Chronic pelvic pain syndrome in women. Pain syndrome Neuropathic pain syndromes

Pain in the pelvic area usually occurs against the background of real-life pathologies of the pelvic organs, primarily reproductive ones. There are gynecological and non-gynecological causes of chronic pelvic pain in women. In 75-77% of patients, the following diseases of the female genital area become the morphological basis:
Inflammatory pathologies. Periodic and constant pain syndrome is accompanied by chronic endometritis, salpingitis, adnexitis, oophoritis.
Adhesive processes. Pelvic pain is one of the characteristic signs of plastic pelvioperitonitis and adhesions of the fallopian tubes.
Volumetric neoplasms. Pain occurs with sactosalpinx, ovarian cyst, submucous myoma, ovarian or uterine cancer, and other benign and malignant neoplasias.
Genital and extragenital endometriosis. Aseptic tissue inflammation due to cyclic rejection of endometriotic growths can provoke pain.
Varicose veins of the pelvic veins. The pathological dilatation of the pelvic vessels and the resulting venous congestion have a stimulating effect on the nerve endings located in the pelvic cavity.
Allen syndrome. Masters. Characteristic pelvic pain appears in women who have suffered trauma during childbirth with rupture of the uterine ligaments.
In 21-22% of cases, chronic pain has an organic non-gynecological basis. These reasons include:
Urological pathology. Pain is observed with urolithiasis, kidney prolapse, dystopia and developmental anomalies, chronic cystitis.
Pathology of the peripheral nervous system. Chronic pain is characteristic of inflammatory and other lesions of the intrapelvic nerve plexuses.
Gastrointestinal diseases. Painful sensations are expressed in irritable bowel syndrome, chronic colitis and proctitis, appendicular-genital syndrome, and adhesive disease.
Retroperitoneal neoplasia. Pelvic pain occurs with kidney tumors, ganglioneuromas and other space-occupying processes localized behind the peritoneum.
Bone diseases. Articular apparatus. Pain syndromes include lumbosacral osteochondrosis, damage to the pubic symphysis, tumors and metastases in the pelvic bones, bone tuberculosis, etc.
In 1.1-1.4% of patients, the causes of chronic pain syndrome are inorganic: pain can be bothersome in mental and some other disorders - abdominal epilepsy, depressive states, psychogenics, hyperventilation syndrome, spasmophilia. In less than 2% of clinical cases, the specific causes of chronic pelvic pain in women remain unidentified.

Acute pain.
Acute pain is defined as pain of short duration of onset with an easily identifiable cause. Acute pain is a warning to the body about the current danger of organic damage or disease. Often persistent and acute pain is also accompanied by aching pain. Acute pain is usually concentrated in a specific area before it somehow spreads wider. This type of pain is usually highly treatable.
Chronic pain.
Chronic pain was originally defined as pain that lasts about 6 months or more. It is now defined as pain that persistently persists beyond the appropriate length of time during which it would normally end. It is often more difficult to heal than acute pain. Particular attention is required when addressing any pain that has become chronic. In exceptional cases, neurosurgeons may perform complex surgery to remove parts of a patient's brain to treat chronic pain. Such an intervention can relieve the patient of the subjective sensation of pain, but since signals from the pain site will still be transmitted through neurons, the body will continue to react to them.
Skin pain.
Skin pain occurs when the skin or subcutaneous tissue is damaged. Cutaneous nociceptors terminate just below the skin and, due to their high concentration of nerve endings, provide a highly precise, localized sensation of pain of short duration.
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Somatic pain.
Somatic pain occurs in ligaments, tendons, joints, bones, blood vessels, and even the nerves themselves. It is determined by somatic nociceptors. Due to the lack of pain receptors in these areas, they produce a dull, poorly localized pain that is longer lasting than that of skin pain. This includes, for example, sprained joints and broken bones.
Inner pain.
Internal pain arises from the internal organs of the body. Internal nociceptors are located in organs and internal cavities. An even greater lack of pain receptors in these areas of the body leads to more dull and prolonged pain, compared to somatic pain. Internal pain is particularly difficult to localize, and some internal organic injuries represent “attributed” pain, where the sensation of pain is attributed to an area of the body that is in no way related to the site of the injury itself. Cardiac ischemia (insufficient blood supply to the heart muscle) is perhaps the best known example of attributable pain; the sensation may be located as a separate feeling of pain just above the chest, in the left shoulder, arm or even in the palm. The pain attributed may be explained by the discovery that pain receptors in internal organs also excite spinal neurons that are excited by skin lesions. Once the brain begins to associate the firing of these spinal neurons with stimulation of somatic tissues in the skin or muscle, pain signals coming from the internal organs begin to be interpreted by the brain as originating from the skin.
Phantom pain.
Phantom limb pain is a sensation of pain that occurs in a lost limb or in a limb that is not felt through normal sensations. This phenomenon is almost always associated with cases of amputation and paralysis.
Neuropathic pain.
Neuropathic pain (“neuralgia”) can appear as a result of damage or disease to the nerve tissues themselves (for example, toothache). This can impair the ability of sensory nerves to transmit correct information to the thalamus (a part of the diencephalon), causing the brain to misinterpret painful stimuli even when there is no obvious physiological cause for the pain.
Psychogenic pain.
Psychogenic pain is diagnosed in the absence of an organic disease or in the case when the latter cannot explain the nature and severity of the pain syndrome. Psychogenic pain is always chronic and occurs against the background of mental disorders: depression, anxiety, hypochondria, hysteria, phobia. In a significant proportion of patients, psychosocial factors play an important role (dissatisfaction with work, desire to obtain moral or material benefit). Particularly strong links exist between chronic pain and depression.

