LATERAL AND NEODONTOHENNI ABSCESSES SCHLD. ACUTE AND CHRONIC, AND NEODONTOHENNI ODONTOGENIC LYMPHADENITIS SCHLD.
The Clinic of Maxillofacial Surgery abscesses and phlegmon of the maxillofacial area and neck, the frequency of its occurrence, is one of the first places. In recent years, the number of patients with this disease has increased significantly, increased the severity of the process, which often leads to severe complications such as mediastinit, sepsis,venous thrombosis face and sinuses of the brain (NA Gruzdev, 1978 I. Kuzin et al., AG Shargey-port, 1985 AA Timofeev, 1988, 1999).
Over the past 20 years the number of patients with abscesses and phlegmon, according to the clinic increased by 16%. Value abscesses (by which to understand cavity filled hnoem and separated from the surrounding tissue pyogenic membrane) and abscesses (not clearly differentiated acute purulent inflammation of the tissue) is 4:1. Share an opinion MM Soloviev (1979) on the need for another form of inflammation of the soft tissues – the so-called cellulite, ie serous inflammation of the soft tissues. This disease we call inflammatory infiltrate.
It has long been attempts to classify inflammatory processes on their location, the nature of changes in bone and depending on the source of infection.
In terms of practical dentistry as a basis for classification of inflammatory processes appropriate to adopt the scheme of AI Evdokimov (1958), which is based on the principle of topographic anatomy (Fig. 10.4.1). Under this scheme, ¬ si abscess and phlegmon of the maxillofacial area and neck are divided into:
• abscesses and cellulitis, located near the upper jaw (pidochna, skulova and orbital region, temporal, and Infratemporal pterygopalatine fossa, solid and
soft palate);
• abscesses and cellulitis, located near the lower jaw (chin, buccal and submandibular regions, pterygoid-mandibular, and navkolohlotkovoho submasseterialnoho space area parotid salivary gland and fossa pozaduschelepnoyi);
• abscesses and cellulitis floor of the mouth (upper and lower);
• abscesses and cellulitis language and neck.
In terms of anatomical and topographical localization of odontogenic abscesses and abscesses GA. Vasilyev and T. Robustova (1981) conventionally divided them into 2 groups.
/. Navkoloschelepni abscesses and cellulitis:
1) tissue adjacent to the mandible, 2) tissue adjacent to the upper jaw. Each of these groups is divided into:
• surface (a-pidochna, buccal, b-submandibular, pidpidboridkova, parotid-masticatory regions);
• depth (a-Infratemporal, pterygopalatine fossa, b-pterygoid-mandibular and navkolohlotkovyy space hyoid region, the bottom of the mouth).
/ /. Abscesses and cellulitis neighboring tissues navkoloschelepnymy areas where suppurative process spreads within (zygomatic, temporal region of the orbit, behind-the jaw area, neck), abscesses and cellulitis tongue.
Location of the abscess:
-submandibular
-submental
– hyoid
-areas of the surface and deep space
– parotid-masticatory
– buccal region
– infratemporal fossa
– temporal area
NA Gruzdev (1978) considers reasonable use of the term “osteoflehmon”, relating it to cellulitis, concomitant osteomyelitis, the term “phlegmonous adenitis” means phlegmon, complicated by suppurative lymphadenitis, which may be associated with a disease of the teeth, under the “odontogenic phlegmon” understand phlegmon that has developed on the basis peryodontitu and periostitis, with a change in bone inflammation are reversible.
IM Mukovozov (1982) points to the feasibility of dividing all processes purulent maxillofacial region abscesses and cellulitis, and the latter in turn – on osteoflehmony, phlegmonous adenitis and odontogenic cellulitis.
Depending on the source of infection of inflammatory processes of the maxillofacial area and neck U. Vernadsky (1985) divides into 8 groups: Odontogenous – the reason for their occurrence is gangrenous teeth and their roots intraossalni – resulting from periostitis, osteomyelytov, difficulty eruption of wisdom teeth, sinusitis, cysts, etc.; hinhivalni – their development is associated with the presence of periodontitis , gingivitis, flour-stomatohenni – due to the presence stomatitis, glossitis, salivatornoy – resulting sialodohitov, sialoadenity; tonzillyarnaya-pharyngeal, and rynohenni Otogenic.
In my opinion, all abscesses and phlegmon of the maxillofacial area and neck enough to split depending on the source of their origin into two groups: odontogenic and neodontohenni. In odontogenic routes of infection are the main cause of diseases of hard tissues of the tooth, periodontal and bone. Wheeodontohennyh inflammatory processes associated with the onset of mechanical trauma, infection of tissues during anesthesia, tonsillitis, otitis, ¬ rini Volume etc.
On the severity of illness of patients with phlegmon is divided into three groups: Group 1 (mild) – patients with cellulitis, localized in the same anatomical area, 2 nd (moderate) – patients with cellulitis, localized in two or more anatomical regions 3-a – seriously ill with soft tissue phlegmon floor of the mouth, neck, half of the face and blend cellulitis temporal region of the infratemporal and pterygopalatine holes.
Clinically, in case of abscesses observed induration, which is accompanied by swelling of the face and neck. Over the area of abscess often appears be ¬ flushing of the skin. If the suppurative process is located in the deep parts of the maxillofacial region (pterygoid-mandibular and okolohlotochnoe space and pterygopalatine fossa double ¬ juicy, etc.), the inflammatory changes in the skin are missing.
An important feature of an abscess is a symptom fluctuations. It is the result of the presence of pus enclosed in the cavity with elastic walls, which transmit impulse from one wall in all directions. This symptom is not available for the localization of abscesses in deep water, especially under a layer of muscle.
When purulent inflammation of the soft tissues of the maxillofacial area and neck clinical symptoms of intoxication usually expressed moderately and weakly developed in the process they may be missing. It is a feature of how abscess purulent process, separated from the surrounding tissue pyogenic membrane – the inner wall of the abscess, granulation tissue lined. Pyogenic membrane separates purulent-necrotic process and produces exudate. The ability of the surrounding soft tissue granulation to create the shaft is a manifestation of the normal defense response aimed at spreading purulent inflammation of the day, as well as a manifestation of nonspecific reactivity, defined as a normal physiological systems of the body healthy. In the tissues of the maxillofacial region pyogenic membrane is thin and not always clearly defined.
