegmons of the ocular space (1), the root of the language (2), the bottom of the oral cavity (3), submandibular (4) and the presidential (5) regions. The spread of the infectious-inflammatory process to the cellular cell of the mediastinum from the occasional space, the root of the tongue occurs first in the translated space, and from there in the fiber along the pharynx and the esophagus - to the rear media. From the submarine, presidential areas, from the area of \u200b\u200bthe sleepy triangle, the infectious-inflammatory process spreads along the tissue down along the main vascular-nervous beam of the neck and then in the front mediastinum.
Clinical picturemediastinitis
The reason to suspect the patient with the phlegmon bottom of the oral cavity, the dissemination of the infectious inflammatory process into the mediastinum is:
the emergence of signs of the inflammatory process in the neck area, especially in the course of the vascular-nerve neck beam;
detection of the overall condition of the patient, despite the good drainage of purulent foci in the head and neck area (temperature to 39-40 o C, chills, tachycardia)
the emergence of clinical symptoms characteristic of the purulent-inflammatory process of this localization.
Characteristic symptoms of mediastinite
1. The appearance of inflammatory infiltration in the course of the main vascular-nerve bundle in the lower neck, in the test area, in the area of \u200b\u200bthe jugular depression.
2. The forced position of the patient: sitting with the head lowered, lying on the side with the legs pursed to the belly.
3. Sharply pronounced shortness of breath at rest (up to 45-50 respiratory movements per minute)
4. The tissue of the tissue of the jugular depression when inhaling (Symptom of Ravich-Shcherba).
5. Pain over the sternum or in the depths of the chest. Pains are intensified with deep breath, cough, swallowing, heading of the head (symptom of coin).
6. Characteristic muffling as a consequence of mucus hypersection due to irritation of the vagus nerve and disruption of the drainage of the bronchial tree due to the appearance / enhancement of pain during intensive coupling.
7. Pain in the depths of the chest at percussion of the sternum, deploying on the heels during the dispersed lower limbs.
8. The X-ray study reveals the expansion of the mediastinum, the effluent in the pleural cavity, and in the presence of a rotary-necrotic process caused by anaerobic infection, the presence of gas in the mediastinum and a paraharaseral fiber of the neck.
TREATMENT.
Opening of a purulent focus - mediastinotomy. The most often used by reasonable - through a cut along the front edge of the breast-curable-bed-like muscle, ranging from the level of the upper edge of the thyroid cartilage and 2-3 cm below the breast-clearable articulation. After opening is washed with furaciline and drain.
2. Thrombophlebitis facial veins. Podrombosis of the cavernous sinus .
Pathogenesis.
In the development of this complication, the main importance is
Rich blood supply to the maxillofacial region
No valves on faces
The presence of anastomoses between the surface veins of the face, the elephants of the soccer and the venous sinus of a solid cerebral shell (cavernous sine): angular vein (v. Angularis) - between the elephants of the society and the facial vein,
Clinic.
The thrombophlebitis of the facial veins is characterized by the appearance of but the move of the angular or facial veins of painful "heavy" infiltrated tissue, hyperemia of the skin with a blue tint, the spread of edema far beyond the limits of infiltrate. There is an increase in body temperature, changes in the blood pattern characteristic of inflammation.
The most serious complication of thrombophlebitis of the facial veins is the thrombosis of the cavernous sinus. This complication can be attributed to intracranial. General symptoms are severe headache, general weakness, an increase in body temperature up to 38-40 ° C, leukocytosis, an increase in ESP to 40-60 mm / h.
Locally marked:
Edema and hyperemia of the skin of the eyelids and forehead
Infiltration of soft orbit fabrics
Exophthalm, Hemosis conjunctiva, ophthalmoplegia, expansion of pupil, eye hyperemia
Could celebrate the rigidity of the occipital muscles
Treatment.
When the first signs of the disease appear intensive antibacterial (wide spectrum antibiotics, immunotherapy), disinfecting and desensitizing therapy. With purulent-septic thrombophlebitis, the introduction of drugs is used directly into the outdoor carotid artery. Internally except antibiotics are injected direct action anticoagulants (heparin) to prevent intravascular blood coagulation. In the abscess of thrombic veins and infiltrates, surgical treatment with active drainage of uluses is carried out. To prevent the thrombosis of the cavernous sinus during the thrombophlebitis of the facial veins, the bandage is recommended
corner or facial vein. The ligature is superimposed through the entire thickness of the tissues without prior allocation of veins.
Treatmentpatients with developed thrombosis of the cavernous sinus are carried out according to the same principles. Along with intense antibacterial, desensitizing, disintellation, dehydration, hormonal and anticoagulant therapy is shown. Sustainable bedding is required. To enhance the effect of therapy, antibacterial drugs are recommended to be introduced intraarterially. It should be noted that the conducting of active anticoagulant therapy in thrombosis of the cavernous sine is not generally accepted, as it is unsafe due to the possibility of hemorrhage and the brain infarction. Various authors offer to use fibrinolytic agents, "soft" anticoagulants (acetylsalicylic acid, butadion).
Intracranial complications
A. Primary rhinogenic hydrocephalus -
t.oxico-infectious edema of brain shells with phenomena of liquor hypertension - occurs under the influence of the inflammatory process in the maxillary sinuses. It is clinically characterized by an intense headache, which can be accompanied by nausea and vomiting, symptoms from the eye (reduction of visual acuity, lesion of the discharge, oxide, trigeminal nerve).
B. Basal Arachnoiditis.
Due to the purulent and polypose process in the topless sinuses. It is characterized by sharp one-sided pains of the area of \u200b\u200bthe face and head, the defeat V, VI and VII pairs of cranial nerves.
V. purulent meningitis
- it is usually developing with purulent melting of the walls of the cavernous sinus (due to its thrombosis). It is characteristic of a sharp beginning, an increase in body temperature up to 39-40 degrees, strong headache, nausea, vomiting, depression of consciousness, meningial symptoms The rigidity of the occipital muscles, the symptoms of Kerniga, Burutzinsky), changes in the liquor (increase in pressure, clouding, pleyocytosis).
Meningoencephalitis
- characterized by the presence of signs of meningitis, towhich joins the focal symptoms, loss of consciousness. Tachycardia, arrhythmia, falling blood pressure.
4. Odontogenic sepsis.
Currently, the following phases of a total purulent infection are distinguished:
1. Night-resorbative fever -the overall syndrome, closely related to the local purulent process, characteristic of all purulent-inflammatory diseases of the maxillion-linea region.
2. Charging phase of sepsis.Diagnosed in the presence of a purulent-resorbative fever after eliminating the purulent focus, its drainage and conducting drug therapy and sowing the pathogenic flora from the blood. In this phase, during intensive therapy, the disease is eliminated within 15-10 days.
