Possible complications in acute odontogenic inflammatory processes of the maxillofacial area.
Complications of acute odontogenic inflammatory diseases of the maxillofacial area include:
Mediastinitis
Thrombophlebitis of the facial veins. Thrombosis of the cavernous sinus.
Intracranial complications
A. Primary rhinogenic hydrocephalus
B. Basal arachnoiditis
B. Purulent meningitis
G. Meningoencephalitis
1. Mediastinitis
Purulent mediastinitis, as a complication of infectious and inflammatory processes in the maxillofacial area, often develops in patients with phlegmon of the peripharyngeal space (1), root of the tongue (2), floor of the mouth (3), submandibular (4) and retromandibular (5) areas. The spread of the infectious-inflammatory process to the tissue of the mediastinum from the peripharyngeal space, the root of the tongue occurs first in the retropharyngeal space, and from there along the tissue along the pharynx and esophagus to the posterior mediastinum. From the submandibular, retromandibular regions, from the area of the carotid triangle, the infectious-inflammatory process spreads along the tissue down along the main neurovascular bundle of the neck and further into the anterior mediastinum.
Clinical picturemediastinitis
Reasons to suspect the spread of an infectious-inflammatory process into the mediastinum in a patient with phlegmon of the floor of the mouth, peripharyngeal, and retromandibular spaces are:
the appearance of signs of an inflammatory process in the neck, especially along the neurovascular bundle of the neck;
deterioration of the patient’s general condition, despite good drainage of purulent foci in the head and neck area (temperature up to 39-40 o C, chills, tachycardia)
the appearance of clinical symptoms characteristic of the purulent-inflammatory process of this localization.
Characteristic symptoms of mediastinitis
1. The appearance of an inflammatory infiltrate along the main neurovascular bundle in the lower part of the neck, in the supraclavicular region, in the region of the jugular cavity.
2. Forced position of the patient: sitting with his head bowed, lying on his side with his legs tucked to his stomach.
3. Severe shortness of breath at rest (up to 45-50 respiratory movements per minute)
4. Retraction of the tissues of the jugular cavity during inspiration (Ravich-Shcherba symptom).
5. Pain behind the sternum or deep in the chest. The pain intensifies with deep inspiration, coughing, swallowing, and throwing back the head (Gercke's symptom).
6. Characteristic coughing as a consequence of hypersecretion of mucus due to irritation of the vagus nerve and impaired drainage of the bronchial tree due to the appearance/increasing of pain with intense coughing.
7. Pain in the depths of the chest when percussing the sternum, rocking the heels with straightened lower limbs.
8. X-ray examination reveals an expansion of the mediastinal shadow, effusion in the pleural cavity, and in the presence of a putrefactive-necrotic process caused by an anaerobic infection, the presence of gas in the mediastinum and paravisceral tissue of the neck.
TREATMENT.
Opening a purulent focus - mediastinotomy. The most commonly used is transcervical according to Razumovsky - through an incision along the anterior edge of the sternocleidomastoid muscle, starting from the level of the upper edge of the thyroid cartilage and 2-3 cm below the sternoclavicular joint. After opening, wash with furatsilin and drain.
2. Thrombophlebitis of the facial veins. Cavernous sinus thrombosis .
Pathogenesis.
In the development of this complication, the main importance is
Rich blood supply to the maxillofacial area
Absence of valves in facial veins
The presence of anastomoses between the superficial veins of the face, the veins of the orbit and the venous sinuses of the dura mater (cavernous sinus): angular vein (v. angularis) - between the veins of the orbit and the facial vein,
Clinic.
Thrombophlebitis of the facial veins is characterized by the appearance along the angular or facial vein of painful “strands” of infiltrated tissue, hyperemia of the skin with a bluish tint, and the spread of edema far beyond the infiltrate. There is an increase in body temperature and changes in the blood picture characteristic of inflammation.
The most serious complication of thrombophlebitis of the facial veins is thrombosis of the cavernous sinus. This complication can be classified as intracranial. Common symptoms are severe headache, general weakness, increased body temperature to 38-40°C, leukocytosis, increased ESR to 40-60 mm/h.
Locally noted:
Swelling and hyperemia of the skin of the eyelids and forehead
Infiltration of soft tissues of the orbit
Exophthalmos, conjunctival chemosis, ophthalmoplegia, pupil dilation, fundus hyperemia
There may be a stiff neck
Treatment.
When the first signs of the disease appear, intensive antibacterial (broad-spectrum antibiotics, immunotherapy), detoxification and desensitizing therapy are prescribed. For purulent-septic thrombophlebitis of a person, drugs are administered directly into the external carotid artery. In addition to antibiotics, direct anticoagulants (heparin) are administered intraarterially to prevent intravascular coagulation. In case of abscess formation of thrombosed veins and infiltrates, surgical treatment is performed with active drainage of abscesses. To prevent thrombosis of the cavernous sinus with thrombophlebitis of the facial veins, ligation is recommended
angular or facial vein. The ligature is applied through the entire thickness of the tissue without prior isolation of the vein.
Treatment patients with developed cavernous sinus thrombosis are treated according to the same principles. Along with intensive antibacterial therapy, desensitizing, detoxification, dehydration, hormonal and anticoagulant therapy is indicated. Strict bed rest is required. To enhance the effect of therapy, antibacterial drugs are recommended to be administered intra-arterially. It should be noted that active anticoagulant therapy for cavernous sinus thrombosis is not generally accepted, since it is unsafe due to the possibility of hemorrhage and cerebral infarction. Various authors suggest the use of fibrinolytic agents, “soft” anticoagulants (acetylsalicylic acid, butadione).
Intracranial complications
A. Primary rhinogenic hydrocephalus -
T oxy-infectious swelling of the membranes of the brain with symptoms of cerebrospinal fluid hypertension - occurs under the influence of the inflammatory process in the maxillary sinuses. Clinically characterized by intense headache, which may be accompanied by nausea and vomiting, eye symptoms (decreased visual acuity, damage to the abducens, oculomotor, trigeminal nerves).
B. Basal arachnoiditis.
Caused by a purulent and polypous process in the maxillary sinuses. It is characterized by sharp unilateral pain in the face and head, damage to the V, VI and VII pairs of cranial nerves.
B. Purulent meningitis
- usually develops with purulent melting of the walls of the cavernous sinus (due to its thrombosis). Characterized by an acute onset, an increase in body temperature to 39-40 degrees, severe headache, nausea, vomiting, depression of consciousness, meningeal symptoms, stiff neck, Kernig, Brudzinski symptoms), changes in the cerebrospinal fluid (increased pressure, turbidity, pleocytosis).
G. Meningoencephalitis
- characterized by the presence of signs of meningitis, To accompanied by focal symptoms and loss of consciousness. Tachycardia, arrhythmia, and a drop in blood pressure are noted.
4. Odontogenic sepsis.
Currently, the following phases of general purulent infection are distinguished:
1. Purulent-resorptive fever - a general syndrome closely related to the local purulent process, characteristic of all purulent-inflammatory diseases of the maxillofacial area.
2. Initial phase of sepsis. It is diagnosed in the presence of purulent-resorptive fever after elimination of the purulent focus, its drainage and drug therapy and sowing of pathogenic flora from the blood. In this phase, with intensive therapy, the disease is eliminated within 15-10 days.
3.Septicemia - characterized by a severe general condition of the patient (body temperature above 38 degrees, tremendous chills, severe headache, insomnia). Pathogenic flora is cultured from the blood. Pyemic foci are not detected.
4.Septicopyemia. In this phase, in addition to the phenomena of septicemia, the appearance of metastatic abscesses is characteristic as a result of the transfer of bacteria by hematogenous route from the primary focus. This stage is characterized by the following symptoms: body temperature above 38 degrees, tachycardia above 100 beats per minute, anemia, shift of the leukocyte formula to the left, increase in ESR more than 60 mm/h, hypoproteinemia, toxic hepatitis and nephritis, isolation of pathogenic microorganisms during blood cultures.
A severe complication of sepsis is septic toxic-infectious shock. The triggering point for the development of shock is the immediate or repeated flooding of the bloodstream with microorganisms and their toxins. In septic shock, dysfunction of the central nervous system, pulmonary gas exchange, peripheral and central circulation, and organic damage are observed. The mortality rate from septic shock currently remains very high, amounting to 50% or more.
Treatment.
Treatment of sepsis should be comprehensive and include the following components:
Inspection of foci of purulent infection and, if necessary, “additional opening” of primary phlegmons, abscesses, purulent leaks.
Ensuring good drainage of purulent foci using perforated polyethylene and polyvinyl chloride tubes inserted through the main incision and removed through an additional (counter-aperture). The purulent focus is washed with antiseptics.
Antibacterial therapy taking into account the sensitivity of microflora to antibacterial drugs.
Detoxification infusion therapy.
Immunotherapy (administration of leukocyte suspension, gammaglobulin, antistaphylococcal plasma if the causative agent is staphylococcus)
Symptomatic therapy (depending on damage to various organs and systems)
Complete nutrition, vitamins.