Odontogenous abscesses often localized in podhlaznychnoy, buccal, zygomatic, blyzkovushnoyi, pidpidborodochniy and during mandibular areas pterygoid-mandibular space, pterygopalatine fossa, oral and lingual grooves and less in other areas navkoloschelepnyh soft tissues. Unlike abscess, phlegmon is spilled in the spread of the inflammatory process. Odontogenous cellulitis are characterized by the same local and general symptoms that are observed in odontogenic abscesses, only in a more severe degree. Local features include: extensive soft tissue swelling, redness of the skin and diffuse, dense infiltrate painful. In the distance there is a further ¬ fluctuation. Spontaneous pain increases, an increase in local temperature. Disrupted function of swallowing, chewing and speech, and in some cases even breathing. Severity of symptoms depends on the local severity of inflammation and purulent foci localization.
AA And PY Maksymenko Stolyarenko (1976) indicate a violation of lung function in patients with purulent-inflammatory diseases of soft tissues, the degree of which depends on the location and spread of the inflammatory process. Thus, the localization of abscess in the jaw, and zygomatic regions pidochnoyi impaired respiratory function recovered within 1-2 days after opening purulent focus, infratemporal and open ¬ lonebnoy holes, temporal region – 5 days; pterygoid-mandibular space and submandibular region – through 5 -7 days.
VA Olszewski et al. (1982) noted a change in soft tissue blood flow in patients with acute odontogenic pathological processes in the area of focus: reducing the rate of blood flow, impaired venous drainage. A day after the operation section venous stasis ulcer is increased by increasing the outflow tissues. Improving all reohrafichnyh performance takes place on the seventh day after surgery.
Odontogenous abscesses and cellulitis often accompanied by severe intoxication body: high body temperature (up to 39-40 (C), leukocytosis, neutrophilic left shift, eosin-singing (aneozinofiliya), ESR high numbers (up to
In phlegmonous adenitis development of the inflammatory process occurs more slowly and is characterized by infiltration of tissues and increase the formation of purulent exudate. If an inflammatory process preceding the previous microbial sensitization of the patient to staphylococcus, streptococcus, E. coli and other microorganisms, the development of phlegmonous adenitis occurs rapidly and is characterized by aggressive flow, which complicates the differential diagnosis of phlegmonous adenitis odontogenic phlegmon.
Differential diagnosis delineated and spilled inflammatory ¬ owls in the early stages of inflammation is quite a difficult task, since the early period of its development abscess and cellulitis are most similar to clinical symptoms and laboratory parameters of blood. We use the following method for differential diagnosis of abscesses and abscesses: first time taking a drop of blood from the finger, the center of the inflammatory infiltrate and on its borders, and then determine in each sample of white blood cells contained in 1 ml of blood, and smears prepared for counting blood counts that stained by Romanovsky-Himzoyu and to determine the leukocyte alkaline phosphatase (ALP activity to identify leukocytes). While increasing the number of neutrophils (more than 2.2 times) and index leukocyte alkaline phosphatase activity (30 arbitrary units) in the center of the inflammatory lesions, and on its borders (against local leukocytosis), compared with blood samples taken of thumb, set the diagnosis of diffuse inflammatory process – cellulitis (auth. testimony. N412012 from 1986). This makes it possible to clarify the diagnosis and his ¬ temporarily assign adequate treatment (AA Timofeev, 1983).
Symptoms neodontohennyh abscesses and phlegmon of the maxillofacial region is virtually identical to the clinical manifestations of these processes odontogenic origin, making it difficult differential diagnosis. Important role in establishing the correct diagnosis plays carefully collected history. The first step is to determine whether or not preceded by an inflammatory disease process thoroughly examine your teeth and mouth to detect the presence of teeth and various infections of odontogenic lesions (abnormal tooth-gingival pocket, on alveolar fistula from ¬ sprouts, pericoronitis, painful thickening of the alveolar process, infiltration by re ¬ tion crease, periodontitis, etc.). Particular attention should be given to X-ray examination of the jaws conducted to determine pathological changes in bone-related diseases of the teeth. It is necessary to conduct differential diagnostics ¬ tion of abscesses and abscesses of odontogenic origin with boils and carbuncles person, erysipelas, acute inflammation of the salivary glands, suppuration cysts of soft tissue.
When boils developing acute purulent-necrotic inflammation of the hair challenge ¬ likula and surrounding connective tissue. Carbuncle is diffuse purulent-necrotic inflammation of the skin and subcutaneous fat, which comes from several hair follicles and sebaceous glands. Thus, the main difference boils and carbuncles from odontogenic abscesses are no odontogenic lesions and the presence of purulent-necrotic cores (ris.10.2.1).
When beshysi person inflammatory process captures only the layers of skin, and due to odontogenic source is not. On the face there is severe congestion area with clear boundaries, which towers above the healthy skin. With its shape resembles erysipelas pictures “flames” can wonder symmetrical facial skin (ris.10.4.2).
The symptoms that distinguish odontogenic phlegmon of calculous and non-calculous sialoadenitiv are: selection for sialoadeniti with duct glands pus in the presence of salivary duct stones in the major salivary glands can be defined palpator-no, radiography of soft tissues of the oral cavity bottom vprykus reveals salivary stones in the submandibular gland.
The difference nahnyvayuchyh soft tissue cysts of odontogenic abscesses is that wheahnyvayuchyh cysts of history can establish that the inflammatory process is preceded by the appearance of education myahkoelastychnoyi consistency. If you can puncture the cyst fluid contents. In the mouth odontogenic source of ignition is not detected.
In the literature, there is evidence that the long-recognized along with aerobic and facultative pathogens abscesses and phlegmon of the maxillofacial region, such as staphylococci, streptococci, gram-negative bacteria and other microorganisms, increasingly as an etiological factor of these diseases are the anaerobic Nekla-stridialnye microbes – bacteroids, veylonelly, peptokokki et al.