3.Septicemia -it is characterized by a severe common state of the patient (body temperature above 38 degrees, stunning chills, strong headache, insomnia). A pathogenic flora is seized from the blood. Food foci are not detected.
4.Septicopemia.In this phase, in addition to the phenomena of septicemia, it is characterized by the emergence of metastatic jets as a result of the transfer of bacteria by hematogenic pathway from the primary hearth. For this stage, the following symptoms are characterized: body temperature above 38 degrees, tachycardia is above 100 shots per minute, anemia, leukocyte formula shift, improving ESP is more than 60 mm / h, hypoprotein, toxic hepatitis and nephritis, discharge during sowing of pathogenic microorganisms.
Septic toxic-infectious shock is a severe complication of sepsis. A starting point for the development of shock is a simultaneous or multiple flooding of blood flow by microorganisms and their toxins. With septic shock, there is disorders of the CNS function, pulmonary gas exchange, peripheral and central blood circulation, organic damage. Mortality from septic shock is currently very high, accounted for 50% or more.
Treatment.
The treatment of sepsis must be comprehensive and includes the following components:
The revision of the foci of purulent infection and, if necessary, "confusion" of primary phlegmon, abscesses, purulent chapels.
Ensuring good drainage of purulent foci with the help of perforated polyethylene and polychlorvinyl tubes introduced through the main incision and derived across additional (contraperture). The purulent focus was washed with antiseptics.
Antibacterial therapy, taking into account the sensitivity of microflora to antibacterial drugs.
Disinfecting infusion therapy.
Immunotherapy (administration of leukocyte suspension, gammaglobulin, antistaphococcal plasma if the pathogen is staphylococcus)
Symptomatic therapy (depending on the defeat of various organs and systems)
Full nutrition, vitamins.
Inflammation as a reflection of the injury of tissues and cells of various genesis is the largest group of outpatient reception diseases and one of the most complex - for the doctors of the annular hospitals.
The patterns of the flow of inflammatory processes in the maxillofacial region in children and their classification
Pathophysiology inflammation.Inflammation is a comprehensive reaction of vascular and connective tissue on damage to them by any phlogen agent (biological, mechanical, thermal, radiation, chemical). Inflammation inherent in autochonity: starting, regardless of the continuation of the flogenic factor, it passes all stages of development. Inflammation develops according to a cascade principle with the participation of chemical regulators arising acting and inactivating in the focus of inflammation. As an increase in the signs of it and the inverse dynamics are governed by autonomous local chemical "signals" - mediators. And even the end of inflammation is not to exhaust all local reserves, but a consequence of accumulation and action on the center of special anti-inflammatory mediators.
The focus of inflammation is always trying to dissociate (blocked) from surrounding healthy fabrics, which is due to the need to prevent the systemic effect of mediators of inflammation to the body, since outside the focus they cause dangerous reactions. In the event of such a situation, the latter causes the phenomena of general intoxication, anaphylactic or septic shock, polyorgan deficiency.
Inflammation always includes three components - alteration, exudation and proliferation. The process of inflammation begins primary alteration of cell membranes, lysosomes, mitochondria, vessels and, as a result, synthesis and aktivation of chemical "signals" - mediators of inflammation I order - biogenic amines (histamine, serotonin), polyamines (sperm, spermadine, etc. n.) accomplished by vascular reactions and the beginning of exudation. Vascular reactions starting with a short-term narrowing of vessels, and then the capillary expansion comes< гиперемией. Гистамин, брадикинин и серотонин повышают проницаемость сосу лов. Через промежутки, возникающие в сосудах эндотелия, происходит проникно вение плазмы в межклеточные пространства. Появляется воспалительный отек, т< есть развивается второй компонент воспаления - экссудация, обеспечивающая транспорт лейкоцитов и других защитных агентов из крови в очаг воспаления.
According to the type of exudate, there is an exudative (liquid prevails) and productive (cells prevail) inflammation.
In turn, exudative inflammation shared on:
1) serous (in exudate a lot of protein);
2) purulent (polyposphonuclear plates prevail, especially lymphocytes;
3) fibrous (revealed coagulation factors forming fibrin;
4) hemorrhagic (necessarily there is an admixture of erythrocytes);
5) Catarial (exudate produced by mucous membranes).
All types of exudative inflammation have their continuation, they pass all the phases of inflammation and necessarily end with the reparative processes.
The continuation of inflammation is to increase the tone in the veul section due to serotoiin, which contributes to the occurrence of hemostasis, and hence the aggregation of platelets, the appearance of blood clots; The formation of fibrin is accelerated. It occurs outside the vessels and partly - inside the capillaries. The appearance of edema and the fibrin layer the body separates the focus of inflammation from healthy tissue. Primary alteration products cause a secondary lesion of tissues, which, in turn, contributes to the formation of autocoids (gumoral agents of secondary alteration) necessary for regeneration processes.
Bradykin, histamine and prostaglasia, together with the material of metabolism and the pressure pressure on pain receptors, cause painful pain typical. Together with the seeping of the plasma, the cell migration occurs in the focus of inflammation. In this process, neutrophils, eosinophilic and basophil granulocytes, lymphocytes and macrophages take part in this process. The nature of the flow of the inflammatory process largely depends on the scale and nature of migration, which cause chemotactic factors (for example, part of the complement), and from the properties of phagocytes.
Reparative processes occurring in the focus of inflammation are reduced to regeneration (replace the dead cells by cells of the same type) and fibroplasia (formation of fibrous tissue).
In the process of regeneration, macrophages and a granule. You, brought to the place of inflammation of the plasma current, capture foreign cells. Own enzymes of the body, which are distinguished from Phagocyte LPZOS and Mastocytes (fat cells), begin to split the fragments of fabrics and products of inflammation. In the next phase of the regeneration of enzymes, the layers of fibrin are cleaved by the layers, and the remaining tissue defects are gradually leveled with the help of fibroblasts, growth factors formed from macrophages, lymphocytes, platelets, etc. Such is the simplified scheme of the phase of the acute inflammatory process.
Chronic inflammation in children can develop as a primary chronic process or be a consequence of the transition of acute inflammation into chronic. This contributes to a violation of the flow of inflammatory reactions - the excessive activation of macrophages and lymphocytes of cytokines, isolated in macro-genial-lymphocyte infiltration, constantly maintains the phenomena of inflammation, immune processes (the development of cytotoxic, immunocomplex and anaphylactic reactions).
The relevance of the problem of inflammatory processes of the maxillofacial area of \u200b\u200bthe Obus.Chov.1 is an increase in the number of such patients with an ambulatory reception
in the hospital, a variety of forms of manifestations of these processes, the severity of the course of the disease, which causes serious complications.