Of the patients admitted to dental hospitals, 42.2% are patients with inflammatory diseases of the maxillofacial area, among them 29.1% are people over 60 years of age. In recent years, along with an increase in the number of dental patients, some of them have also experienced an increase in the severity of the clinical course of these processes. The cause of death of patients is severe complications: mediastinitis, sepsis, brain abscess.
The main reasons for the increase in inflammatory diseases are insufficient oral care and sanitation, untimely diagnosis and hospitalization of patients, their early discharge from hospital and irrational use of antibacterial agents. The processes that occur in the body as a result of aging are important in the course of inflammatory diseases of the maxillofacial area.
In elderly people and the elderly, the source of infection that causes the occurrence of phlegmon in the maxillofacial area is most often not periodontitis, but colds, infectious diseases and pathological periodontal pockets during periodontitis. The onset of the disease can be caused by trauma to the oral mucosa during eating, brushing teeth, treating them and preparing for prosthetics. The appearance of phlegmon can also be preceded by an inflammatory process of the oral mucosa.
As patients age, the immunological reactivity of the body decreases; the inflammatory process is sluggish, with a slight increase in temperature. The wound, a day after opening, is usually covered with fibrinous plaque, the discharge is usually moderate and liquid. Cleansing the wound from necrotic tissue occurs slowly, and the granulations that appear are atrophic. Sometimes exacerbations of inflammatory phenomena occur, which is associated with a delay in purulent discharge or with the depletion of the compensatory capabilities of the patient’s body. A weak local tissue reaction in the general serious condition of the patient is a sign of reduced resistance of the body as a whole. The prognosis becomes doubtful.
Clinic. In some patients, the disease begins violently, with a significant rise in temperature, fever, accompanied by chills and insomnia. The purulent-inflammatory process quickly spreads to adjacent cellular spaces and to vital organs.
Odontogenic inflammatory processes of the soft tissues of the face have their own characteristics that must be taken into account when diagnosing and treating them, especially in elderly patients.
1. The possibility of rapid spread of the purulent-inflammatory process from the primary focus to neighboring anatomical areas is one of the differences between odontogenic phlegmons and abscesses. The basis for this is the topographic and anatomical features of the face and neck, in particular, the presence in the maxillofacial region of a significant number of masticatory and facial muscles, a well-developed network of blood vessels, nerves, and the Bisha fat pad. This creates a danger 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 spread of pus occurs primarily within the interfascial space in which the suppurative process arose. When any wall of this formation melts, the process moves into adjacent cellular spaces. Often, during odontogenic inflammatory processes of the soft tissues of the face, pus spreads along the fiber located in the interfascial and intermuscular spaces surrounding the vessels, nerves, salivary glands with their ducts, and processes of the Bichat lump.
The spread of the purulent-inflammatory process to adjacent cellular spaces and vital organs is accompanied by severe intoxication and a general reaction of the body. The patient's condition becomes serious, pain in the wound area intensifies, weakness increases, and poor sleep and appetite are noted. The purulent-inflammatory process of the soft tissues of the face is characterized by pale skin, anemia, elevated body temperature and other symptoms of intoxication.
In such cases, it is necessary to open the wound wide, open purulent leaks and “pockets”, remove necrotic tissue, and create conditions for the constant outflow of discharge from the wounds.
2. Late appearance of fluctuation is one of the features of odontogenic phlegmon, which is associated with the localization of the pathological process medially from powerful muscle formations (deep phlegmon of the temporal region, inflammation in the infratemporal, pterygopalatine fossa, masseter and pterygomaxillary regions, floor of the mouth). In this case, a dense painful infiltrate without clear boundaries and signs of fluctuation is detected. The skin over it is initially pale and mobile, then hyperemia and swelling appear. This feature explains the need for early opening of the abscess. At the same time, a sleepless night is an absolute indication for surgical intervention. Untimely opening of the inflammatory focus can lead to the spread of infection through the blood and lymphatic vessels.
Metastasis and formation of pyemic foci occur mainly by hematogenous route. The lymphogenous route of metastasis is also possible. Pyemic foci most often occur in the form of abscesses of various sizes, infiltrates such as phlegmon. On the part of the internal organs during sepsis, mainly severe degenerative-necrobiotic and inflammatory phenomena and edema are detected. In elderly people, the excretory function of the kidneys is most noticeably affected, as a result of which one of the most important links in the body's defense mechanism is disrupted - the evacuation of bacterial toxins and products of impaired metabolism of the inflammatory focus with urine. This circumstance largely determines the general condition of the patient and the course of the disease.
Blood cultures in sepsis do not give growth if a small amount is taken (up to 2 ml). Blood for testing must be taken at the moment the daily rise in temperature begins.
3. The proximity of vital organs (brain, upper respiratory tract, mediastinum, organ of vision) to the maxillofacial area leads to severe complications. In this case, the inflammatory process spreads from the source of inflammation in various directions through the lymphogenous and hematogenous route, through the fascia and cellular spaces.
Through the lymphatic vessels of the mandibular and maxillary nerves, the infection can penetrate through the oval and round openings to the meninges. Thrombophlebitis of the anterior facial, and then the angular and superior ophthalmic veins also leads to brain damage, and orbital phlegmon also occurs. The proximity of the larynx and trachea causes the risk of asphyxia, which is significant with phlegmon of the floor of the mouth, neck, and abscesses of the root of the tongue.
Mediastinitis - develops as a result of the spread of pus along the neurovascular bundle of the neck, as well as along the peri-esophageal and pretracheal tissue. Mediastinitis can occur at lightning speed and occur simultaneously with phlegmon of the floor of the mouth and neck, so diagnosing them is not always simple.
4. Anaerobic infection is often present in purulent-inflammatory foci of odontogenic etiology. Microorganisms represent a very large group, including both coccal and rod flora. Aerobic or anaerobic conditions are required for their development. The occurrence of a purulent process is based on the damaging effect of the microorganism and the compensatory and adaptive reactions of the patient.
Along with staphylococci, streptococci, Proteus, Escherichia coli and Pseudomonas aeruginosa, every third microflora study also identifies anaerobes: bacteroides, clostridia, anaerobic gram-positive cocci, bacilli. They are representatives of normal human microflora. Anaerobes are found on the mucous membranes of the oral cavity, sweat glands, and lower intestines.
Obligate anaerobes are very sensitive to oxygen. Their growth requires a very low oxidation-reduction potential of the environment: they are difficult to isolate from clinical material. To a certain extent, the sterility of the punctate when examining pus from inflammatory foci indicates the presence of an anaerobic infection.
The role of microflora as an etiological factor in the purulent-inflammatory process is very complex and cannot be reduced to a simple relationship between a macroorganism and a microorganism. Often the simultaneous detection of aerobic and anaerobic flora during these processes is not accidental. The occurrence of an anaerobic inflammatory process is prepared by aerobes, which penetrate the pathological focus and in a certain way “prepare” the tissues for the development of 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 treat anaerobic infections, especially those caused by bacteroids, metronidazole and metragil are prescribed. Antibiotics should include chloramphenicol, tetracycline, and cefatoxin, which are used only in cases where traditional therapy is ineffective and the wound is covered with grayish films.
5. The increased regenerative ability of facial tissues is due to good blood supply and innervation of the maxillofacial area, as well as the presence of low-differentiated cellular elements with a high potential for regeneration. This can lead to healing of wounds of the oral mucosa earlier than the inflammatory process in the soft tissues is stopped. Therefore, wide incisions (for phlegmon of at least 6 cm) with careful drainage are advisable.
6. Inflammatory contractures arise as a result of reflex-painful contraction of the masticatory muscles or its damage by an odontogenic inflammatory process. Inflammatory contractures are observed with odontogenic abscesses and phlegmons, which are localized in the area of the muscles that lift the mandible, and are also observed with periostitis and osteomyelitis of the mandible. Long-term inflammatory contracture as a result of destructive and degenerative processes in the muscles leads to scar contracture. Inflammatory contracture makes it difficult to examine the oral cavity and local diagnosis of the inflammatory process. In addition, the functions of chewing and swallowing are impaired, which can lead to exhaustion of patients. Contracture requires careful special oral care.
7. The need for special care for the oral cavity is determined by the fact that during the inflammatory process of the maxillofacial area, the process of self-cleaning of the oral cavity is disrupted. The nature of the microflora changes dramatically due to the proliferation of putrefactive microbes, which causes a characteristic fetid odor. The patient performs oral care independently or by medical personnel. The thoroughness of these measures largely determines the outcome of patient treatment.
Treatment. As a result of a decrease in inflammatory and other reactions in elderly and senile patients, the indications for surgical intervention in acute purulent inflammatory processes of the soft tissues of the face and neck change. You should not wait for the appearance of hyperemia of the skin over the source of inflammation and fluctuation, since purulent exudate can spread to neighboring areas. The indication for opening an inflammatory focus is a dense, sometimes painful infiltrate of soft tissue that can be detected by palpation.
When choosing the type of anesthesia in elderly patients, it is necessary to take into account not only the reduced compensatory capabilities of the respiratory, circulatory, and endocrine apparatus, but also the fact that 70-80% of patients in this category have concomitant diseases, often more severe than the main one. The cardiovascular system is most often affected. Coronary circulation is often disrupted, the contractility of the heart muscle decreases, and the minute volume of blood decreases. Blood pressure often increases. The pulse is usually slow.