Mal.10.4.2. Appearance patients with erythematous form of erysipelas person (two-a-, b – one-way)
According to AG Tyshko et al (1984), bacterial infection deserves special attention of clinicians not only because of the high percentage of human pathology, but also because of the diversity of clinical manifestations caused by the localization process, pathogens and species composition as the patient.
On the basis of our microbiological studies found that the most common odontogenic lesions were seeded monoculture Staphylococcus (47.6%) and epidermal (33.3%), staphylococci, rarely – strep (19.1%).
Microorganisms are sown with purulent lesions in patients with odontogenic abscesses were both aerobic (94.5%) and anaerobic (5.5%) microflora. Monocultures of bacteria occurred more frequently (in 92.7%) than their association (7.3%), among aero ¬ bov most frequently encountered Staphylococcus (52.9%) and epidermal (19.7%), staphylococci, rarely – strep (11.8%), gastrointestinal (5.9%) and Pseudomonas (5.9%) coli, Proteus (3.8%). Playing ¬ motritsatelnye anaerobes (veylonelly, bacteroids) and Gram-positive anaerobes (eubacteria) were only associative links with aerobic microbes.
In patients with odontogenic phlegmon in septic foci detected not only aerobes (in 78.8%), but anaerobes (21.2%). Microorganisms were both in monoculture – 67.5% (-56.7% aerobes, anaerobes – 8.8%) and in associations – 32.5% (aerobic – 20.0%, anaerobes – 2.5% aerobes and anaerobes – 10.0%). Aerobic and are golden staph ¬ epidermal we Escherichia coli, hemolytic streptococci, enterococci, Proteus and dyplokokkom. Among the Gram-negative anaerobes met (bacteroids, veylonelly) and gram (peptostreptokokky, eubacteria). In monoculture gold plated and Staphylococcus epidermidis, veylonelly, peptostreptokokky and eubacteria.
Thus, in patients with limited odontogenic inflammatory processes in soft tissue purulent foci were detected most frequently monoculture aerobic microorganisms that are mainly Gram-positive microbial (Staphylococcus epidermidis and Staphylococcus, Streptococcus) and rare – hramvid’yemnoyu microorganisms (Escherichia and Pseudomonas aeruginosa, Proteus). Anaerobes, the current limi ¬ inflammatory processes of the soft tissues were always in association with aerobes. Patients who have lesions with purulent sown association of aerobic and anaerobic microorganisms were particularly severity of the disease, severity of general and
local clinical symptoms. In diffuse purulent processes of the soft tissues, which were located in the same anatomical region (usually phlegmonous adenitis) found monoculture microorganisms in patients with cellulitis, which had two or more anatomical regions (floor of the mouth, face half) – monoculture anaerobes, associations only anaerobov, associations of different types of aerobic and anaerobic and aerobic bacteria.
Determination of antibiotic showed that staphylococci crop, sown in patients with limited odontogenic purulent-inflammatory diseases of soft tissues ¬ we are sensitive to most of the antibiotics studied. In the penicillin group of drugs they were resistant to potassium and sodium salt of penicillin and were sensitive to the semisynthetic penicillins (methicillin, ampicillin, ca-satsillinu, karbenitsyllinu), as well as antibiotics protystafilokokkovyh reserve (erythema ¬ romitsyn, oleandomycin, lincomycin, ristomitsin). Showed little sensitivity to aminohlikozidnyh antibiotics (gentamicin, neomycin, monomitsin, kanamycin).
Staphylococci in association with aerobes had changed their antibiotiks, and anaerobes – are sensitive only to the aminoglycoside drugs tsefallosporyniv and TIYENAMU ®.
In patients with diffuse purulent inflammation of soft tissue monoculture staphylococci showed sensitivity to aminoglycoside drugs, cephalosporins Tien ®, and to a lesser extent – to the semi-synthetic penicillins and antistaphylococcal antibiotics reserve. In association with aerobes antibiotiks staphylococci significantly decreased, and anaerobes – staphylococci were resistant to all antibiotics except Tienamu.
In considering the pathogenesis of acute odontogenic inflammatory diseases of soft tissues, we tried to figure out where is formed pus, which we find in bilyaschelepnyh soft tissues. In the literature there are different opinions. The theoretical possibility of mechanical spreading manure from the tooth socket bone marrow space of the mandible and soft tissue navkoloschelepni confirmed by experimental studies AM Vasilenko (1966). However, this mechanism is difficult to explain why most of the signs of acute inflammation in soft tissues bilyaschelepnyh appear almost simultaneously with signs of acute inflammation in periodontal disease. GA. Vasiliev (1973) believes that the infectious process spreads from odontogenic foci in the soft tissue around the lymph vessels. In the opinion of M. Soloviev and I. Hudoyarove (1979), abscess formation in soft tissues around the jaw is not due to the breakthrough of pus under the periosteum over the bone defect and the formation of pathological focus “own” pus under the influence of microorganisms, bacterial toxins and products of tissue decay that penetrated here along the vessels that are in the channels of compact bone substance.
To elucidate the mechanism of formation of pus we studied its morphological composition in patients with this pathology. Cytological examination of the purulent exudate found that when purulent lymphadenitis and phlegmonous adenitis he has degenerative modified segmented neutrophils, lymphocytes, monocytes, macrophages, eosinophils isolated, basophils and plasma cells. A significant number of typical and atypical forms of lymphocytes (up to 20-26 pieces. Counted per 100 cells in the smear) indicates that the abscess comes from the lymph node. In patients with odontogenic abscesses in pus are degenerative change segmented neutrophils, monocytes, macrophages, and cells of lymph single row, eosinophils, plasma cells. Patients with purulent exudate odontogenic phlegmon was introduced almost one degenerative modified sehmentoneytrofilamy. In blood smears were found isolated monocytes, macrophages and lymphocytes. Noted law that the heavier the abscess process proceeded, the less related degenerative modified segmented neutrophil cells we met (until their complete absence).