The proportion of children with inflammatory diseases of the maxillofacial region in the hospital ranges from 27 to 61% in relation to other patients. In the conditions of an ambulance at the reception at the children's surgeon dentist, the number of children with inflammatory processes is: in the age group from 1 to 3 years - 16 "h\u003e (relative to other diseases); 4-6 years - 26%; 7-12 years -38 %; 13-15 years-20%.
Among the reasons for the oscillation of the growth of inflammatory processes of the oral cavity organs and the maxillofacial region are most significant:
1. Social, economic and environmental situations that determine the conditions for the growth and development of children.
2. Changing the virulence of microorganisms, strains and their compounds, an increase in the effects of anaerobic microflora, the effect on the organism of viruses and the simplest.
3. An increase in the number of factors causing inflammation (biological, chemical, physical, etc.).
4. Low sensitivity of microorganisms to different frequently used drugs.
5. The presence of factors of instability of the homeostasis of macroorganism due to the growth of background diseases of the endocrine (diabetes and the disease of the thyroid gland), immune (number of primary and, more often, secondary immunodeficiency) systems, metabolic diseases, blood, and the like.
6. Inefficiency or low efficiency of the prevention of major dental diseases in children and their treatment.
The patterns of the flow of inflammatory processes of the maxillofacial region are due to age, socio-biological and socio-hygienic premature factors.
Among the socio-biological factors should be allocated:
1. Low level of physical development of the child. Socio-economic and environmental conditions are currently not promoting the health of children and their parents. Today it is difficult to imagine almost healthy parents.
2. An unfavorable course of the newborn period ™ and the first year of life. Only 30% of children at the age of 6 months feed breast milk. Most of them are early translated on mixed and artificial feeding. All of this, of course, affects the further development of the child's body.
3. Power is one of the main factors affecting the health status. Observations indicate a significant deterioration in the main mass of the population of Ukraine.
4. In children who often sick with sharp chronic inflammatory diseases of the breathing apparatus, digestive and urinary systems, the inflammatory processes of the maxillofacial region are most often developed.
Social and hygienic premorbid factors include: 1) non-compliance with the rules of the oral hygiene - only 30% of children at the age of 6 years (residents of cities) use a toothbrush and partially perform
Section 3.
new rules of oral hygiene. In rural areas, this percentage is significantly lower (10%);
2) Reducing the number of children engaged in physical culture, non-compliance (possibly, on an objective reason) of the correct nutritional mode - qualitative and quantitative - adversely affect the specific and non-specific reactivity and the harness of the body.
A significant role of the immunobiological characteristics of the body of the child and immunity factors is sometimes perceived incorrectly. In the scientific literature, data appear on the occurrence of certain processes in the body of the child due to its "immature" immunological reactivity. The term "immature" rather categorical. If you imagine that greater antigenic load from viruses, microorganisms, simplest and other biological agents to the child's body from the first days to 10-15 years, it is difficult to explain the organism's compensatory possibilities to such "immaturity". But, of course, immunological reactivity, that is, the ability to enable the necessary protective-adaptive reactions in a timely manner, aimed at preserving homeostasis and ensuring the harmonious development of the child. A different age of the child provides an unequal type of body response to an inflammatory process. Thus, small children react much more often according to the hypo-ergic type and only at 3-7 years old - on the pshrsrgic.
Functional imperfection of the reticulous endothelial system, the immaturity of the components of the immune system, local and central regulation mechanisms in young children do not provide sufficient antibody and phagocytic reactions. This often causes the generation of purulent infection.
A characteristic feature of the flow of inflammatory processes in childhood is pronounced intoxication. This is due to the fact that the liver and kidneys exercising with the withdrawal of metabolism products, finish their formation mostly until 6-8 years. Their capabilities are quickly exhausted, which is manifested by a significant deterioration in the state of the child even with limited forms of inflammation. The appearance of a protein in the urine, which is observed in adults after months after the disease, in childhood it arises early and indicates the defeat of the kidney products by the decay of tissues and toxins; In the growing body, intoxication and the strength of the water-salt balance increase. A newborn body weight consumes liquids 20 times more than an adult. Inflammatory processes are accompanied by a rapid loss of water due to an increase in body temperature and evaporation of it, enhancement of exchange processes. This causes an increase in the concentration of toxins in the blood, it makes it difficult to derive the metabolites. The inadequacy of the CNS reaction in children on the local effect of the infectious factor is characterized by the common excitement, manifested by convulsions, nausea, vomiting, diarrhea.
The child, especially at an early age, is distinguished by the fact that the metabolism and vital activity does he occur in a high energy level against a background of several reduced reserve capabilities. This acquires particular importance for prolonged inflammatory processes requiring significant energy costs.
In connection with the peculiarities of the development of basic organism systems, the flow of inflammatory processes has a special equivalent of local manifestations:
1) the predominance of productive forms of inflammation over exudatives;
2) the rarity of autonomous processes:
3) a quick transition to generalized forms;
4) General reactions - answers to the inflammatory agent are often ahead of the development of local processes;
5) As a result of intoxication, general symptoms come to the fore.
1 [Azvannaya General features of the responses of the child's body into an inflammatory process are accompanied by the peculiarities of a local nature caused by the anatomical and immunobiological patterns of the development of a children's body. Among them are the mains are:
1. Temporary and constant teeth in children are in a state of permanent
development (bookmark and intake period; period of teething,
growth, formation and resorption of the roots of temporary teeth).
Temporary and teething constant teeth are relatively less mineralized, have a large pulp chamber and wide root channels. Blood vessels pulp are widely anastomosed with jaw bones and vessels. A large assault hole in the formative and re-torn roots, the absence of a generated periodonta creates a close connection of them with bone (with an "immature" bone marrow).
2. Jewish bones in childhood are rich in organic and poor minerals. They are in a state of constant growth and restructuring associated with the change of teeth. The cortical bone layer is thin, and its main mass is a spongy substance. It has wide bone tubules, a subtle and gentle structure of bone beams, between which is preferably a red bone marrow, less resistant to different stimuli. The periosteum is thick, tightly covers the bone.
3. Rich vascularization and lymphotod of the maxillofacial region in children determine the developed anastromization of the vessels of soft tissues, teeth, periodontal, jaws and periosta. This, on the one hand, provides active regeneration of soft tissues and the high potential of reparative osteogenesis, and on the other, it helps the spread of inflammation with a hematogenic way.
4. Rising jaw bones uneven intensity and time. More active jaws are growing during teething (1-3 years, 6-10 years). Age 13-15. Tests "puberty", because during this period the growth of bones is significantly activated. The uneven growth is that the bone grows in length not by the whole of the mass, but only by separate areas - growth zones; The growth of bones in the thickness is carried out at the expense of periosteum.