As a result of atrophic changes, the respiratory surface of the lungs decreases by approximately 25%. Due to ossification of the costal cartilages and sclerotic changes in the lung tissue, the lungs are fixed in the inhalation position. At rest, such a person is in balance (his heart rate and breathing are normal), but a small amount of physical or nervous tension (excitement, anxiety before surgery, etc.) is enough and hypoxia may occur, which will immediately affect the state of the function of the heart muscle.
When choosing a method of pain relief, the general condition of the patient, concomitant diseases and the extent of surgical intervention are taken into account.
Elderly and senile patients require systematic observation by a therapist, repeated ECG, blood and urine tests. Since the recovery of such patients is often delayed, the issue of their follow-up treatment in the clinic must be decided together with the therapist.
An oral and maxillofacial surgeon is a doctor whose job is to study and treat diseases of the jaws and face. Let's look at what diseases the doctor treats, diagnostic methods and tips for maintaining health.
Oral and maxillofacial surgeon is the most popular, but at the same time complex medical specialty today. A person’s face is his business card; it is appearance that determines individuality and provides a number of vital functions (breathing, speech, facial expressions, eating). The doctor treats abscesses, periostitis, difficult teething, inflammation of the salivary glands and maxillary sinuses. The doctor helps with the treatment of injuries to the facial skeleton, tumors on the jaw bones, birth defects, pathologies and deformities.
During the treatment process, the doctor uses multi-stage surgical methods to treat both children and adults. Particular difficulties during surgical treatment arise with maintaining a normal respiratory process. The result of treatment of maxillofacial lesions depends on the tactics of its management (anesthesia, surgery, rehabilitation) and the professionalism of doctors.
Who is an oral and maxillofacial surgeon?
What is an oral and maxillofacial surgeon? This is a qualified doctor who treats the oral cavity, damaged teeth, pathologies and deformities of the bones of the facial skeleton, neck and face. The area of the disease is innervated and supplied with blood, so all lesions are painful, leaving behind defects and serious deformities.
Before treating the disease, the maxillofacial surgeon conducts a detailed diagnosis of the patient. This is due to the fact that the treatment area has proximity to vital organs and the brain. All this suggests that the maxillofacial surgeon must be a true professional, be able to recognize the symptoms of serious diseases and promptly treat inflammation and lesions of the maxillofacial area.
When should you contact an oral and maxillofacial surgeon?
When should you contact a maxillofacial surgeon for help, and what defects of the jaws and face require mandatory treatment? Let's look at the symptoms of diseases that are treated by a doctor and that require immediate help.
- Periodontitis is a disease accompanied by severe and increasing pain in the teeth. Pain sensations are associated with pressure on nerve endings. Teeth that are affected by periodontitis change color and become mobile.
- Periostitis is an inflammation of the jaw that occurs due to the remaining tooth root after extraction, and is accompanied by a slight compaction on the gum, which gradually affects the soft tissues of the face.
- Osteomyelitis of the jaws - symptoms of the disease are accompanied by throbbing pain in the jaw, chills, headache and high fever. The disease occurs due to necrotic tooth pulp.
- An abscess is a collection of pus. The disease is accompanied by weakness, headaches, high fever and other symptoms that are typical for purulent-inflammatory processes.
- Lymphadenitis is a disease that causes inflammation of the lymph nodes. Most often it affects the head, oral cavity and pharynx.
What tests should be taken when visiting an oral and maxillofacial surgeon?
Treatment of any disease is accompanied by tests that help diagnose the cause of the lesion and create the most effective treatment plan that matches the individual characteristics of the patient’s body. Standard tests that are mandatory for all patients are a general and biochemical blood test, as well as a general urinalysis.
An oral and maxillofacial surgeon can give a referral for histology, that is, skin scraping from the affected area. If the disease occurs in the neck and or in the area of the lymph nodes, then the patient must be tested for hormones.
What diagnostic methods does the maxillofacial surgeon use?
Diagnostic methods help to determine the disease as accurately as possible, focusing on its symptoms and test results. Let's look at what diagnostic methods an oral and maxillofacial surgeon uses. The most common method that allows you to visually see the extent of damage is x-rays and intraoral x-rays, which are used for lesions of the jaw and teeth.
In case of defects of teeth and bone tissue, the doctor conducts radiovisiographic diagnostics and radiography. To diagnose facial lesions, tomography, MRI, CT, and cephalometric radiography are performed.
What does an oral and maxillofacial surgeon do?
What does an oral and maxillofacial surgeon do and what are the responsibilities of a doctor? The specialist is engaged in the diagnosis, treatment and prevention of diseases, lesions and pathologies of the maxillofacial area. The doctor corrects congenital deformities, malocclusions and performs aesthetic surgical treatment of the face and neck.
An oral and maxillofacial surgeon treats emergency patients who present with injuries and mutilations that require medical attention. As a rule, these are people who have suffered in accidents and accidents. The doctor diagnoses and treats planned patients and performs operations. The surgeon accompanies the patient until complete recovery.
What diseases does an oral and maxillofacial surgeon treat?
An oral and maxillofacial surgeon is a qualified doctor who treats pathologies and defects of the maxillofacial area. Let's take a closer look at what diseases the doctor treats. All diseases are divided into certain groups, which depend on the causes of the lesions. The groups include tumors, inflammation, trauma, and acquired and congenital defects.
An oral and maxillofacial surgeon is a qualified doctor whose task is to timely diagnose and properly treat lesions of the jaws and face. To do this, the doctor uses modern diagnostic techniques and treatment methods.
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Diseases of the nerves of the maxillofacial region include lesions of the trigeminal, facial, glossopharyngeal, and hypoglossal nerve systems of various etiologies.
Classification
There are different classifications depending on the location of the lesion and the nature of the pathological changes.Based on the location of the lesion, the following are distinguished:
- damage to the trigeminal nerve;
- damage to the facial nerve;
- damage to the glossopharyngeal nerve;
- damage to the hypoglossal nerve.
- neuralgia;
- neuropathy (neuritis).
Etiology and pathogenesis
In the etiology of nerve lesions of predominantly central origin, the following are important:- acute traumatic brain injury;
- development of benign and malignant neoplasms in the cranial cavity;
- trophic changes due to cerebrovascular accidents;
- development of inflammatory processes (meningitis, meningoencephalitis, etc.).
- trauma (fractures of the jaw and facial bones; changes due to traumatic tooth extraction and other surgical interventions; injury from instruments and filling materials when filling dental canals; chronic trauma due to the use of irrationally manufactured prostheses and orthodontic devices, etc.);
- acute and chronic inflammatory processes (chronic periodontitis; osteomyelitis; odontogenic maxillary sinusitis; rarely - acute inflammatory processes);
- neoplasms of the maxillofacial region (malignant neoplasms of the maxillofacial region, neuroma);
- infectious and colds (specific and nonspecific).
Clinical signs and symptoms
The clinical picture depends on the location and nature of the lesion. Trigeminal neuralgia of predominantly central origin is characterized by:- short-term painful, paroxysmal pain that suddenly arises and quickly stops;
- attacks of pain are accompanied by vegetative manifestations on the face (skin hyperemia, lacrimation, salivation, reflex contractions of facial and masticatory muscles);
- painful attacks are often preceded by prolonged pain in the zone of innervation of the corresponding trunk.
Neuralgia of the nasociliary nerve (unilateral and bilateral Charpin syndrome) is characterized by:
- attacks of excruciating pain in the area of the eyeball, eyebrow and corresponding half of the nose;
- pain occurs at night and is accompanied by lacrimation, swelling of the nasal mucosa;
- There may be changes in the anterior part of the eye in the form of keratoconjunctivitis and pain on palpation of the inner corner of the eye.
- pain in the temple, inner ear, anterior wall of the external auditory canal, temporomandibular joint;
- Pathognomonic is sweating and redness of the skin in the area of innervation of the auriculotemporal nerve during meals.
Neuritis of the trigeminal nerve is characterized by pain, parasthesia and sensory disturbances in the areas of innervation of the affected branches. Neuritis of the facial nerve is characterized by acutely developed prosopoparesis, sensory and autonomic disorders. Neuritis of the glossopharyngeal nerve is characterized by paroxysmal short-term pain in the root of the tongue or tonsil, spreading to the velum, throat, and ear. The pain radiates to the corner of the jaw, eyes, and neck.
Neuritis of the hypoglossal nerve is characterized by:
- with isolated neuritis, motor disorders of the tongue muscles occur, sometimes pain in the root of the tongue and headache;
- in the initial stages of the disease, upon careful examination, it is possible to note that the suture of the tongue has the shape of an arc, curved towards the healthy side, the root part of the tongue on the affected side is slightly higher due to paralysis;
- when protruding, the tongue deviates towards the lesion.
Complications
The nature of the complications is due to the weakening or shutdown of individual functions due to damage to one or another nerve branch. The diagnosis is made based on the results of a physical examination (pay attention to the medical history, the patient’s complaints and the presence of sensory and functional disorders). An X-ray examination is carried out to identify areas of damage to the jaw and facial bones that may cause neuropathology. In order to clarify the localization of the affected nerve branch, diagnostic blockades are performed with a 1-2% lidocaine solution.To identify central (intracranial) pathological changes, computed tomography of the skull is indicated. To clarify the diagnosis, electroodontodiagnosis, ultrasound examination, color Dopplerography, magnetic resonance imaging (MRI), encephalography, etc. are performed.