Thus it was found that patients with purulent exudate of acute odontogenic inflammatory processes of soft tissue represented only blood cells. Bone marrow cells, unlike EK Zelentsova (1948), the pus we have found. This, in my opinion, proves correct assumption MM Soloviev and I. Hudoyarove (1979) that acute odontogenic inflammatory processes in bilyaschelepnyh soft tissues formed “a” pus and its formation is not associated with mechanical “breakthrough” (spread) from the hole in the bone marrow of the tooth space bottom navkoloschelepni jaw and soft tissue.
It is noted that the presence of mixed wound infection promotes ana ¬ erobnyh bacteria as aerobes, absorbing oxygen, promote the development of anaerobes (IG Rufanov, 1948 I. Kuzin et al., 1981, V. et al Struchkov ., 1984).
Clinical disease caused by anaerobic infection is particularly severity and lack of positive dynamics of the process, even with adequate drainage of the inflammatory foci. It is characterized by rapid growth, etc. ¬ intoxication symptoms, patients have tachycardia, disturbances of microcirculation. The general pro ¬ phenomena infection caused by anaerobes asporohennymy refers subikterichnist sclera and yellowness of the skin, anemia, significant leukocytosis and high ESR. Signs participate in the infectious process anaerobes can be considered bad fluid, a large number of necrotic tissue in septic foci, dirty-gray pus from the presence of fat droplets in it. Reproduction Bacteroides you may be accompanied by dividing ¬ gases that contribute to more light penetration of bacteria beyond the inflammatory foci. Increased pressure in the tissues of the pathological focus more on ¬ touched by circulation, contributing to the development of hypoxia and anaerobic microorganisms. After the operation the wound separates small amount ihoroznym fetid pus. Muscles look like boiled meat. When participating in inflammatory processes of bacteria species melaninohenikus selection wounds often dark or brown color. Typically used to treat antibiotics are ineffective.
Dangerous manifestations of anaerobic infection is septic shock, which causes extremely high (50-70%) mortality (Y. Shaposhnikov, 1984). There is the development of septic phlebempraxia not only near the site of infection, but also in distant cities – in the lungs, brain, liver, joints and other areas.
The clinical picture is not always possible to distinguish infections caused by anaerobic microflora of putrefactive anaerobic infection caused by Escherichia coli, Proteus and other organisms (EA Reshetnikov, 1984). In all cases of severe course of acute inflammatory process should take a piece of necrotic tissue for bacterioscopic and biological research.
SN Efuni et al (1981) believe that making sampling secretions and tissues, cha ¬ a muscle of the lesion should be on the slides. Then the glass to dry over a flame burner to cool for a minute and paint smears with methylene blue. After their washing and re-drying author recommends microscopy preparation. The presence of a small amount of “gross” rods located between muscle fibers fragmented, there is evidence of participation of anaerobic microorganisms in the inflammatory process. Fence pus to identify anaerobes produce into special transport medium (AG Tyshko et al., 1984).
Me studied the local and general non-specific resistance of patients with this pathology. Found that acute odontogenic lymphadenitis refers only to a slight decrease levels of lysozyme in saliva mixed against unmodified general nonspecific resistance and secretion of mixed saliva, large and small salivary glands. Lymph node abscess occurs when further reducing the content of lysozyme in mixed saliva and in blood and secretion of mixed saliva. Odontogenous abscesses develop in an even greater decrease in both local immunity – mixed saliva lysozyme and total nespetsifi ¬ Czech resistance – lysozyme levels, and reducing the number and secretory function of minor salivary gland secretion of mixed saliva. Odontogenous cellulitis observed in patients with a significant decrease in the level of lysozyme mixed saliva and blood, further reducing the secretion of mixed saliva and major salivary glands, and the number and function of minor salivary glands (AA Timofeev, 1988).
After the medication level of lysozyme in mixed saliva and blood is restored not earlier than 2-4 weeks after discharge patients (depending on the severity ¬ sti disease).
Thus, the author found that purulent-inflammatory diseases of soft tissues occurring against a temporary immune deficiency – low lysozyme content of saliva and blood persists traditional medical treatment and requires the appointment immunokorehuyuchoyi therapy.
We determined the pharmacokinetics of antibiotics in the blood and tissue inflammatory foci maxillofacial area and neck while its intramuscular administration in patients with acute odontogenic inflammatory diseases. Found that all persons within 4-6 hours after drug administration creates therapeutic concentration in the blood. In the altered inflammatory soft tissue pathological focus antibiotic
not penetrate at all or there created such a concentration that is well below the prevailing minimum dose. This indicates a general lack of effect of antibiotic therapy in the treatment of patients with this pathology. Therefore, we faced the question of whether antibiotics in patients with acute serous odontogenic lymphadenitis, with inflammatory infiltrates and purulent-inflammatory diseases of soft tissues. Moreover, antibiotics, we found that further inhibit nonspecific resistance. Therefore, the treatment of all our actions are aimed at improving the defenses of the patient (AA Timofeev, 1988) through immunocorrective lizotsymom therapy.
Phlegmon of the orbit – Acute diffuse purulent inflammation of orbital fat with its purulent melting and necrosis.
What triggers phlegmon of the orbit:
Cause:
· Injury orbit with infikuvannyamtkanyn pyogenic microbes;
· Introduction into the orbit of infected foreign bodies;
· Suppurative processes in the face – boils, erysipelas, barley;
· Purulent dacryocystitis, cellulitis century, purulent sinusitis;
· Common infection (influenza, scarlet fever, typhoid).
The process is often developed to extend the field of v. angularis thrombophlebitis small orbital vessels, which leads to the formation of many small pustules, which then gradually merge into one or Several major abscesses, cellulitis of the orbit may occur as a result of the spread of purulent process from a neighboring cell to retrobulbarno fiber (broken subperiosteal abscesses).