5. The occasional soft tissues in children have a smaller density of fascia and aponeurosis, limiting cellular spaces, are characterized by low barrier properties of them, and a significant amount of subcutaneous fluid fiber. The inflammatory process quickly extends to 2-3 topographic-anatomical areas.
Thus, the listed features predetermine the specific
Inflammatory diseases of the maxillofacial region
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the conditions for the emergence of inflammatory processes of the maxillofacial region in children of different age groups.
The classification of inflammatory processes of tissues and the oral cavity organs and the maxillofacial region in children is shown in Scheme 3.
Scheme 3.Classification of inflammatory processes of tissues and oral oral organs and maxillofacial area
In the maxillofacial region, the special group consists of inflammatory diseases caused by specific pathogens: radiant mushroom, pale trepalia, mycobacterium tuberculosis. Diseases caused by these pathogens (actinomycosis, syphilis, tuberculosis) is made to allocate in a group of specific inflammatory processes.
Actinomycosis
Aktinomycosis, or launch-fungal disease, an infectious disease resulting from the introduction of actinomycete (radiant fungi) into the body. The disease can affect all organs and tissues, but more often (80-85% of cases) maxillofacial area.
Etiology.Aktinomicosis pathogens - radiant mushrooms (bacteria). The culture of actinomycetes may be aerobic and anaerobic. With a person in 90% of cases, an anaerobic form of radiant mushrooms (proactinomycene) is distinguished, less often - individual types of aerobic actinomycetes (thermophiles) and micromonosphere. In the development of actinomycosis, a significant role is played by mixed infection - streptococci, staphylococci, diplococci and other coccis, as well as anaerobic microbes - bacteroids, anaerobic streptococci, staphylococci, etc. Anaerobic infection helps the penetration of actinomycetes in the tissue of the maxillofacial region and the further distribution of them by cell spaces .
Pathogenesis. The actinomycosis occurs as a result of autoinfection, when radiant mushrooms penetrate into the tissue of the maxillofacial area, and a specific actinist granuloma is formed or a somewhat granulul. In the oral cavity, actinomycetes are in dental, carious cavities of teeth, pathological seashest pockets, on almonds; Actinomycetes make up the main stroma of the dental stone.
The development of the actinomycotic process reflects complex changes in the immuno-biological reactivity of the organism, non-specific protection factors in response to the introduction of infectious agent - radiant fungi. Normally, the constant presence of actinomycetes in the oral cavity does not cause an infectious process, since there is a natural equilibrium between the immunological mechanisms of the organism and antigens of radiant fungi.
The leading mechanism for the development of actinomycosis is the violation of the immune system. For the development of actinomycosis in the human body, special conditions are needed: a decrease in or impairment of the organism's immunobiological reactivity, a factor of non-specific protection in response to the introduction of infectious agent - radiant fungi. Among the general factors that violate immunity can be distinguished primary or secondary immunodeficient diseases and conditions. Local pathogenetic causes are great importance - odontogenic or dentogenic, less often - tonsilogenic and rinegenic inflammatory diseases, as well as tissue damage that violate the normal symbiosis of actinomycetes and another microflora. With the actinomyosis, violations of specific immunity and phenomena of immunopathology are developing, of which the lead is allergic.
The entrance gate of the introduction of the actinomyosis infection during the damage to the tissues and organs of the maxillofacial region can be carious teeth, pathological seashest pockets, damaged and inflamed mucous membrane of the oral cavity, zea, nose, ducts of salivary glands, etc.
Actinomycetes from the place of implementation are applied to contact, lymphogenic and hematogenic paths. Typically, a specific focus develops into well-vascularized tissues: loose fiber, connective tissue muscle layers and bone organs, where actinomycetes form colonies - dubs.
The incubation period ranges from several days to 2-3 weeks, but can be longer - up to several months.
Pathological anatomy. In response to the introduction of radiant fungi in tissue, a specific granuloma is formed. Directly around the colonies of the radiant mushroom - polynuclears and lymphocytes and lymphocytes accumulate. According to the periphery of this zone, a granulation tissue is rich in thin-walled vessels, consisting of round, plasma, epitheloid cells and fibroblasts. Here are the occasionally gigantic multi-core cells. Characteristic is the presence of xanthome cells. In the future, in the central departments of the actinomy granuloma, cells occurred and their disintegration. At the same time, macrophages rush to the colonies of the friends of a radiant mushroom, capture pieces of mycelium and migrate with them into neighboring tissue with a specific granuloma. A secondary granuloma is formed there. Further, such changes are observed in the secondary granuloma, tertiary granuloma is formed, etc. The daughter granuloma gives rise to diffuse and focal chronic infiltrates. According to the periphery of a specific granuloma, granulation tissue matures and turns into fibrous. At the same time, the number of vessels and cell elements decreases, fibrous structures appear, dense scar connecting tissue is formed.
Morphological changes in the actinomycosis are directly dependent on the reactivity of the organism - the factors of the specific and non-specific protection. This causes the character of the tissue reaction - the predominance and combination of exudative and proliferative changes. An important meaning is to attach the secondary global infection. Strengthening necrotic processes, the local distribution of the process is often associated with the addition of purulent microflora.
Clinical picture Diseases depends on the individual characteristics of the organism, determining the degree of general and local reaction, as well as from the localization of the specific granuloma in the tissues of the maxillofacial region.
The actinomycosis often proceeds as acute or chronic inflammatory process, characterized by a normergic reaction. With a duration of a disease of 2-3 months and more in persons burdened by concomitant pathology (primary and secondary immunodeficiency diseases and states), the actinomycosis acquires a chronic flow and is characterized by a hypergic inflammatory response. A relatively rare actinomycosis proceeds as an acute progressive and chronic hyperblastic process with a hypergic inflammatory response.
Often, the overall hypergic chronic flow is combined with local hyperblastic changes in tissues, expressing in scar changes in tissues adjacent to lymph nodes similar to muscle hypertrophy, hyperostotic jaw thickening.
Depending on the clinical manifestations of the disease and the peculiarities of its flow associated with the localization of a specific granuloma, it is necessary to distinguish the following clinical forms of actinomycosis of the face, neck, jaws and oral cavity: 1) skin, 2) subcutaneous, 3) subliminity, 4) mucous membrane, 5) Odontogenic actinist granule, 6) subcutaneous intermushkinic (deep), 7) actinomycosis of lymphatic components, 8) actinomycosis of the periosity of the jaw, 9) actinomycosis of the jaws, 10) actinomycosis of the oral cavity - language, almonds, salivary glands, topless sinuses. (Classification Robustova T. G.)
Skin shape. It is rare. It occurs both odontogeneously and as a result of damage to the skin. Patients complain of minor pains and sealing on a small leather leather, in surveys indicate a gradual increase and sealing of the focus or foci.