Differential diagnosis
Diseases of the nerves of the maxillofacial region are differentiated from each other. Neuralgia and neuropathy of the II and III branches of the trigeminal nerve are differentiated from pulpitis and periodontitis. Neuralgia and neuropathy of the second branch of the trigeminal nerve are also differentiated from maxillary sinusitis. It should be remembered that symptoms of neuritis of the trigeminal, facial and other nerves can occur with malignant extra- and intracranial neoplasms. In the early stages, conservative treatment is carried out; in later stages and in case of mechanical (due to injury) rupture of the nerve trunk, surgical treatment is possible.Neuralgia
Treatment of neuralgia should be combined and prescribed with the participation of a dentist and neurologist. If these specialists are not available, the treatment is carried out by a dentist. The choice and tactics of treatment depend on the etiology of the disease, its duration, the intensity of the pain syndrome and the age of the patient.Typically, treatment begins with the appointment of carbamazepine (minimum doses are used initially, gradually increasing them until an analgesic effect is obtained):
Carbamazepine 100 mg orally 2 times a day until clinical improvement.
Other drugs can be used:
Thiamine/pyridoxine/cyanocobalamin IM 2 ml (100 mg/100 mg/1 mg) 1 time per day or every other day, 10 injections
±
Glycine orally 100 mg 3 times a day, 30 days, then a 30-day break, then a repeat course or
Piracetam 800 mg orally 2 times a day, 6-8 weeks.
For severe pain syndromes, NSAIDs may be included in the treatment regimen:
Diclofenac 50 mg orally 2-3 times a day, until clinical improvement or
Indomethacin 25 mg orally 3 times a day until clinical improvement.
Neuritis
NSAIDs are used to treat neuritis:Diclofenac orally 50 mg 2-3 times a day, 10 days or
Indomethacin orally 25 mg 3 times a day, 10 days or
Ketoprofen 50 mg 3-4 times a day (1 capsule in the morning and afternoon and 2 capsules in the evening) or
Ketorolac orally 10 mg every 4-6 hours, 10 days or
Nimesulide orally 100 mg 2 times a day, 10 days.
NSAIDs can be combined with vitamins:
Thiamine/pyridoxine/cyanocobalamin IM 2 ml (100 mg/100 mg/1 mg) 1 time per day, 10 days or orally 1 tablet (100 mg/200 mg/200 mcg) 3 times per day, 20 days or
Pyridoxine IM 100 mg once a day, 10 days
+
(alternate every other day) Thiamine IM 100 mg 1 time per day, 10 days
+
Cyanocobalamin IM 1 mg 1 time per day, 10 days.
In the treatment of neuritis, in addition to pharmacotherapy, the following are additionally prescribed:
- physiotherapy;
- acupuncture;
- hirudotherapy;
- transcutaneous electrical neurostimulation.
Evaluation of treatment effectiveness
Treatment is effective in the absence of attacks (long-term remission).Errors and unreasonable assignments
Unreasonable prescriptions are a consequence of erroneous diagnosis. It is necessary to take into account concomitant diseases to exclude polypharmacy (simultaneous use of a large number of drugs from different groups).Forecast
With correct diagnosis and adequate treatment, the prognosis is relatively favorable.G.M. Barer, E.V. Zoryan
MINISTRY OF HEALTH OF THE REPUBLIC OF UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF SURGICAL DENTISTRY
LECTURE No.5
FOR STUDENTS3 DENTAL FACULTY COURSE
COMPLICATIONS OF INFLAMMATORY DISEASES OF THE FACIAL VEINS (THROMBOPHLEBITIS OF THE FACIAL VEINS, THROMBOSIS OF THE CAVERNOUS SINUS, MENINGITIS, MEDIASTENITIS, SEPSIS)
Prepared by: Professor
TASHKENT 2008
Lecture No.5
Complications of inflammatory diseases of the maxillofacial area (thrombophlebitis of the facial veins, thrombosis of the cavernous sinus, meningitis, mediastenitis, sepsis)
Number of hours: 2 hours.
Purpose of the lecture:
Familiarize yourself with the complications of inflammatory diseasesmaxillofacial area (thrombophlebitis of the facial veins, thrombosis of the cavernous sinus, meningitis, mediastenitis, sepsis), outline the nature and features of the course of complications of inflammatory diseases of the maxillofacial area.
Lecture objectives:
1. Familiarize yourself with the complications of inflammatory diseases of the maxillofacial area.
2. Explain etiopathogenesis
3. Outline the general clinical manifestations of thrombophlebitis of the facial veins, thrombosis of the cavernous sinus, meningitis, mediastenitis, sepsis.
4. Explain the features of diagnosing complications of inflammatory diseases of the maxillofacial area.
5. Explain the general principles of treatment of complications of inflammatory diseases of the maxillofacial area.
Lecture outline:
1. Etiology and pathogenesiscomplications of inflammatory diseases of the maxillofacial area.
2. Features of clinical manifestationscomplications of inflammatory diseases of the maxillofacial area.General and local symptoms.
3. Features and modern principles of diagnosticscomplications of inflammatory diseases of the maxillofacial area.New research methods.
4. The main points of surgical treatment and features of postoperative management of patients with complications of inflammatory diseases of the maxillofacial area.
The problem of purulent infections affecting p.l.o. and their complications are currently extremely relevant. More than forty years ago, during the period of mass use of antibiotics, even small doses of these drugs prevented the development of purulent complications. Currently, odontogenic inflammatory diseases are one of the most common types of pathology. In recent years, the number of patients with these diseases has increased significantly, the severity of the process has worsened, which often leads to such severe complications as thrombophlebitis of the facial veins, thrombosis of the cavernous sinus, meningitis, and sepsis.
Thrombophlebitis of facial veins - this is an acute inflammation of a vein with its thrombosis, which develops in purulent-inflammatory diseases.
As a rule, the development of thrombophlebitis due to acute odontogenic infection is preceded by colds or viral diseases, as a result of which the body's resistance is reduced. The following factors are important in the pathogenesis of thrombophlebitis: microbial allergy and autoallergy as a result of tissue breakdown during infection; inflammatory and traumatic damage to the endothelium of the veins, especially in a sensitized organism, which predisposes to intravascular coagulation with transition to thrombosis at the site of damage to the vein (Balude, 1975), a dense network of lymphatic and venous vessels in the facial area with numerous anastomoses; damage to the vascular wall can occur: with a decrease in the reactivity of the body, a slowdown in blood flow, damage to the venous wall, a change in the composition of the blood and an increase in its coagulation (endophlebitis) or with the transition of the inflammatory process from the fiber to the outer wall of the vein (periphlebitis). In both cases, the inflammatory process involves the entire venous wall and thrombus formation occurs in the vein (and co-author, 1984). Thrombophlebitis of the facial veins is most often formed when the inflammatory process passes from the surrounding soft tissues to the outer wall of the vein, followed by the formation of a blood clot. This pathology is most often a complication of boils and carbuncles of the face, acute polysinusitis, phlegmon of the infratemporal and pterygopalatine fossae.
In the pathogenesis of thrombophlebitis of the facial veins and cavernous sinus, the presence of a dense network of lymphatic and venous vessels of the face with numerous anastomoses, the connection of the veins of the face, nasal cavity and pterygopalatine fossa with the veins of the orbit of the cavernous sinus, decreased reactivity of the body after colds and viral diseases, microbial allergies and autoallergy are important. in inflammatory processes t.l.o., mechanical damage to skin pustules.
The main anastomosis connecting the deep veins of the face, the pterygoid plexus with the veins of the orbit, the veins of the dura mater, and the cavernous sinus, is the inferior ophthalmic vein. IN
In the anastomoses of the veins of the face with the sinuses of the dura mater, valves are almost absent. During inflammatory processes in the area of the upper lip, blood flows through the angular vein into the veins of the orbit.
Thrombophlebitis of the facial veins most often occurs when patients squeeze out skin pustules or accidentally or through injury. The disease is characterized by the appearance of painful “strands” of infiltration along the angular or facial vein. tissue, hyperemia of the skin with a bluish tint, spreading of edema far beyond the infiltrate. The saphenous veins are dilated and diverge radially. There is severe intoxication, high body temperature, chills, general weakness, leukocytosis, high ESR. Clinical symptoms resemble the course of erysipelas.
When the thrombophlebitic process spreads through the veins of the orbit and the retrobulbar tissue space, exophthalmos of one or both eyeballs occurs, and subsequently thrombosis of the cavernous sinus may occur. (1957) recommends identifying variants of the clinical picture of thrombophlebitis of the cavernous sinus, which are characterized by two main signs: circulatory disorders in the eye and loss of functions of the cranial nerves combined with a septic condition. In this case, there is a severe headache, body temperature rises to 39-40 C, sharp pain in the eyes, exophthalmos. Changes in the cardiovascular system may be observed.
Treatment of thrombophlebitis is always urgent and is aimed at combating the threat of septicopyemia, preventing the spread of inflammation and normalizing hemostasis.