Symptoms of orbital phlegmon:
The process is usually unilateral. Acute onset: inflammation develops suddenly and rapidly (within hours or 1-2 days). Pain in the eye and eye socket, headache. Pain aggravated by palpation and eye movements. Hyperemic eyelids, swollen and tense, almost impossible to open them. The general condition of severe fever, weakness. Fast-paced limited mobility of the eyeball and exophthalmos. In cases where the development of cellulitis or abscess preceded osteitis walls of the orbit, the possible displacement of the eyeball, the direction of displacement of the eye may help to identify the pathogenesis process. With the development of inflammation appears hemoz conjunctiva of the eyeball, edematous mucosa falls out, the eyelids, exophthalmos increased, the eyeball becomes almost motionless, eyes sharply reduced. Among the speakers forward edge of the eye and orbit can test the swollen orbital contents.
In engaging in inflammatory optic neuritis develops its dominated by stagnation and retinal vein thrombosis. As a result of trophic disorders caused by pressure oerves, sometimes develops purulent keratitis and corneal ulcer. Inflammation can go to the choroid and retina and cause purulent horioydit and panoftalmit result in atrophy of the eye.
In the separation process in the orbital abscess formed, which can inadvertently reveal the skin or conjunctiva. Inflammation can go to the meninges and venous sinuses (cavernous sinus) or may develop sepsis. In such cases, possible death.
Diagnosis of orbital phlegmon:
Diagnosis is based on characteristic clinical picture. The rapid onset, rapid progression and severity distinguish phlegmon of the orbit tenonita. Required radiography of the paranasal sinuses and orbit, which is important for the differential diagnosis of orbital cellulitis orbital periostitis wall and to exclude foreign body in the eye socket injury.
Prevention of phlegmon of the orbit:
Timely and proper treatment of various inflammatory processes in the face of chronic processes in orbit, with infected wounds it – vigorous treatment with antibiotics and sulfonamides.
Treatment
The main method of treating abscesses eye socket is a fairly wide opening cavity boil for emptying. When you perform an access to the boil perform skin incision along the upper eyelid or lower outer edge of eye socket to the bone and stupidly pushing the tissue penetrating between the wall of the eye socket bone and the eyeball in the center of the inflammatory foci. If the spread of purulent process of the maxillary sinus discharging boil carry through an open maxillary sinus with simultaneous perforation of the upper wall of the bone in its distal part. For 1-2 weeks. The wound from the mouth sewn tightly and put rynostomu. Drainage of purulent wounds when opening abscesses orbital plots carried supple perforated drainage pipe or napivtrubkoyu. Active drainage of purulent foci do not make enough to wash it 2-3 times a day with antiseptic solutions.
Displaying antibiotics orally, intramuscularly and intravenously in severe cases. Intramuscular – benzylpenicillin sodium salt of 500 000 units 4 times a day, methicillin sodium salt of 1-
Abscesses and cellulitis which soft and hard palate abscess
In the soft palate or infection penetrates directly from
navkoloverhivkovoho fire upper third molar, or when
spreading of manure infratemporal or pterygopalatine fossa.
The severity of the clinical course is determined by the prevalence of cellulitis abscess
to other cellular spaces. Soft palate is much larger in
size, shifted towards a healthy, muscles it into a state of tension.
Treatment of cellulitis and abscess of soft palate surgery, conduct
Showdown at the place of greatest severity of abscess to drain injected
rubber strip.
Abscesses palate resulting distribution
infection within areas near the apical lesions of teeth of the upper jaw, the roots of which are located closer to the palatal surface of the alveolar ridge / second incisor, first molar palatal root /. The clinical course is characterized by pustules palate intense pain, because in this area there is no submucosal layer of loose and dense plum shell peeled from the bone with the periosteum. For the same reason there are often difficulties in implementing proper drainage: elastic, thick wound edges closer together and eliminate drainage strip. To avoid delays manure recommend carving small portion of tissue along the edge of the cut, ie yku of tissue along the edge of the cut, ie, to form drainage hole in the lining.
Abscesses and cellulitis infraorbital area.
Limits infraorbital area:
– Upper – lower edge of the eye socket
– Internal – lateral wall of the nose
– Lower – alveolar process of maxilla
– External – zygomatic – jaw bone joint.
On the upper wall perdniy jawbone are soft tissue. Each has its own facial muscles loose fascial sheath, and between them are thin layers of fat that spoluchayutsya together. Topographic – anatomical features infraorbital areas causing significant soft tissue swelling with inflammation. In ikloviy hole located nasolabial lymph node that receives lymph from the superficial parts of the face.
Cellular space infraorbital areas with iklovoyi holes through the infraorbital canal, combined with fiber eye socket. When the angular vein thrombophlebitis facial vein lesions undergo eye socket, which flow into the venous sinus skull.
Etiology and pathogenesis.
The main sources of infection are the upper incisors, canines, small molars. If the inflammatory process in the nasolabial lymph node having glandular (serous, purulent) periadenit or phlegmonous adenitis.
Klnichni manifestations. In the initial stage of phase inflammatory process localized in the anterior surface of the upper jaw and the upper jaw and upper lip, reminding acute suppurative periostitis. Further swelling of the upper lip increases and inflammatory infiltrate may extend to the entire infraorbital, buccal and zygomatic areas. Smoothed nasolabial furrow, raised wing of the nose, there is swelling of the upper and lower eyelids. Infraorbital skin hyperemic areas in the crease is not taken, the inflammatory infiltrate is higher than in acute periostitis. Because it can be irritating infraorbital nerve, which is accompanied by intense pain. Open your mouth is not broken, determine the pain during deep palpation in the area iklovoyi fossa.
Diagnosis. Unlike suppurative periostitis of the upper jaw, with abscess and phlegmon infraorbital area no smoothing (bulging) of the mucous membrane on a transitional fold. Inflammatory processes in the nasolabial lymph node differ vidmezhovanistyu, zatyazhnymperebihom, a tendency to retsedyviv if the lymph node is collapsed, was not removed.