The actinomyosis of the skin flows without increasing body temperature. In case of inspection, inflammatory skin infiltration is determined, one or more foci, germinating outwards. It is accompanied by thinning of the skin, by changing its color from bright red to the drow-blue. On the skin of the face and neck can prevail the pustulas or tubercles, their combination occurs.
The skin shape of actinomycosis is distributed through the length of the tissue.
Subcutaneous form It is characterized by the development of the pathological process in subcutaneous tissue, as a rule, near the odonogenic focus. Patients complain of pain and swelling. From the history you can find out that the subcutaneous form arose as a result of the preceding purulent odontogenic disease. Also, this form can develop during the decay of lymph nodes and involvement in the process of subcutaneous fiber.
The pathological process with this form of actinomycosis is distinguished by a long but calm current. The period of decay of the specific granuloma may be accompanied by minor pains and subfebrile temperature.
In case of inspection in subcutaneous tissue, a rounded infiltrate is determined, initially dense and painless. During the decay period, the granuloma, the skin is soldered with the subjectable tissues, becomes bright pink to the red, in the center of the focus there is a softening section.
Submembrance the form It occurs relatively rarely, if the oral mucosa is damaged - biting, insertion, ingress of foreign bodies, etc.
The form develops without lifting body temperature. Pain sensations in the focus of the lesions are moderate. Depending on the localization of pain can be intensified when opening the mouth, conversation, swallowing. Next appears a feeling of a foreign body, awkwardness. When palpation is determined by the round shape of a dense infiltration, which is further limited. The mucous membrane is soldered.
Actinomycosis of the mucous membrane The mouth is rare. The radiant mushroom penetrates through damaged mucosa, traumatic factors most often are foreign bodies, sometimes sharp edges of the teeth.
The actinomyosis of the mucous membrane of the oral cavity is characterized by a slow, calm current, is not accompanied by an increase in body temperature. Pain in the focus is insignificant.
In case of inspection, the superficially located inflammatory infiltrate with a bright red mucous membrane above it is determined. Often there is a dissemination of the focus outside, its breakthrough and the formation of individual small fistula moves, of which granulation sput.
Ondogenic actinomy granulomain the tissues of periodonta, it is rare, but recognized with difficulty. This focus always tends to spread to other fabrics. In the localization of granuloma in the skin and subcutaneous tissue, there is a severity of a transitional fold, which comes from the tooth to the hearth in soft tissues; With the subclosure, the focus is not. The process often applies to the mucous membrane, with the next exacerbation it is thinning, forming a fistula.
Subcutaneous intermushny (deep) formactinomicosis is common. In this form, the process develops in subcutaneous, intermushkin, interfascial fiber, applies to the skin, muscles, mining and other facial bones. It is localized in the puzzleless, chewing and the near-chewing and chewing area, and also affects the tissue of temporal, under-judicial, zicky regions, omperable and wonderland-palate pits, wonder-jaw and occupation spaces and other areas of the neck.
With a deep form of actinomycosis, patients indicate the appearance of swelling due to inflammatory edema and subsequent infiltration of soft tissues.
Often, the first sign is the progressive restriction of the opening of the mouth, because the radiant mushrooms growing into the cloth are striking the chewing and inner wing muscles, as a result of which the disturbing patient arises the restoration of the mouth opening.
During the inspection, the sinusiness of the skin cover over the infiltrate; Arriving in certain areas of infiltrate foci of softening resemble the forming abscesses. The breakthrough of the thinned area of \u200b\u200bthe skin leads to its perforation and isolating the tight fuel fluid, often containing small whitish grains - dubs of actinomycetes.
The acute beginning or exacerbation of the disease is accompanied by an increase in body temperature to 38 - 39 ° C, pain. After opening the actinomy focus, sharp inflammatory phenomena verses. There is a proxy density of peripheral departments of infiltrate, sections of softening in the center with fistula strokes. Leather over the affected plot of fasting, Sinah. Subsequently, the actinometric process is developing in two directions: there is a gradual resorption and softening of infiltrate or distribution to neighboring tissues, which sometimes leads to secondary damage to the bones of the face or metastasis in other organs.
Actinomycosis Lymph nodes It occurs in an odontogenic, tonsillogenic, all-heated paths of infection.
The process can manifest itself in the form of actinometric lymphangitis, abscessive lymphadenitis, adenoflems or chronic hyperplastic lymphadenitis.
The clinical picture of lymphangitis is characterized by a superficially located flat infiltrate, initially dense, and then softening and soldering with the skin. Sometimes infiltrate is in the form of a dense heavyweight, coming from the affected lymph node up or down the neck.
Absoing actinomikosis lymphadenitis is characterized by complaints with a limited, slightly painful dense node. The disease develops sluggish, without increasing body temperature. The lymph node is increased, gradually saves with adjacent tissues, tissue infiltration increases around it. In abscess, the pain is enhanced, the body temperature increases to subfebrile, there is airsdown. After opening the abscess, the process is subjected to reverse development, there remains a dense biting and changed conglomerate.
Adenoflemmon is characterized by complaints about sharp pain in the affected area, the clinic will move the picture of phlegmon caused by a glorodular infection.
With hyperplastic actinomaic lymphadenitis, an increased, dense lymphatic assembly resembling a tumor or tumor-like disease is observed. Characteristic slow, asymptomatic current. The process can exacerbate and abscess.
Actinomycosis Period of jaws Compared to other forms, it is rare. Proceeds in the form of exudative or productive inflammation.
With an exudative periostite jaw, inflammatory phenomena are developing in the field of tooth and switch to the vestibular surface of the alveolar process and the body of the jaw. Pain sensations are poorly expressed, well-being is not violated.
Clinically develops a dense infiltration on the eve of the oral cavity, the smoothing of the lower arch. The mucous membrane above it is red, sometimes with a bluish tint. Then the infiltrate slowly softened, limited, soreness appears. Percussion of the tooth is painless, it's like a "spring". At the opening of the focus it is not always released by the pussy, the growth of granulations is often marked.
With productive actinomycase periostite, the base of the lower jaw due to the periosteum is observed. The process with the periosteum of the alveolar part goes to the base of the jaw, deforming and thickening its edge.
X-ray outside the alveolar part, the base of the body of the jaw and especially at the bottom edge, loose periosal thickening of the inhomogeneous structure are determined.
Actinomycosis of the jaws.The pathological process with primary lesion of the jaw is often localized on the lower jaw and is very rare on the top. The primary actinomyosis of the jaw can be in the form of a destructive and productive-destructive process.
The primary destructive actinomyosis of the jaw can manifest itself in the form of an intraosseous abscess or intra-apart gum.
With intraoscience abscess patients complain of pain in the affected bone area. With the neighborhood of the focus with the channel of the lower jaw, the sensitivity in the area of \u200b\u200bthe branching of the chiffer nerve is disturbed. In the future, pain become intense, acquire the nature of neuralgic. There appears swelling of soft tissues.