1. When the first signs of this disease appear, it is necessary mandatory hospitalization of patients and placement in a ward intensive care or resuscitation. Take from the source of inflammation exudate (to identify the sensitivity of pathogenic microflora to antibiotics) and blood from a vein (to determine indicators coagulograms and bacteremia)
2. Based on the presence of a background aggravating the inflammatory process, it is determined the degree of likelihood of developing complications, studying the functional activity of neutrophil granulocytes in peripheral blood and identify the nature and degree of microbial sensitization of the body (skin tests with allergens, etc.)
3. They will scream catheterization. The operation is affordable, safe and easy to perform. P. Ya. Shimchenko and Saeva (1981) indicate that the effectiveness treatment of patients using the method of continuous intracarotid infusion largely depends on compliance with the following requirements: a) when more than two are simultaneously involved in the inflammatory process deep anatomical areas or there are thromboses of facial veins, the catheter must be installed in a. sagopz ex! eta on level C-2 C-3 vertebrae; b) when an infectious disease spreads process on the substance and membranes of the brain, the catheter is installed in the common carotid artery and aortic arch, when the purulent-inflammatory process spreads to the mediastinum at the level of C-4 C-6 vertebrae; c) the catheter should pass without undue effort;
d) The infusate must be administered at a constant rate, which should not exceed 16-22 drops per minute; e) the infusate should consist of an isotanic solution of NaCl, novocaine, anticoagulants (heparin, fibrinolysin), re-opoly/glgokine and an antibiotic acceptable for intra-arterial administration.
4. Early dissection of the purulent-inflammatory infiltrate is performed, which creates decompression of soft tissues and prevents generalization of infection. Due to the fact that the purulent focus is located superficially, actively wash the wound through tubular drainage is not possible.
5. To reduce intoxication of the body, the patient is given intravenous drips. inject 400 ml. hemodesa, 500 ml. 5% glucose solution, antibiotics broad spectrum of action, dioxidin 5.0 ml., kontrikal 10,000-20,000 BD., 1-4% solution of amidopyrine, diphenhydramine, vitamins (ascorbic acid and B vitamins). According to indications it is necessary prescribe cardiovascular drugs. To prevent heart overload, it is necessary to control the amount administered fluid and daily diuresis. Daily dose of administered liquids are determined at the rate of 50-70 ml. per kilogram body weight of the patient and should not exceed 3-4 liters.
6. Thrombophlebitis leads to a violation of the acid-base state in the body towards acidosis, sodium deficiency occurs. That's why patients are prescribed an isotonic NaCl solution or a 4% solution bicarbonate Ma 200-400 ml. To enhance detoxification effect, forced diuresis should be used (administer 10-20% mannitol solution at the rate of 1.5 drugs per 1 kg. body weight).
7. To combat infection, broad-spectrum antibiotics are initially administered. spectrum of action, and, after identifying the microflora and determining its sensitivity is assigned accordingly anti-inflammatory drugs.
8. To prevent intravascular coagulation in a dose ED heparin is administered every 4-6 hours, and upon reaching mild hypocoagulemia switch to intramuscular administration drug in the same doses and intervals.
9. In order to stimulate immune factors, the patient is prescribed administration of hyperimmune antistaphylococcal plasma (4-6 ml per 1 kg of body weight after 1-2 days for 5-10 days), antistaphylococcal gamma globulin (4-5 ml. every 1 day during 8-10 days, plasma albumin with an increased content of antibodies, etc.
10. With pronounced sensitization of the body to microbial allergens nonspecific hyposensitizing therapy is prescribed. Diphenhydramine, suprastin, pernovin, tavegil, etc. are used. In case of untimely and inadequate care for patients with thrombophlebitis of veins t.l.o inflammatory process very quickly spreads to intracranial venous sinuses. Forecast at thrombophlebitis of the cavernous sinus is unfavorable. Considering the fact that mortality in sinus thrombophlebitis brain still remains at a fairly high level, it is necessary to pay great attention to prevention, as well as early detection and adequate treatment of purulent-inflammatory diseases h.l.o.
When the inflammatory process moves to the digestive sinus, damage of varying degrees occurs (from limited phenomena of phlebitis to thrombosis with purulent inflammation of the sinus), the symptoms are far from clear.
Severe headaches appear, sharp pain in the eye area, general weakness, chills, body temperature reaches 8-40
Local manifestations include swelling and hyperemia of the skin of the eyelids and forehead, infection of the soft tissues of the orbit, conjunctival chemosis, ophthalmoplegia, pupil dilation and fundus hyperemia.
These symptoms may progress on the side opposite to the source of inflammation. Rigidity of the neck muscles is often noted.
In peripheral blood, the number of leukocytes reaches 15-20 x 10 */l, TER increases to 40-60 mm/g.
<жнуса, как меншлтг, менинго-энцефалит, абсцесс шповного мозга, сепсис.
The same list of infusion-transfusion therapy measures is used as for phlebitis syndrome.
Anticoagulant therapy is particularly sensitive. The most commonly used is one of the following 2 methods:
Scheme of Rukavishnikov AI (1981): consists of catheterization of acagons ex^ or a.8ubc! aV1a and the administration of antibiotics, heparin, hydrocartisonitis S^emodes
Antithrombic therapy proposed by Zatevakhin II (1977) is a continuous intravenous infusion of heparin (150-250 SD/kg per day), reopolizhin (0.5-1.0 g/kg per day), nicotinic acid (2.5 mg/g per day), 1-b in this background, trental (3 mg/gg) is administered intravenously, gradually moving to oral administration of 100-200 mg treptal Zr per day. Pasle graduation
continuous infusion - heparin intravenously (50-75 IU/kg every 3 hours), after 1 week heparin is administered in the same dose, but every 4 hours with a further decrease in pain.
Although an increase in blood clotting is considered
sinus, K. Vashyzher (1969) indicates that the use of anticoagulants is unsafe due to the possibility of hemorrhages and cerebral infarction. GЪ opinion of the author, as well as EZ. Nzhtmarko (1975) in such cases, it is more correct to prescribe fisrinolithmic drugs against the background of hypothermia, and anticoagulants are prescribed only if there is a clear general tendency to thrombus formation (presence of thrombophlebitis of extracrural localization, risk of thromboembolism of the pulmonary artery).
Among the numerous and varied complications of acute odontogenic infection, sepsis occupies a special place, against which the development of contact mediastinitis and secondary intracranial inflammatory processes.
Despite the constant improvement of comprehensive programs therapy, the treatment results cannot be considered satisfactory. One of the most significant reasons is the untimely diagnosis of sepsis. At the same time, it is known that optimal results (up to 100% recovery) can be obtained in the initial stage of sepsis. In the septicopyemic form of sepsis with multiple organ failure syndrome (MODS), septic shock (SS), mortality can be 70-80% or more.
One of the ways to solve the problem of odontogenic sepsis is post-graduation special training of dentists of various profiles, as first-contact doctors, in the main sections of clinical sepsisology, adapted to dental practice.
Acute sepsis
The polymorphism of clinical manifestations of diseases, due to the nature, localization, prevalence of the source of primary infection, the type of pathogen and its biological properties, the initial state and functionality of vital organs and systems of the body, the degree of compromise of natural defense and detoxification mechanisms, makes the early diagnosis of sepsis quite problematic.
The difficulties of early diagnosis of sepsis are pointed out by clinicians dealing with the problem of acute surgical infection [, 1977; , 1982; , 1984; , 1987; , 1996; Tchervenkov J. et al., 1996].
Most often, sepsis has to be differentiated from a local purulent infection, accompanied by severe intoxication and choroid-resorptive fever (SRF), as well as acute infectious diseases [Svetukhin A. M ., 1982; , 1989; et al., 1997].
It is most difficult to establish the moment of transition of a local purulent infection into sepsis [, 1995; Holloway W, 1983; Grant L., 1984; Deitch E., Dobke M. ., 1996]. In this regard, it is appropriate to cite the statement of I.V. Davydovsky (1956) about purulent-resorptive fever as a normal general reaction of the body to a local infection, which distinguishes this syndrome from sepsis caused by “altered reactivity of the body.” There are diametrically opposed opinions on this matter: firstly, sepsis leads to a change in the reactivity of the body, secondly, the quantitative side of various constants changes the dynamics of the clinical picture of the disease [et al., 1983; Kuchler R., 1985; Wilson R ., 1995]. Most researchers understand GRF as a syndrome that occurs as a result of the resorption of tissue decay products from a purulent focus and is accompanied by general symptoms of intoxication [, 1981; Popkirov S, 1981; , 3983; Aronoff V., 1983, Williams E., Caruth J., 1992].
The course of GRF and the severity of general symptoms always correspond to the severity of the lesion in the local focus. Typically, GRF develops when there is a significant amount of dead tissue in the lesion, undrained purulent pockets and a high level of contamination of the purulent wound with microorganisms. As a rule, GRF proceeds without sharp deterioration and is rarely accompanied by bacteremia. According to (1982), Go et al. (1996), F. Tally (1982), transient bacteremia is one of the main signs of GRF.