Treatment. Surgical intervention for abscess and phlegmon infraorbital area is revealing purulent focus internally or pozarotovoyu cut. Deep boils are cut to reveal a transition skldatsi, hemostatic clamp pushing muscles, and held in iklovu hole. For surface localization process hnyinoho skin incision is carried out over the course of the nasolabial grooves or parallel nyzhnoochnoyamkovu edge. Purulent drainage is carried out by perforated elastic washing antiseptic substances ..
INTRODUCTION
Ludwig’s angina is a bilateral infection of the submandibular space that consists of two compartments in the floor of the mouth, the sublingual space and the submylohyoid (also known as submaxillary) space (figure 1). It was first described by the German physician, Wilhelm Frederick von Ludwig in 1836. This infection most commonly arises from an infected second or third mandibular molar tooth. It is an aggressive, rapidly spreading cellulitis without lymphadenopathy with potential for airway obstruction and requires careful monitoring and rapid intervention for prevention of asphyxia and aspiration pneumonia.
The anatomy, microbiology, clinical manifestations, imaging, and treatment of submandibular space infections (Ludwig’s angina) will be reviewed here. Other deep neck space infections are discussed separately. (See “Deep neck space infections”.)
DEFINITION
Although the term Ludwig’s angina has been loosely applied to a heterogeneous array of infections involving the sublingual and submylohyoid (submaxillary) spaces, this diagnosis should be restricted to the following classical description:
- The infection begins in the floor of the mouth. It is characteristically an aggressive, rapidly spreading “woody” or brawny cellulitis involving the submandibular space.
- The infection is a rapidly spreading cellulitis without lymphatic involvement and generally without abscess formation.
- Both the submylohyoid and sublingual spaces are involved.
- The infection is bilateral.
ANATOMIC CONSIDERATIONS
The submandibular space lies within the submental and submandibular triangles between the mucosa of the floor of the mouth and the superficial layer of the deep cervical fascia. It is subdivided by the mylohyoid muscle into the sublingual space (which contains the sublingual gland, hypoglossal nerve, part of the submandibular gland, and loose connective tissue) and the submylohyoid space (which contains the submandibular salivary gland and lymph nodes) (figure 1). The two divisions communicate posteriorly around the mylohyoid muscle. This accounts for the bilateral involvement by contiguous spread of infection within the submandibular space in Ludwig’s angina.
[Cause]
submental space infection is caused by what the?
space under the chin (submental space) located in the suprahyoid region, the submental triangle within a single space. A small amount of adipose tissue within the gap and lymph nodes, this gap for the mylohyoid muscle, the submental hyoid muscle and the sublingual space apart. Connected with the submandibular space on both sides, the infection spread easily with each other (Figure 1).
Figure 1 submental space anatomy
submental space infections come from the lymph node inflammation. Lower lip, tongue, floor of mouth, sublingual caruncle, mandibular anterior teeth and periodontal tissues of the lymphatic flow can be remitted directly to the submental lymph nodes, it is more than one region of inflammation, mouth ulcers, mouth under the chin can cause go far lymphadenitis and cellulitis secondary to the submental space.
[Symptoms]
submental space infection early symptoms?
submental space as much as the lymph nodes caused by infection, it is generally slow progression, early limited lymph node enlargement, obvious clinical symptoms. When extranodal spread to the lymph node inflammation, the gap was caused by cellulitis tissue inflammation, swelling extended to cover different time to the submental triangle development area, skin redness, pain. Abscess formation after local skin purple, palpable pressure fluctuations have pitting edema, and infection. Back when the infection spread to submandibular space, and can demonstrate the appropriate symptoms.
[Prevention]
submental space infection should be how to prevent?
prevention
lower lip, tongue, floor of mouth, sublingual caruncle, mandibular anterior teeth and periodontal tissue lymphatic drainage can be remitted directly to the submental lymph nodes, so the need to actively treat more than one region of inflammation, oral ulcers, mouth go far, avoid submental lymphadenitis, cellulitis and secondary to the submental space.
[Treatment]
submental space infection precautions before treatment?
abscess formation, swelling in the submental area to do the most prominent transverse skin incision, separated from the submental platysma of the gap and establish drainage.
submental space infection medicine treatment
No information
Western submental space infection treatment
No information
[Check]
submental space infection should be how?
oral examination.
obvious sense of deep abscess fluctuations, sometimes required by the puncture diagnosis.
[Confused]
submental space infection and the diseases easily confused?
detailed analysis of the history, combined with clinical and anatomical features, coupled with the biopsy, etc., is not difficult to make a correct diagnosis.
Abscesses of the second and third mandibular molars may perforate the mandible and spread into the submandibular and submental spaces. Ludwig’s angina is manifested by swelling of the floor of the mouth and elevation and posterior displacement of the tongue. A rapidly spreading gangrenous cellulitis produces a brawny edema of the suprahyoid region of the neck. The infection begins unilaterally but quickly spreads to include the entire neck. The most common presenting symptoms are oral, neck, and dental pain. In addition, there is neck swelling, odynophagia, dysphagia, dysphonia, trismus; and tongue swelling. Airway patency is the main concern. In many of these patients, it is impossible to introduce an endotracheal tube and therefore, tracheotomy under local anesthesia is the only way to ventilate them.
Submental space abscess, secondary to dental disease
Submental Abscess
Ludwig’s Angina.
LUDWIG’S ANGINA is an inflammation of the submandibular space, usually starting in the submaxillary space and spreading to the sublingual space via the fascial planes, not the lymphatics. As the submandibular space is expanded by cellulitis or abscess formation, the floor of the mouth becomes indurated and the tongue is forced upward and backward, causing airway obstruction. Ludwig’s angina does not necessarily mature to form an abscess, it is more likely to produce a cellulitis or a phlegmon. It is typically bilateral and presents with drooling, trismus, pain, dysphagia, submandibular swelling airway obstruction caused by displacement of the tongue. The tongue may protrude outside the mouth. This is a life-threatening condition that requires tracheotomy. Before antibiotics, the mortality rate of Ludwig’s angina was 50%. With modern antimicrobial and surgical therapies, the mortality rate is less than 5%.