The clinic of the bone gum is characterized by a slow, calm current with minor painful feelings; accompanied by exacerbations under which an inflammatory contracture of chewing muscles occurs.
The radiographically primary destructive actinomycosis of the jaws is manifested by the presence of one or more spilled cavities in the bone, not always clearly contiguous. In the gum of the hearth can be surrounded by the sclerosis zone.
The primary productive and destructive damage to the jaws is observed mainly in children, adolescents, the cause is an odontogenic or tonsilogenic inflammatory process. The bone thickening is noted due to periosal overlays, which progressively increases and compacted, simulating the neoplasm.
The course of the disease is long - from 1-3 years to several decades. Against the background of chronic flow, there are separate exacerbations similar to those with a destructive process.
The radiograph of the bone, coming from the periosteum, the sealing of the structure of the compact and spongy substance in the body area, the branch of the lower jaw is visible. Separate foci of resorption are found; The days of cavity are small, almost point, other large. More or less expressed sclerosis of the bone in the circumference of these foci.
Aktinomikosis of the oral cavity It meets relatively rare and presents significant difficulties for diagnosis.
Clinic aktinomycosis language It may proceed as a diffuse inflammatory process by type of phlegmon or abscess. On the back or tip of the tongue there is a small-breaking node, which remains for a long time unchanged, and after 1-2 months. It is resolved with abscess and opening outwards with the formation of fistula and empty of heavy granulation.
Aktinomikosis of salivary glands It can be primary and secondary. The clinic is diverse, depending on the length of the process in the gland and the nature of the inflammatory reaction, you can distinguish the following forms of actinomycosis of the salivary glands: 1) an exudative limited and diffuse actinomycosis; 2) productive limited and diffuse actinomycosis; 3) Aktinomycosis of deep lymph nodes in the parole salivary gland.
Diagnosis. Diagnosis of actinomycosis due to a significant variety of clinical picture of the disease presents some difficulties. The sluggish and long-term course of odontogenic inflammatory processes, the unsuccessfulness of the anti-inflammatory therapy is always alarmed with respect to actinomycosis.
The clinical diagnosis of actinomycosis should be supported by the microbiological study of separated, conducting a skin-allergic test with actinolizat and other methods of immunodiagnostics, with a pathological study. In some cases, repeated, often multiple diagnostic studies are required.
The microbiological study of the discharge should be to study the native drug, cytological study of painted smears and in some cases in the release of pathogenic culture by sowing.
The study of the native drug separated is the simplest method of determining the friends and elements of radiant fungi. A cytological study of painted smears makes it possible to establish the presence of the Micsence of actinomycete, secondary infection, as well as to judge the cellular composition of the organism's jet abilities (phagocytosis, etc.).
Differential diagnosis. The actinomycosis is differentiated from a number of inflammatory diseases: abscesses, phlegmon, periostite and osteomyelitis of jaws, tuberculosis, syphilis, tumors and tumor-like processes. Clinical diagnostics help microbiological research, specific reactions, serodiagnostics. Morphological data is played an important role in difdiagnosis of tumors.
Treatment. Therapy of the actinomicosis of the maxillofacial region should be complex and include: 1) surgical treatment methods with local impact on the wound process; 2) impact on specific immunity; 3) an increase in the overall reactivity of the body; 4) the impact on the accompanying purulent infection; 5) prosthetic, desensitizing, symptomatic therapy, treatment of related diseases; 6) Physical methods of treatment and leaps.
Surgical treatment of actinomycosis is: 1) detection of teeth, which appeared in the entrance gate of infection; 2) Surgical treatment of actinometric foci in soft and bone tissues, removing areas of redundantly neoplated bone and in some cases of lymph nodes affected by the actinomycous process.
Large importance is care for the wound after opening the actinomy source. Its long-term drainage, the subsequent scraping scraping, the processing of the affected fabrics of 5% of the iodine tincture, the introduction of the yodoform powder is shown. When the secondary global infection is attached, deposited administration of antibiotics is shown.
With the normargic flow of actinomycosis, actinolizatotherapy is carried out or specially selected immunomodulators are prescribed, as well as secrets of stimulating agents and in some cases biologically active drugs.
The therapy of actinomycosis with a hypergic inflammatory response is beginning with a detoxification, tall and stimulating treatment. Actinolizat and other immunomodulators prescribe strictly individually. In order to remove intoxication, a solution of hemodesa, refooliglucin with the addition of vitamins, kocarboxylase is injected intravenously. The complex of treatment of chronic intoxication includes polyvitamins with trace elements, enterosorbents, abundant drinking with the presentation of medicinal herbs. Such treatment is carried out for 7-10 days with intervals of 10 days as part of 2-3 courses. After 1-2 courses, immunomodulators are prescribed: T-activin, thymazine, actinolizat, stafilicococcal anatoxin, levamizol.
With a hypergic type of process with a pronounced sensitization to a radiant mushroom, treatment begins with a general antibacterial, enzymatic and complex infusion therapy, aimed at correction of hemodynamics, the elimination of metabolic disorders, disinfect. Prescribed preparations with desensitizing, constructing and tonic properties. In the treatment complex, vitamins of groups B and C, Cocarboxylase, ATP are used. After the course of such treatment (from 2-3 weeks before 1-2 months), on the basis of the data of the immunological study, they prescribe a course of immunotherapy with actinolization or levamizol.
An important place in complex treatment is occupied by stimulating therapy: hemotherapy, the purpose of antigenic stimulants and tensile agents - polyvitamins, vitamins in 1, B 12, C, aloe extract, pregoiosis, pentoxyl, methyluracil, levamizol, T-activin, thimaline. Treatment should be combined with the purpose of antihistamine, pyrazolone derivatives, as well as symptomatic therapy.
Forecast With the actinomyosis of the maxillofacial region, in most cases favorable.
Prevention. Sange the mouth cavity and remove odontogenic, dentogenic pathological foci. The main in the prevention of actinomycosis is the increase in the overall anti-infectious protection of the body.
Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis. Tuberculosis is a transmissive disease. In recent years, the disease of the jaws, fabrics of the face and the oral cavity has become rare.
Etiology.The causative agent of the disease is mycobacterium tuberculosis, - thin, straight or curved sticks, 1..10 μm long, 0.2..0.6 μm width. Three types of tuberculosis bacteria are isolated: human (causes 92% of cases of disease), bull (5% of cases) and intermediate species (3%).
Pathogenesis. The source of the propagation of infection is more often a sick tuberculosis man, the disease is transmitted by an alimentary path through milk of patient cows. In the development of tuberculosis, the immunity and sustainability of a person to this infection is of great importance.