The results of surgical treatment of the wound play an important role in the diagnosis of forms of purulent infection. If 7-10 days after radical surgical treatment the severity of the local inflammatory reaction (clinical and laboratory manifestations of endogenous intoxication syndrome - EIS) decreases, an inflammatory process should be assumed to occur in a localized form. In cases where, after surgical treatment against the background of antibacterial therapy, symptoms of intoxication persist, and microflora is sown from the blood, there is reason to suspect acute sepsis [, 1995; Clowes G ., 1986]. However, a number of researchers note that a single positive blood culture for pathogenic microflora does not always allow diagnosing sepsis. Only the clinical symptom complex characteristic of acute sepsis helps to diagnose the disease, although often in such cases blood cultures for sterility turn out to be negative [Savelyev B. C. et al., 1981; , 1988].
To increase the efficiency of diagnosing sepsis in general and improve treatment results, the so-called initial phase of sepsis is distinguished. The practical feasibility of this approach is beyond doubt. However, the theoretical basis for the early phase of sepsis is vulnerable to criticism, since there is no characteristic symptom complex of a generalized infection.
According to (3981), et al. (1982), M. Coshu and D. Perrott (1994), true surgical sepsis should be considered a form of purulent infection that manifests itself in the form of septicemia or septicopyemia. However, not everyone shares this point of view. It is customary to make a diagnosis based on clear differential diagnostic signs of GRF and sepsis [G, Etina G E., 1980].
In the primary purulent focus of GRL, the pathogenic agent appears as a decay product, while in sepsis it is represented by a wound infection. A severe clinical course of GRL is noted when the infection is introduced, whereas in sepsis this occurs some time after the introduction of the pathogen. In GRF, local symptoms predominate, while in sepsis, symptoms of a general infectious disease predominate. GRF is accompanied by transient bacteremia, and in sepsis bacteremia is natural and it is often accompanied by metastasis to distant organs and systems. Surgical treatment for GRF gives a positive sanitizing effect, while for sepsis the positive results are inconsistent and short-lived. The above differential diagnostic signs of GRF and sepsis to a certain extent suggest the generalization of infection when the symptom complex has a characteristic clinical picture.
Currently, acute sepsis has a blurred clinical picture. The classic symptom complex occurs only at the height of the infectious process or in the terminal phase of the disease. Differential diagnosis of sepsis should be carried out with systemic and chronic diseases accompanied by high body temperature, the presence of purulent foci, and often bacteremia [, 1987; Currer R., 1983; Stone R., 1994; Faist E., 1996].
Superficial skin necrosis, ulcerations, rashes on it, and minor damage are classified as atypical septic lesions [, 1987; , 1988]. Sepsis without a pronounced primary purulent focus should always raise doubts. On the contrary, the diagnosis becomes certain with secondary pyemic foci [Voino-, 1981; , Svetukhin A. M ., 1986]. Symptoms such as high body temperature and bacteremia in the absence of purulent foci cannot be the basis for a diagnosis of sepsis.
In the presence of uncharacteristic purulent foci and in the absence of a clinical picture of sepsis, it is necessary to carry out differential diagnosis with collagenosis and tuberculosis [Svetukhin A. M ., 1989]. In this regard, cytological and morphological studies of biopsies from purulent foci and bone marrow punctures, detailed X-ray examination, as well as ultrasound echolocation and radioisotope studies are of great help. The remark (1978) is correct regarding the correct interpretation of symptoms confirming the diagnosis of sepsis. High fever, the presence of a purulent atypical focus is not sepsis.
In addition to the three main symptoms, sepsis has a characteristic clinical picture: a primary purulent focus (a reasonable cause of high body temperature), intoxication, and corresponding changes in the blood and internal organs. In all cases, symptoms must be assessed comprehensively.
Complications that arise during the course of the disease play an important role in the clinical picture. However, it is practically difficult to decide what we are dealing with: the normal course of sepsis or its complication.
Septic shock(SS) should be considered as wound exhaustion, and disseminated intravascular coagulation syndrome, thrombophlebitis and bleeding are specific complications of sepsis. SS is considered the most dangerous complication, in which mortality can be 60-80% [Grinev M V, 1996; Stansley G., Byzne M., 1994].
Septic shock. According to data from both E. D. Kostin (1980) and (1983), M. Molomy (1982), the frequency of SS ranges from 10-40% of sepsis cases.
The most common causative agents of septic shock are gram-negative microorganisms. There are two known theories of the development of SS. First [, 1984; , 1987] explains it by the fact that under the influence of toxins, intravascular hemolyzed thrombus formation occurs. According to the second theory [, Gerega I.I., 1980; , 1989; Jawetz E., 1986; Dionigi R., Dominion! L ., 1991], SS is caused by stimulation of receptors by toxins, which leads to peripheral vasoconstriction and deterioration of peripheral circulation. A. M . Svetukhin et al. (1981), (1982), (1984) believe that both mechanisms take part in the development of SS - vasoconstriction and intravascular thrombus formation, which lead to a sharp deterioration in peripheral circulation. In addition, factors such as prolonged hypoxia, decreased circulating blood volume (CBV), acute adrenal insufficiency, toxic damage to parenchymal organs with the development of multiple organ failure play an important role [, 1982; 1984; , 1984; Eckant 1., 1983].
Septic shock can occur in any phase of sepsis, which depends on many reasons: worsening of the local purulent process, changes in microflora, intra-hospital infection, exacerbation of chronic diseases.
The clinical picture of SS is characterized by a certain symptom complex: a sudden sharp deterioration in general condition, a decrease in blood pressure below 80 mm Hg. Art., the appearance of shortness of breath, respiratory alkalosis, a sharp decrease in diuresis, neuropsychic manifestations, severe microcirculation disorders and dyspeptic disorders.
(1995), M. Heading and D . Henrich (1995) note that the following conditions are necessary for the development of SS: extensive or multiple highly contaminated foci, the presence of gram-negative flora, concomitant chronic diseases.
In most cases, when SS occurs, patients complain of a sharp deterioration in their general condition, increasing weakness, chills, feelings of fear and anxiety, and increased headaches. As a rule, body temperature rises to 40-41.5 °C. The skin becomes pale, a petechial rash may appear on the skin of the extremities and the anterior surface of the abdominal wall. Heart sounds are muffled, and a systolic murmur is detected at the apex of the heart. Hard vesicular breathing, dry and moist rales, and pleural friction noise can be heard in the lungs. The liver enlarges and palpation becomes painful. Acute respiratory failure is typical for patients with SS. There is a feeling of lack of air, increased shortness of breath, cyanosis and acrocyanosis are determined. As a rule, after the application of a tracheostomy, the symptoms of acute respiratory failure (ARF) do not disappear. Almost all patients exhibit mental disorders: from excitement, euphoria and mild confusion to delirium and coma.
As can be seen from the above data, the severity of clinical manifestations and laboratory data in SS depends on the degree of functional activity of vital organs and systems and the preservation of the body’s reactivity. In our opinion, it is advisable to distinguish between the early and late stages of SS [, 1987]. The most constant clinical signs of SS should be considered the presence of hyperthermia, chills, hypotension, tachycardia, shortness of breath, and disturbances of consciousness in the late stage of SS.
It should be noted that changes in the morphological and biochemical composition of the blood are not specific to SS and can be observed in all patients with severe purulent infection. However, SS is characterized by a decrease in blood volume (51.8±1.2 ml/kg), cardiac and stroke indices, an increase in blood flow time (10.8±0.6 s) and total peripheral vascular resistance.
Thus, SS is the most dangerous manifestation of acute odontogenic sepsis. In its diagnosis, analysis of the dynamics in the clinical picture of the disease is crucial. The presence of a symptom complex in the form of hyperthermia, hypotension, tachycardia, a sharp increase in breathing, and impaired consciousness indicates the development of SS.
When comparing clinical and laboratory parameters in patients with a local form of purulent infection and sepsis, it was found that many symptoms of sepsis can be observed in both the first and second nosological groups.
The conducted studies made it possible to identify early, intermediate and late signs of odontogenic sepsis, which are characterized by certain clinical and laboratory parameters.
Early signs of sepsis are: febrile fever for 3 days, dysfunction of the central nervous system according to the type of depression, the presence of multiple purulent foci, the development of SS with hypocirculation syndrome and ARF, decompensated hemocoagulation disorders with hemorrhagic syndrome, necrosis of the skin and mucous membranes, the presence of anemia. However, it should be noted that the above clinical and laboratory complex was observed only during the fulminant course of odontogenic sepsis.
As a rule, on the 7th-14th day of the disease, intermediate signs of odontogenic sepsis appear: loss of body weight, hectic type of temperature curve, pale gray skin color, jaundice, cyanosis, acrocyanosis, anemia with a steady decrease in the content of red blood cells and hemoglobin level, the appearance new pyemic foci of inflammation, low detoxifying effect of surgery on purulent foci, hepatosplenomegaly, toxic myocarditis (according to electrocardiography); progressive metabolic disorder (decrease in the content of total protein and albumin by 30% or more, decompensated forms of disorders of the CBS and hemocoagulation system, hyperenzymeemia); decrease in the content of lymphocytes (up to 40-50%) or more, phenomena of imbalance of the immune system, high levels of circulating immune complexes, positive blood cultures, refractoriness to treatment.