Spontaneously occurring attacks of pain in the tooth associated with inflammation of the pulp. Constant, localized pain in the area of one tooth, often pulsating, aggravated by touching the tooth, is associated with inflammation of the peri-apical tissues. Acute toothache can also be caused by periodontitis, exacerbations of which are accompanied by the formation of periodontal abscesses.

The projection zones of toothache are irradiated cutaneously and zones for up to 4 minutes on the field. The total irradiation time is up to 15 minutes.

Modes of exposure to a tooth crown in the treatment of acute pain The duration of treatment is determined by the onset of positive dynamics. It should be noted that even after effective pain relief, it is necessary to contact a dentist for specialized help.

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Description of dental lesions regarding the classification of caries according to ICD 10

The caries classification system is designed to categorize the degree of damage. It helps to choose a technique for further treatment.

Caries is one of the most famous and common dental diseases throughout the world. If tissue damage is detected, mandatory dental treatment is required to prevent further destruction of dental elements.

General information

Doctors have repeatedly made attempts to create a single, universal system of classifications of human diseases.

As a result, in the 20th century the “International Classification - ICD” was developed. Since the creation of the unified system (in 1948), it has been constantly revised and supplemented with new information.

The final, 10th revision was carried out in 1989 (hence the name ICD-10). Already in 1994, the International Classification began to be used in countries that are members of the World Health Organization.

In the system, all diseases are divided into sections and marked with a special code. Diseases of the oral cavity, salivary glands and jaws K00-K14 belong to the section of diseases of the digestive system K00-K93. It describes all dental pathologies, not just caries.

K00-K14 includes the following list of pathologies related to dental lesions:

Item K00. Problems with development and teething. Edentia, the presence of extra teeth, abnormalities in the appearance of teeth, mottling (fluorosis and other darkening of the enamel), disturbances in the formation of teeth, hereditary underdevelopment of teeth, problems with teething.
Item K01. Impacted (sunk) teeth, i.e. changed position during eruption, in the presence or absence of an obstacle.
Item K02. All types of caries. Enamel, dentin, cement. Suspended caries. Pulp exposure. Odontoclasia. Other types.
Item K03. Various lesions of hard dental tissues. Abrasion, enamel grinding, erosion, granuloma, cement hyperplasia.
Item K04. Damage to the pulp and periapical tissues. Pulpitis, pulp degeneration and gangrene, secondary dentin, periodontitis (acute and chronic apical), periapical abscess with and without cavity, various cysts.
Item K06. Pathologies of the gums and the edge of the alveolar ridge. Recession and hypertrophy, trauma to the alveolar margin and gums, epulis, atrophic ridge, various granulomas.

Item K07. Changes in bite and various jaw anomalies. Hyperplasia and hypopalsia, macrognathia and micrognathia of the upper and lower jaws, asymmetry, prognathia, retrognathia, all types of malocclusion, torsion, diastema, trema, displacement and rotation of teeth, transposition.

Incorrect jaw closure and acquired malocclusions. Diseases of the temporomandibular joint: looseness, clicking when opening the mouth, painful dysfunction of the TMJ.

Item K08. Functional problems with the supporting apparatus and changes in the number of teeth due to exposure to external factors. Loss of teeth due to injury, extraction or disease. Atrophy of the alveolar ridge due to long-term absence of a tooth. Pathologies of the alveolar ridge.

Let's take a closer look at section K02 Dental caries. If a patient wants to find out what entry the dentist made in the chart after treating a tooth, he needs to find the code among the subsections and study the description.

K02.0 Enamels

Initial caries or chalk stain is the primary form of the disease. At this stage, there is still no damage to hard tissues, but demineralization and high susceptibility of the enamel to irritation are already diagnosed.