It is customary to distinguish between the primary and secondary tuberculosis defeat. The primary lesion of the lemph nodes of the maxillofacial region occurs when myfobacteria is hit through the teeth, almonds, the mucous membrane of the oral cavity and the nose, damaged skin. Secondary damage occurs when the localization of primary affect in other organs or systems.
Pathological anatomy. Tuberculosis can affect any organ or system of organs, while remaining a common disease. Tuberculle is formed at the place of deployment of the pathogen - banal inflammation develops, in the proliferation phase, acquiring a specific nature. A shaft of cell elements are formed around the inflammatory focus, in which epitheloid cells are present, the giant Pyrogo-Langkhans cells are present for the inflammation of the cells. In the center of the inflammatory hearth, a section of caseous necrosis is formed. Another specific form of inflammation is a tuberculosis (tuberculosis granuloma), morphologically similar to a tuberculus.
Clinical picture.In the maxillofacial region, the lesion of the skin, mucous membranes, the submucous base, subcutaneous fiber, salivary glands, jaws are distinguished.
Primarydefeat lymphatic nodes It is characterized by their single appearance either in the form of soldes in the package. Lymph nodes are dense, in the dynamics of the disease are even more compacted, reaching a cartilage or bone consistency. In patients of young age, the disintegration of the node is often observed with the output of the characteristic secretary secret. Primary tuberculosis of lymph nodes is accompanied by general symptoms characteristic of the inflammatory process.
Secondary tuberculosis lymphadenitis It is one of the most common forms of this pathological process. It develops in the presence of a focus in other organs. The disease is more often chronically accompanied by a subfebrile temperature, general weakness, loss of appetite. In some patients, the process may have an acute start, with a sharp increase in body temperature, symptoms of intoxication. There is an increase in lymph nodes, they have a density consistency, sometimes a bug stem, clearly contoured. Their palpation is slimless, sometimes painless. In some cases, there is a quick decay of the focus, in others - slow cavity with the formation of a curly decay of tissues. At the output of the contents, there remains fistula or several fistulas. In recent years, the number of cases of slow-member lymphadenitis has increased.
Tuberculosis of the skin and subcutaneous fiber. Distinguish between several clinical forms:
Primary skin tuberculosis (tuberculous Shankr) - erosion and ulcers are formed on the skin, having a compacted bottom. Regional lymph nodes are applied. After healing ulcers, the deforming scars remain.
Tuberculosis lupus. The primary element is a lupoma, which is characterized by a symptom of "apple jelly" - when pressing a yellow zone on a lumber in the center of the element is formed. Lyupes have a soft consistency, the tendency to merge, forming infiltrate, when resolving which deforming scars are formed.
The crotheloderma is most often formed in close proximity to the tuberculous focus in the jaws or lymph nodes, less often - when the infection is distributed from remote foci. It is characteristic of the development of infiltrate in the subcutaneous tissue in the form of nodes or their chain, as well as spilled gummime foci. The foci are located superficially coated with atrophic, thinned skin, the foci are opened to the formation of single fistula or ulcers, as well as their combinations. After opening, the bright red or red-purple color of the affected fabrics is characteristic. In the pus separation, the crust closes the fistula or the surface of the ulcer is formed. The process is inclined to spread to new fabric sites. After healing of foci on the skin, the characteristic atrophic scars of the star form are formed.
Dissimiliated miliar tuberculosis of the face - the emergence on the skin of the face and neck of small painless nodules of red or brown color, which can be ulcerated and heated with the formation of a scar or without a trace.
Rosaceao-like tuberculoid - against the backdrop of rosacea-like redness and teleangio-extasses, pinkish-brown papules arise, rarely with pustulas in the center. The sprinkled pustulas are covered with crust, heal with the formation of a scar.
Papul-necrotic tuberculosis. Soft rounded papules with a diameter of 2-3 mm are formed on the skin with a diameter of 2-3 mm, ultery, cyanotic brown color. In the center of Papula may form a pustula containing necrotic masses driving in crust. Perifocal inflammation is observed around the papula.
Defeat Tuberculosis salivary glands It is relatively rare. Tuberculosis bacteria spread to the hematogenic gland, lymphogenically or less often - contact path. The process is often localized in the parole iron, and there may be a focal or diffuse lesion, with a tuberculosis of the lifting gland - only diffuse. The clinically disease is characterized by the formation of dense, painless or weakly heated nodes. Over time, the skin is soldered above them. On the site of the breakthrough of the thinned area of \u200b\u200bthe skin are formed by fistula or peptic surfaces. From the fiber of the gland, the selection of saliva is scarce or not. When decaying the focus and hinders of its contents in the duct in the saliva appear flakes. Sometimes paralysis of the Mimic muscles from the affected side may occur.
With radiography in the projection of the salivary gland in the chain of lymph nodes, foci of occurrence are detected. In the sialography, there is a blurry of the drawing of gland ducts and individual strips corresponding to the resulting cavities.
Tuberculosis jawsit occurs secondly, as well as due to the contact transition from the oral mucosa. Accordingly, it is distinguished by: a) damage to the bone in the primary tuberculous complex; b) damage to the bone with the active tuberculosis of the lungs.
Jaw tuberculosis is observed more often with lung damage. It is characterized by the formation of a single focus of bone resorption, often with a pronounced periosal reaction. On the upper jaw, it is localized in the area of \u200b\u200bthe under-judicial edge or the zickthrower, on the bottom - in its body or branch.
Initially, the tuberculous focus in the bone is not accompanied by painful sensations, and as they spread to other parts of the bone, periosteum, soft tissues appear pain, inflammatory contracture of chewing muscles. When moving a process from the depth of bone to the adjacent fabric, infiltration is observed, smelling the skin with subjectable tissues, the change in its color from red to bluish. One or more cold processes are formed, which are prone to spontaneous autopsy with a watery exudate separation and lumps of cotton decay, launched with affected bone, have multiple fistulas with sputtering granulations. Their probing allows you to detect the focus in the bone filled with granulations, sometimes small dense sequesters. Slowly such foci are completely silt, leaving drawn, atrophic scars; Fabric decreases, especially subcutaneous fiber. More often, the fistulas are preserved for several years, and some fistulas are scarceed, and new people arise near.
The radiograph is determined by the resorption of the bone and single intracerene foci. They have clear boundaries and sometimes contain small sequesters. With the prescription of the disease, the intraosteous focus is separated by the sclerosis zone from a healthy bone.
Diagnosis. The diagnosis of the tuberculosis of the maxillofacial region is composed of a number of methods and primarily from tuberculinidiagnostics, which allows you to establish the presence of tuberculous infection in the body. Tuberculin solutions are used in various techniques (manta samples, pirk, koch). Conduct a general study of patients with the use of radiological methods of the study of the lungs. In addition, it is investigated by MAKS from foci, prints of cells from an ulcers, distinguish cultures to detect tuberculosis bacteria.