Late signs of odontogenic sepsis, which are determined in the 2-3rd week of hospitalization, include: lack of weight gain against the background of stabilization of the general condition, elimination of acute manifestations of the inflammatory process in the maxillofacial area and neck, significant reduction in the severity of symptoms of intoxication, pale gray coloration of the skin, hepatosplenomegaly, toxic myocarditis, slow dynamics of changes in metabolic processes and immunity against the background of complex therapy, the characteristic appearance of purulent wounds, indicating reduced regenerative processes.
Based on clinical and laboratory comparisons, we have identified the following absolutely reliable signs of odontogenic sepsis: the presence of a purulent focus, increasing metabolic disorders and immunity, persistent anemia, weight loss, positive blood cultures.
The data presented indicate the need for a thorough analysis of the dynamics of the clinical picture of the disease and indicators of homeostasis for the purpose of early diagnosis and provision of effective treatment for SS and ARF in patients with odontogenic sepsis.
Studies have shown that odontogenic sepsis is characterized by increasing intoxication, disruption of the functions of life-supporting organs and body systems. However, the classic version of the clinical course of odontogenic sepsis is rare. Its symptoms and syndromes manifest most clearly in the late stage of the disease. For these reasons, timely diagnosis of odontogenic sepsis can be carried out with a clear understanding of the diversity and different combinations of general and local clinical symptoms and laboratory data.
In order to diagnose odontogenic sepsis, one should actively and purposefully identify this most dangerous complication of purulent diseases, without waiting for the progression of the process and the development of a life-threatening condition.
Contact mediastinitis
Contact odontogenic mediastinitis (CM) is traditionally considered one of the most severe complications of acute purulent diseases of the face and neck [, 1985; , 1987, etc.]. According to (1971), CM develops in 1.78% of patients with phlegmon of the maxillofacial area and neck. (1973), (1973) observed CM in 0.3% of patients, (1973) - in 1.3%, (1988) - in 0.4%, (1988) - in 0.7% of patients (1985), (1985), (1978), (1985) note that the incidence of CM ranges from 0.3-2.72%. Most authors indicate an increase in the number of cases of this complication. Data for recent years are presented in table. 16.1.
CM is more often observed in men aged 15 to 70 years [, 1996].
In the practice of general surgeons, primary mediastinitis dominates, arising as a complication in the postoperative period due to open heart surgery as a result of perforation of the esophagus, cases of CM injuries of the trachea during intubation, during catheterization of the subclavian vein. In dental practice, as a rule, mediastinitis of odontogenic, less often tonsilogenic origin is observed, which is caused by the progression of the phlegmonous process of the soft tissues of the face, neck and its spread into the mediastinum.
1 According to existing classifications, mediastinitis is distinguished taking into account pathogenesis (primary or secondary), etiology (staphylococcal, streptococcal, etc.), nature and intensity of inflammation (serous, purulent, putrefactive, gangrenous, etc.), localization and prevalence (anterior, posterior , total, limited and progressive), clinical course (acute and chronic) [, 1946; , 1959; , 1971, etc.].
In recent years, most clinicians adhere to the classification proposed by (1977). The authors distinguish between non-purulent (serous), purulent and chronic mediastinitis.
More detailed classifications can be used only in the postoperative period as clinical and laboratory information is accumulated and are important for the retrospective assessment of the clinical manifestations of the disease, their relationship with factors of bacteriological aggression, pathomorphological, topographic and anatomical data [, 1977, etc.] .
Pathogenesis.The ways of infection spreading in patients with phlegmon of the head and neck into the mediastinum have been studied experimentally and clinically by many authors. A959) considered the most likely spread of descending phlegmons of the neck into the mediastinum along the prevertebral fascia into the posterior mediastinum and along the vascular bundle of the neck into the anterior mediastinum. Similar routes of spread of infection into the mediastinum were noted by A965).
Research conducted by T. V. Stepenova A971), N. G. Popov A972), V. P. Golbreich A984), allowed us to establish two main ways: 1) the inflammatory process spreads into the mediastinum from the posterior part of the peripharyngeal space along the vascular nerve bundle of the neck; 2) with phlegmon of the floor of the mouth or the root of the tongue, the pus overcomes the natural barrier in the area of the hyoid bone and enters the cellular space betweenThe parietal and visceral layers of the endocervical fascia of the neck and along the trachea freely descend into the mediastinum. Very often, the inflammatory process spreads downwards along several interfascial gaps, which leads to the development of total purulent mediastinitis. However, N.G. Popov A969) pointed out that in the experiment, when the dye spreads through the subcutaneous fatty tissue and muscle, its transition to the mediastinal tissue is not observed. Through the fiber located in the lateral spaces of the pharynx, trachea and esophagus, the ink penetrated into the mediastinum along the fiber of the neurovascular bundle.
With odontogenic infection and diffuse phlegmon of the peripharyngeal space, floor of the mouth, anterior and lateral surfaces of the neck, the infection may spread through several interfascial spaces with the development of total purulent or putrefactive-necrotic mediastinitis.
It has been established that with an odontogenic source of infection, anterior mediastinitis develops more often. Posterior or total KM is more often observed in patients with putrefactive-necrotic phlegmon, which is characterized by the spread of the inflammatory process to numerous spaces, including the base of the root of the tongue, the floor of the mouth and the neck (Fig. 16.1) [Talyshinsky A. M., 1982].
Bacteriological examination of discharge from the mediastinum reveals staphylococci, streptococci and their associations, and Proteus and Escherichia coli are often found.
In recent years, most authors point to gram-negative and a combination of gram-negative and gram-positive microflora, including anaerobic non-clostridial microflora, as the causative agent of infection in patients with KM.
Clinical picture KM is characterized by a combination of general and local symptoms of the disease [et al., 1985]. Patients complain of spontaneous pain in the chest, aggravated by tilting or turning the neck, as well as malaise, dizziness, cough, difficulty breathing, increased body temperature to 39-40 0C. The intensity of both local and general complaints can vary: from moderate to extremely pronounced. Based on the anamnesis, as a rule, it is possible to establish the odontogenic nature of the disease. Most often this is aggravated chronic periodontitis of the 48th, 47th, 46th, 36th, 37th, 38th teeth, difficult eruption of the 48th, 38th teeth and the subsequent development of the inflammatory process in the soft tissues of the jaw -facial area and neck [, 1985]. The general condition upon admission can be different - from moderate to extremely severe and agonizing. Noteworthy is the forced position of the patient, often on his side.
The skin is pale, with a grayish-icteric tint, expressed to varying degrees by acrocyanosis. “Marble spots” and a petechial rash may be visible on the skin in the area of the hands, feet, and knee joints, and extensive hematomas in the injection area. The skin may feel cold to the touch and covered with sticky sweat. The skin of the face is often pale, sometimes purple-bluish. The dilated saphenous veins of the face and neck are visually determined.
Changes in the circulatory system are manifested by tachycardia, increased blood pressure, expansion of the boundaries of the heart, and systolic murmur at the apex. In some patients, reduced or unstable blood pressure is detected against the background of extreme tachycardia.
In the lungs, upon physical and x-ray examination, except for hard breathing and increased bronchovascular pattern, there may be no pathological changes. Along with this, with KM, clear signs of focal or diffuse pneumonia, abscess formation with the development of pleurisy, pyopneumothorax, or even gangrenization of the lungs can be detected.
Local changes are also characterized by significant differences, depending on the location and extent of the primary and purulent lesion and the duration of the disease. Many authors consider the characteristic signs of the spread of the inflammatory process into the mediastinum to be the appearance of edema and hyperemia on the anterolateral surface of the neck, spreading to the projection of the manubrium of the sternum, supra- and subclavian regions, anterolateral and upper parts of the chest [, 1986].
Pastosity of the skin of the head, neck, and upper limb on the affected side is observed as a manifestation of superior vena cava syndrome (SVVC) [Popov N. G., 1971]. Disturbances of homeostasis have been established, reflecting the state of organs and life support systems.
The blood revealed leukocytosis with a shift to the left and lymphopenia, and an increase in ESR. Significant disorders of protein metabolism, characterized by dysproteinemia, hyperfermentemia, and an increase in the concentration of protein metabolites, were discovered in patients with mediastinitis by V. I. Karandashov A988). In addition, significant changes in the parameters of CBS, gas and electrolyte composition of the blood were revealed [, 1988].
Diagnostics.Based on the data we obtained [Gubin M. A., 1987, 1990], differential diagnostic signs were established that reflect the phases and dynamics of the development of KM. Each phase is characterized by certain clinical and laboratory parameters. Thus, in the reactive phase of the disease, the clinical picture includes local complaints (pain when swallowing, aggravated by eating and turning the neck in a healthy direction, limited mouth opening, painful swelling on the side of the neck, spontaneously occurring pain in the chest, against the background of moderate intoxication ) predominate in the toxic phase - appear against the background of pronounced intoxication. The terminal phase is typically characterized by the predominance of a general infectious syndrome, indicating deep and persistent intoxication with characteristic signs of central nervous system depression up to complete loss of consciousness. In a comparative assessment of homeostasis indicators in accordance with the phase of the disease, it was found that their changes are nonspecific, reflecting a compensated state in the reactive phase, a subcompensated state in the toxic phase, and a decompensated state of the life support systems in the terminal phase.