This patient developed acute upper respiratory obstruction. The swelling became so severe that the tongue protruded outside the mouth. A tracheotomy was performed to provide an airway. After resolution of the infection, a large stone was found in the submandibular gland duct (Wharton’s duct). The radio-opacity in the occlusal film on the left represents the stone that was removed.
Stages of Infection
l I. Cellulitis
II.l Abscess
III.l Sinus Tract/Fistula
CELLULITIS
A painful swelling of the soft tissue of the mouth and face resulting from a diffuse spreading of purulent exudate along the fascial planes that separate the muscle bundles.
Abscess
l Well defined borders
Pus accumulation in tissuesl
Fluctuant to palpationl
Cellulitis – “spreading” infectionl
Abscess – “localized” infectionl
FISTULA
A drainage pathway or abnormal communication between two epithelium-lined surfaces due to destruction of the intervening tissue.
Management of Infection
Determine the severity of the infectionl
Evaluate the host defensel
Decide on setting of carel
Treat surgicallyl
Support medicallyl
Choose and prescribe antibiotics appropriatelyl
Evaluate patient frequentlyl
Severity of Infection
Rate of progressionl
Potential for airway compromise or affecting vital organsl
Anatomic location of infectionl
HISTORY
Duration of infectious process.l
Sequence of events and changes in symptoms or signs.l
Antibioticsl prescribed, dosages and responses.
Review of systems with emphasis oeuro-ophthalmologic and cardiopulmonary and immune systems.l
Social history – exposure, travel, (fungal or parasitic infections), chemical dependency.l
SIGNS OF SEVERITY
Feverl
Dehydrationl
Rapid progression of swellingl
Trismusl
Marked painl
Quality and/or location of swellingl
Elevation of tonguel
Difficulty with speech and swallowingl
Anatomic Location
Graded in severity by level to which the airway and vital structures are threatenedl
Lowu
Buccal, Vestibular, SubperiostealF
Moderateu
Masticator spaceF
Severeu
Lateral pharyngealF
RetropharyngealF
Danger SpaceF
What are the primary fascial spaces?
The spaces directly adjacent to the origin of the odontogenic infections. Infections spread from the origin into these spaces, which are:
Vestibular Submental
Canine Sublingual
Buccal Submandibular
VESTIBULAR
BUCCAL
Likely from
Upper Premolaru
Upper molaru
Lower molarsu
SUBMENTAL SPACE
l Anterior mandibular teeth
l Deep to mentalis muscle
Submental Space
Most likely caused by lower anterior teeth or mandibular sympysis fracturel
SUBLINGUAL SPACE
Presents in floor of mouthl
l
Drained intraorally parallel to Wharton’s ductl
Submandibular Space
Likely cause:l
Lower molarsu
SUBMANDIBULAR SPACE
Extra-oral presentationl
l Deep to mylohyoid
Il & D through skin with blunt incision
LUDWIG’S ANGINA
l Bilateral submandibular, sublingual, and sub-mental involvement
l Rarely fluctuant
l Often fatal
l Requires early, aggressive intervention
What are the secondary fascial spaces?
Fascial spaces that become involved following spread of infection from the primary spaces.
The secondary spaces are:
Pterygomandibular Infratemporal
Masseteric Lateral pharyngeal
Superficial and deep temporal Retropharyngeal Prevertebral
PHARYNGEAL SPACE INFECTIONS
Lateral pharyngeall
Retro-pharyngeall
(both can lead directly to mediastinum)
What factors influence the spread of odontogenic infection?
Thickness of bone adjacent to the offending toothl
Position of muscle attachment in relation to root tipl
Virulence of the organisml
Status of patient’s immune systeml
INCISION AND DRAINAGE
The production of “laudable pus” by:
– mucosal incision
– extraction
– endodontic access
– periodontal curettage
INCISION AND DRAINAGE
Incise in healthy skinl
Incise in gravity-dependent, esthetic area – if possiblel
Explore entire abscess cavityl
Non-absorbable drainsl
PRINCIPLES IN
THE USE OF DRAINS (II)
Drained wounds should be cleansed frequently.l
Bacteria can migrate into a wound along the drain surface.l
Latex Penrose drains are best used unmodifiedl
INDICATIONS FOR CULTURE
Nonresolving infection in spite of appropriate carel
l Atypical flora expected
= long term antibiotic treatment
= age extremes (<2 or >65)
= patients with malignancies
Infections with systemic involvementl
Immunocompromised or myelosuppressed patientsl
EMPIRIC THERAPY OF ODONTOGENIC INFECTIONS
Penicillinl
Penicillin + metronidazolel
PCN allergy —— clindamycinl
MANAGEMENT OF ODONTOGENIC INFECTIONS
1. Determine severity Assess history of onset and progression perform physical examination of area:
(1) Determine character and size of swelling
(2) Establish presence of trismus
2. Evaluate host defenses Evaluate:
(1) Diseases that compromise the host
(2) Medications that may compromise the host
3. Perform surgery Remove the cause of infection Drain pus Relieve pressure
4. Select antibiotic
5. Follow up
Determine:
(1) Most likely causative organisms based on history
(2) Host defense status
(3) Allergy history
(4) Previous drug history
Prescribe drug property (route,dose and dosage interval, and duration)
Confirm treatment response
Evaluate for side effects and secondary infections
Patient should be monitored frequentlyl
out-patient should return for f/u in 2-3 daysu
Patient should have decreased swelling, discharge, airway edema, malaise in 2-3 daysu
l If no improvement consider:
Re-cultureu
Re-imageu
Repeat I and Du
Sublingual Space Infections
The sublingual space (SLS) is located inferior to intrinsic muscles of the oral tongue, lateral to the genioglossus-geniohyoid complex and superomedial to the mylohyoid muscle. Anteriorly, it is related to the mandible. Posteriorly, the SLS communicates with the submandibular space (SMS) with no fascia separating these spaces.
Sublingual Space Abscess
Abscesses originating in this space are usually due to sublingual or submandibular duct stenosis or calculus disease. Dental infection or mandibular osteomyelitis may also extend into the SLS. The most commonly encountered organisms in SLS abscess formation are S. aureus and Streptococcus viridans.