Differential diagnosis. The primary and secondary lesion of lymph nodes should be differentiated from abscesses, lymphadenitis, chronic osteomyelitis of jaw, actinomycosis, syphilis, as well as malignant neoplasms.
Crofoferma is differentiated from the skin and subcutaneous forms of actinomycosis, cancer tumor.
The damage to the tuberculosis of the jaw bone should be differentiated from the same processes caused by global microbes, as well as malignant neoplasms.
Treatmentpatients with a tuberculosis of the maxillofacial region are held in a specialized hospital. General treatment should be complemented by local: hygienic content and sination of the oral cavity. Operational interventions are carried out strictly according to the testimony: with the clinical effect of treating and eliminating the local process in the oral cavity, in bone tissue. Output intraosseous foci, scraps screamed from them, sequesters are removed, the fistulas are excised and crushed into the ulcers or refresh their edges for healing by tissue with a secondary tension under a tampon from iodoform gauze. Teeth with affected tuberculosis periodontal are necessarily removed.
Forecast With a timely conducted with general anti-tuberculosis treatment favorable.
Prevention. The use of modern methods of treatment of tuberculosis is the main in the prevention of tuberculous complications in the maxillofacial area. Caries and its complications, diseases of the mucous membrane and periodontal should be carried out.
SYPHILIS
Syphilis is a chronic infectious venereal disease that can affect all organs and fabrics, including the maxillofacial area.
Etiology. The causative agent of syphilis is a pale treponema (spirochete), a spiral microorganism, 4..14 μm long, 0.2..0.4 μm wide. The human body develops as an optional anaerob and is most often localized in the lymphatic system. Spirochete has a small resistance to external factors.
There is no congenital and acquired immunity to syphilis.
Pathogenesis. Syphilis infection occurs in sexual path. Pale treponem falls on the mucous membrane or on the skin, more often when violating their integrity. Infection can also occur in a non-flowing path (household syphilis) or intrauterine from the patient of the mother.
Clinical picture. The disease has several periods: incubation, primary, secondary and tertiary. With congenital syphilis, specific changes are observed in the tissues of the maxillofacial region.
The primary period of syphilis is characterized by the appearance on the mucous membrane, including in the oral cavity, primary syphil or solid Shankra. In the secondary period of syphilis, the mucous membrane of the oral cavity is most often affected, pustular and rose-sized elements are formed.
A rare manifestation of syphilis in the secondary period is the defeat of the periosteum. It is characterized by a slow and sluggish flow. The thickened periosteum acquires a test consistency, but the perception of an eye is not formed. Gradually, the velocity seals are compacted, flat elevations arise.
The tertiary period of syphilis is developing in 3-6 years and more after the start of the disease and is characterized by the formation of the so-called gum. Gumma can be localized in the mucous membrane, periosteum and bone jaw tissue. The manifestations of syphilis in the tertiary period arise not always, in connection with this, the manifestal or hidden tertiary syphilis is distinguished.
When the syphilitic gumm is formed, a dense painless node appears at first, which over time is revealed with the rejection of the gummime rod. The ulcer occurred has a crater shape, with a painless palpation. The edges of it are smooth, dense, bottom covered with granulations.
The syphilitic lesion of the language is manifested in the form of a gummime glossite, diffuse interstitial glossite.
The defeat of the periosteum in the tertiary period of syphilis is characterized by diffuse, dense infiltration of periosta. Next, the thickened periost is soldered with the mucous membrane, and in the field of the body of the jaw - with the skin; Gumma softened and revealed out with the formation of fistula or ulcers in the center. A ulcer on an assault jaw gradually wars, leaving on the surface of the thickening, often rolic-shaped form. Teeth can be involved in the process, they become painful and movable. The process of the appaulus can go to the bone.
Changes in bone tissue in the tertiary period of syphilis are localized in the area of \u200b\u200bjaws, nasal bones, nasal partitions. The process begins with the thickening of the bone increasing as the gum is growing. The patient is disturbed by severe pain, sometimes a violation of sensitivity in the field of branching of the chore, under- and superlord nasticultural nerves. In the future, Gumba germinates in one or several places to the periosteum, mucous membrane or leather, is revealed out, forming fistula. The sequesters are not always formed, they are small. Only the joining of the secondary global infection leads to the term of more significant bones. In this case, on the upper jaw it is possible to form messages with the cavity of the nose and the maxillary sinus.
After the decay of the gum in the bone there is a gradual healing of tissues with the formation of coarse, dense, often tightening scars. Exostositions, hyperostosis develop in the bones.
The radiological picture of gummime bone lesions is characterized by foci of destruction of various sizes with clear even edges surrounded by a sclerosic bone tissue.
Diagnosis. The clinical diagnosis of syphilis is confirmed by the Vasserman reaction and other serological reactions. An important importance is microbiological research, as well as a morphological study of the affected tissues.
Differential diagnosis Syphilitic lesions of the oral cavity, teeth and jaws are certain difficulties. The peptic form of primary syphils on the lip can resemble a split cancer tumor. The gum of the oral mucosa of the oral sheath has common symptoms with traumatic ulcers. Gummime glossy should be differentiated with a tuberculosis ulcer, cancer defeat.
Syphilitic lesions of the periosteum and bone tissue should be distinguished from non-specific and specific lesions of these tissues. The gummime process in the bone can simulate cancer or sarcomatous diseases.
Treatmentsyphilis is carried out in a specialized venereological hospital.
Under the damage to the syphilis of the bone tissue of the jaws, periodic studies of the electrically excavability of the teeth pulp are appropriate, according to the testimony - the trepanation of teeth with the deceased pulp and treatment on the principle of chronic periodontitis therapy. Do not remove moving teeth, after the treatment, they are well strengthened.
Active surgical treatment with the defeat of the periosteum of jaws during syphilis is not shown even in the case of the formation of sequesters. They are removed after specific treatment against the background of the thorough process.
The hygienic content of the oral cavity is important. Dental stones are removed, sharp the sharp edges of the teeth are made, the oral cavity is carried out.
Forecast With timely diagnosis, proper treatment and further dispensary observation is mainly favorable.
Prevention. In the prevention of syphilis, except for its social aspect, the hygienic content of the oral cavity, the warning of cracks and erosions in it is important.
USED \u200b\u200bBOOKS:
1) "Surgical dentistry" - ed. Robustova. M. Medicine, 1996 from. 295-308.
2) "Surgical dentistry" near Ed V. A. Dunaevsky - M. Medicine, 1979. from. 221-224
3) "Guidelines for Maxillofacial Surgery and Surgical Dentistry" - A.A.Timofeev. Kiev, "Chervona Ruta-Tours", 1997. from. 345-350.
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