X-ray examination occupies an important place in the diagnosis of KM [Zhadovsky M. H., 1973; Shcherbatenko M.K., 1977]. Superexposure or hard photographs with overexposure are recommended, allowing one to determine the position and shape of the trachea, bronchi, and mediastinal vessels, and to more clearly see the limitation of the shadow of inflammatory processes. Other methods of X-ray examination (tomography, pneumomediastinography, etc.), used to diagnose mediastinal diseases, are also used in clinical practice, including computed tomography. N. G. Popov A969), A. M. Sazonov et al. A977) ambiguously assess the value of radiological research methods for diagnosing mediastinitis. The value of these methods increases with multi-projection studies, especially in the dynamics of the disease [et al., 1977].
Along with radiological methods, when diagnosing mediastinitis, electrophysiological research methods are also used: ultrasound dowsing and thermal imaging of the mediastinum [Vishnevsky A. A., 1974; , 1975; , 1978], however, these methods have not yet become widespread. Early diagnosis of KM and their differentiation from phlegmons of the maxillofacial area of the face and neck are significant. telial difficulties. KM is often diagnosed only through pathological examination. The lack of effectiveness of treatment, especially for patients with advanced mediastinitis, also indicates the real difficulties of its early diagnosis, even in a specialized hospital [, 1996].
Differential diagnosis. Schemes for the differential diagnosis of mediastinitis, including those of odontogenic origin, were proposed in different years by N. G. Popov. The main criteria for recognizing phlegmon of the maxillofacial area and neck are given in table ice.
Differential diagnostic signs of phlegmon of the neck and contact mediastenitis
Thus, the spread of the inflammatory process into the mediastinum is characterized by a significant deterioration in the general condition, the appearance of chest pain, choking, difficulty breathing, disruption of neuropsychic activity, severe swelling and infiltration of the peri-maxillary tissues, spreading to the anterior and lateral surfaces of the neck, supraclavicular area and in some patients to the upper chest.
The diagnosis of mediastinitis is confirmed by typical x-ray changes in the form of expansion of the boundaries of the mediastinum, as well as the appearance of additional pathological signals during ultrasound dowsing of the mediastinum.
In patients secondary meningitis and meningoencephalitis clinical manifestations of the disease are more significant. In our observations, all patients complained of a severe headache of a bursting nature without clear localization. In 27% of patients it was accompanied by vomiting. Almost 60% of patients complained of weakness or a feeling of awkwardness in the right or left limbs. In 77% of cases, certain types of consciousness disorders were noted (lethargy, drowsiness, stuporous state). Occasionally, excitement and euphoria may be observed, which, as a rule, are briefly and quickly replaced by mental depression up to loss of consciousness. Convulsions or epileptiform attacks, photophobia are possible. A forced position with the head thrown back is rarely observed.
In all patients, the disease develops against the background of a severe febrile reaction. A sharp rise in body temperature, already elevated due to the underlying disease to 40 0C or more, with chills and heavy sweating, is one of the characteristic first manifestations of the spread of the inflammatory process to the meninges and brain matter. Assessment of regional neurological symptoms is always difficult due to extensive inflammatory swelling of the soft tissues of the facial part of the head and neck. Nevertheless, stiffness of the neck muscles in secondary meningitis and meningoencephalitis is almost always detected. Kernig's sign is characteristic. We detected it in more than half of the patients, but its severity varied. Brudzinski's symptom was observed infrequently in 15-20% of patients. In most cases, damage to the oculomotor nerves was noted in the form of gaze paresis, strabismus, ptosis, and decreased pupillary response to light. In 1A patients, central paresis of the facial nerve was detected. Damage to the branches of the trigeminal nerve was manifested by a decrease in the sensitivity of the skin of half the face. In a number of cases, hemiparesis was noted with increased tendon reflexes, sometimes a decrease in muscle tone on the healthy side, Babinsky's symptom, much less often Rossolimo and Gordon's symptoms,
The cerebrospinal fluid is turbid, the pressure in it increases in all patients C00-450 mmH2O. Art.). Leukocytosis E00-2000 cells in 1 μl), neutrophilia D0-60%), protein content 2.0-5.5 g/l are observed.
A special comprehensive neurological examination reveals congestive changes in the fundus, while an otoneurological examination reveals spontaneous nystagmus and asymmetric hyperreflexia.
Thus, complaints of severe headache, nausea, impaired consciousness, damage to cranial nerves, the presence of paresis, paralysis, inflammatory changes in the cerebrospinal fluid give grounds to diagnose meningitis or meningoencephalitis. The objective factor is lumbar puncture.
For the sick with cavernous sinus thrombosis The most characteristic headaches are of significant intensity, predominantly in the frontal region. It is often accompanied by pain in the eyeball area, nausea and vomiting. Consciousness is often not impaired. In some cases, lethargy, drowsiness, and sometimes anxiety and agitation are noted.
The general condition is often severe, body temperature is always elevated up to hyperthermia D0 0C or more), chills and rapid pulse A00-120 per minute are noted). Rigidity of the neck muscles is revealed; Kernig's sign is usually absent.
Upon examination, in all patients on the affected side, pronounced swelling and congestive hyperemia of the skin of the eyelids and adjacent tissues with dilatation of the superficial veins, chemosis, exophthalmos, ptosis, and limitation of movement of the eyeballs are determined.
Pressure on the eyeball is often accompanied by moderate pain. Swelling of the eyelids may also be on the opposite side. Damage to the oculomotor nerves is characteristic, manifested by limited movement of the eyeballs up to ophthalmoplegia on the affected side. Anisocoria and diplopia are possible. Damage to the trigeminal nerve can be manifested by decreased sensitivity in the half of the forehead and upper eyelid, decreased corneal reflexes, and severe pain in the eye and supraorbital region. Both revival and suppression of tendon reflexes, the appearance of a positive Babinsky sign, and uncertain performance of coordination tests cannot be excluded. Cerebrospinal fluid pressure, as a rule, increases B80-300 mm H2O); it is transparent, the cellular composition is not changed.
Stagnant changes in the fundus are detected. Otoneurological examination reveals a violation of vestibular function. Echoencephalography often reveals an increase in the amplitude of echo signal pulsations, expansion of the third ventricle to 7-10 mm, and the appearance of additional echo complexes. Rheoencephalography can detect signs of diffuse disturbances in blood supply.
In our observations, changes in blood circulation were identified in patients with cavernous sinus thrombosis, which were characterized by a hyperdynamic circulatory regime. An increase in systolic and diastolic pressure, an increase in pulse rate against the background of a deficit of blood volume, a decrease in SI and an increase in CI with a normal level of blood circulation were noted.
Dysproteinemia was revealed due to a decrease in the content of total protein and albumin, an increase in the content of α1-, α2- and γ-globulins with an unchanged level of ß-globulins.
Along with this, the coagulating potential of the blood was increased, and depression of the fibrinolytic activity of the blood was noted. Blood CBS indicators indicated the development of compensated metabolic acidosis.
In a significantly smaller number of patients, a hypodynamic circulatory regime and changes in metabolic processes of a decompensated nature were identified.
The final diagnosis of cavernous sinus thrombosis is established based on the results of a comprehensive clinical and laboratory examination. The most characteristic and reliable symptoms are exophthalmos, ptosis, chemosis, and damage to the oculomotor nerves.
In the early stage of thrombosis of the cavernous sinus, MP Oskolkova and T. K Supiev observed pronounced cyanosis of the mucous membrane of the lips, skin of the forehead, nose, and upright, which, according to the authors, indicates intoxication of the body and disruption of the CVS.
Such complications of gastrointestinal thrombosis are considered especially dangerous.<жнуса, как меншлтг, менинго-энцефалит, абсцесс шповного мозга, сепсис.
Treatment of cavernous sinus thrombosis is carried out in intensive care or intensive care units.
The same list of infusion-transfusion therapy measures is used as for thrombophlebitis.
Antithrombic therapy proposed (1977) is a continuous intravenous infusion of heparin (150-250 SD/kg per day), rheopolyglucin (0.5-1.0 g/kg per day), nicotinic acid (2.5 mg/day). ig per day), against this background, trental (3 mg/dg) is administered intravenously, gradually moving to oral administration of 100-200 mg trental Zr per day. After the end of the continuous infusion, heparin is given intravenously (50-75 IU/kg every 3 hours); after 1 week, heparin is administered at the same dose, but every 4 hours, with a further dose reduction.
Despite the fact that an increase in blood clotting is considered in the sinus, the authors point out that the use of anticoagulants is unsafe due to the possibility of hemorrhage and cerebral infarction. according to the authors, as well as (1975), in such cases, it is more correct to prescribe desinolytic drugs against the background of hypothermia, and anticoagulants are prescribed only if there is a clear general tendency to thrombus formation (presence of thrombophlebitis of extracrural localization, risk of pulmonary embolism).
Literature:
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3. , “Fundamentals of surgical dentistry” Kyiv, 1984 G .
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5. , “Differential diagnosis of inflammatory diseases of the maxillofacial area”, Leningrad, 1982.
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