Clinically, patients with SLS abscess usually present with pain, tenderness and swelling in the anterior floor of the mouth. There may be a history of salivary colic, recent dental disease or dental manipulation. Treatment of an SLS abscess should commence with antibiotic therapy followed by surgical drainage.
CT shows an enhancing mass involving the SLS associated with subcutaneous streaking and thickening of the platysma muscle. The genioglossus-geniohyoid complex is often displaced medially or across the midline (Figure 4). If an SMS component is present, this abscess may track into parapharyngeal space, where further spread can take place in the craniocaudal axis. Infection may also spread to the medial pterygoid or masseter muscles.
Sublingual Space Infections
The sublingual space (SLS) is located inferior to intrinsic muscles of the oral tongue, lateral to the genioglossus-geniohyoid complex and superomedial to the mylohyoid muscle. Anteriorly, it is related to the mandible. Posteriorly, the SLS communicates with the submandibular space (SMS) with no fascia separating these spaces.
Sublingual Space Abscess
Abscesses originating in this space are usually due to sublingual or submandibular duct stenosis or calculus disease. Dental infection or mandibular osteomyelitis may also extend into the SLS. The most commonly encountered organisms in SLS abscess formation are S. aureus and Streptococcus viridans.
Clinically, patients with SLS abscess usually present with pain, tenderness and swelling in the anterior floor of the mouth. There may be a history of salivary colic, recent dental disease or dental manipulation. Treatment of an SLS abscess should commence with antibiotic therapy followed by surgical drainage.
CT shows an enhancing mass involving the SLS associated with subcutaneous streaking and thickening of the platysma muscle. The genioglossus-geniohyoid complex is often displaced medially or across the midline (Figure 4). If an SMS component is present, this abscess may track into parapharyngeal space, where further spread can take place in the craniocaudal axis. Infection may also spread to the medial pterygoid or masseter muscles.
Figure 4.
Sublingual space abscess. Axial contrast-enhanced CT (A) shows an abscess involving the left sublingual space (arrow). The bone algorithm (B) shows that the cause of the abscess is due to a “rotten” tooth (arrow).
MR imaging is rarely used for inflammatory disease involving the floor of the mouth. A floor-of-the-mouth abscess shows the typical enhancing mass on T1W images and high signal intensity on T2W images. In contrast-enhanced images, a central area of no enhancement, indicating pus collection, can readily be demonstrated. Mandibular marrow edema is more readily demonstrated on MR as intermediate signal tissues replacing high signal intensity fat on T1W images.
Sublingual abscess
Localization
Accumulation of pus between the mucosa of the floor of the mouth and the mylohyoid muscle.
Tongue muscles lay medially, the mandible ventrally and laterally.
- elevated floor of mouth
- glass-like reddening of the mucosa of the floor of the mouth
- difficulties speaking due to dislocation of the tongue to the healthy side
Treatment
- Incision in the alveolar ridge near the floor of the mouth, touching the periosteum of the affected tooth.
Caveat! The course of the lingual nerve goes laterally close to the periosteum of the lower wisdom tooth! - Drainage, rinsing
- Elimination of causes
Submandibular abscess
- between mylohyoid muscle and superficial fascia colli and the anterior belly of the digastric muscle
Causes
- Periapical periodontitis of molar teeth
- Periapical periodontitis of premolar teeth
Specific symptoms
- reddening and swelling of the inner mandibular surface
- The floor of the mouth is reddened, swollen and hardened dorsally.
- The margin of the mandible is laterally palpable, contours disappear medially.
- occasional trismus
Treatment
- extraoral incision, approx. width 4 cm, parallel to the margin of mandible
- drainage, rinsing
- elimination of causes
Massetericomandibular abscess
Localization
Causes
periapical periodontitis of molar teet
Specific symptoms
- reddening and pain on pressure in masseter region
- non-movable extraoral swelling
- The margin of mandible can usually not be palpated.
- trismus
Treatment
- intraoral incision in the lateral region of the pterygomandibular plica
- drainage, rinsing
- antibiotic treatment obligatory
- treatment of the affected tooth
Perimandibular abscess
Localization
- accumulation of pus laterally from the mandibular body, which encompasses the mandibular margin medially
Causes
- infection usually originates from the mandibular molars
Specific symptoms
- reddening and pain on pressure in the lower buccal region
- non-movable extraoral swelling
- fluctuation
- mandibular margiot palpable
- trismus
Treatment
- extra oral incision (4 cm width) parallel to and below the edge of the mandible
- drainage
- antibiotic treatment obligatory
- treatment of the affected tooth
Chin abscess
Location
Causes
- Periapical periodontitis of incisors
Specific symptoms
- reddening and pain on pressure of the chin
- non-movable, usually central, extraoral swelling above the chin
- intraoral swelling of the oral vestibule
Treatment
- Isolated chin abscess can be incised from an intraoral access.
- drainage, rinsing
- elimination of causes
Pterygomandibular abscess
Localization
Causes
infections of the lower wisdom teet
Specific symptoms
- extreme trismus
- minor swelling from outside
- collateral edema in the parotid bed (on occasion)
- pain on pressure at the mandibular angle and retromandibular
- difficulties swallowing
- swelling of the soft palate
Treatment
- extraoral incision, approx. width 4 cm, parallel to the margin of mandible (in rare cases intraoral incision)
- drainage, rinsing
- antibiotic treatment obligatory
- secondary tooth restoration
Retromandibular (parotid bed) abscess
Localization
Causes
- usually through an inflammation spreading into the masseterico-mandibular space
- abscess formation of a parotitis
Specific symptoms
- swelling of the parotid region (behind the ascending ramus of the mandible) to the sternocleidomastoid muscle
- A fluffy, purulent discharge from the parotid duct is indicative of parotitis.
Treatment
- intra- or extra-oral incision
- drainage, rinsing
- antibiotic treatment
Complications of soft tissue infections around the mandible
- necrotizing fasciitis
- mediastinitis (Bräuing et al. 1997)