In dentistry, 2 forms of initial caries are defined:

Active (white spot);
Stable (brown spot).

During treatment, caries in an active form can either become stable or disappear completely.

The brown spot is irreversible; the only way to get rid of the problem is by preparation and filling.

Symptoms:

Pain – toothache is not typical for the initial stage. However, due to the fact that demineralization of the enamel occurs (its protective function is reduced), the affected area may experience strong susceptibility to influences.
External disorders - visible when caries is located on one of the teeth of the outer row. It looks like an inconspicuous white or brown spot.

Treatment directly depends on the specific stage of the disease.

When the stain is chalky, remineralizing treatment and fluoridation are prescribed. When the caries is pigmented, preparation and filling are performed. With timely treatment and oral hygiene, a positive prognosis is expected.

K02.1 Dentine

A huge number of bacteria live in the mouth. As a result of their vital activity, organic acids are released. They are the ones responsible for the destruction of the basic mineral components that make up the crystal lattice of the enamel.

Dentin caries is the second stage of the disease. It is accompanied by a violation of the structure of the tooth with the appearance of a cavity.

However, the hole is not always noticeable. It is often possible to notice irregularities only at a dentist’s appointment when a diagnostic probe is inserted. Sometimes it is possible to notice caries on your own.

Symptoms:

the patient is uncomfortable chewing;
pain from temperatures (cold or hot food, sweet foods);
external disturbances, which are especially visible on the front teeth.

Painful sensations can be provoked by one or several foci of the disease, but quickly disappear after the problem is eliminated.

There are only a few types of dentin diagnostics - instrumental, subjective, objective. Sometimes it is difficult to detect a disease solely based on the symptoms described by the patient.

At this stage, you can no longer do without a drill. The doctor drills the diseased teeth and installs a filling. During the treatment process, the specialist not only tries to preserve the tissue, but also the nerve.

K02.2 Cement

Compared to damage to enamel (initial stage) and dentine, cementum (root) caries is diagnosed much less frequently, but is considered aggressive and harmful to the tooth.

The root is characterized by relatively thin walls, which means that the disease does not take much time to completely destroy the tissue. All this can develop into pulpitis or periodontitis, which sometimes leads to tooth extraction.

Clinical symptoms depend on the location of the disease focus. For example, when the cause is located in the periodontal area, when the swollen gum protects the root from other influences, we can talk about a closed form.

With this outcome, no obvious symptoms are observed. Usually, with a closed location of cement caries, there is no pain or it is not expressed.

Photo of an extracted tooth with cement caries

In an open form, in addition to the root, the cervical area can also be destroyed. The patient may be accompanied by:

External disorders (especially pronounced in the front);
Inconvenience while eating;
Painful sensations from irritants (sweets, temperature, when food gets under the gum).

Modern medicine makes it possible to get rid of caries in several, and sometimes even in one, dentist appointment. Everything will depend on the form of the disease. If the gum covers the lesion, bleeds, or greatly interferes with the filling, then gum correction is performed first.

After getting rid of the soft tissue, the affected area (with or without exposure) is temporarily filled with cement and oil dentin. After the tissue has healed, the patient comes back for a second filling.

K02.3 Suspended

Suspended caries is a stable form of the initial stage of the disease. It appears as a dense pigment spot.

Typically, such caries is asymptomatic, patients do not complain about anything. The stain can be detected during a dental examination.

Caries is dark brown, sometimes black. The surface of tissues is studied by probing.

Most often, the focus of suspended caries is located in the cervical part and natural depressions (pits, etc.).

The treatment method depends on various factors:

The size of the spot - too large formations are prepared and filled;
From the wishes of the patient - if the stain is on the external teeth, then the damage is eliminated with photopolymer fillings so that the color matches the enamel.

Small dense foci of demineralization usually occur over a period of time with a periodicity of several months.

If the teeth are properly cleaned and the amount of carbohydrates consumed by the patient is reduced, then the future progressive development of the disease may be stopped.

When the spot grows and becomes soft, it is prepared and filled.

K02.4 Odontoclasia

Odontoclasia is a severe form of dental tissue damage. The disease affects the enamel, thinning it and leading to the formation of caries. No one is immune from odontoclasia.

The appearance and development of damage is influenced by a huge number of factors. Such prerequisites even include poor heredity, regular oral hygiene, chronic disease, metabolic rate, and bad habits.

The main visible symptom of odontoclasia is toothache. In some cases, due to a non-standard clinical form or an increased pain threshold, the patient does not feel this.

Then only the dentist will be able to make the correct diagnosis during the examination. The main visual sign indicating problems with enamel is tooth damage.

This form of the disease, like other forms of caries, is treatable. The doctor first cleans the affected area, then fills the painful area.

Only high-quality oral cavity prevention and regular dental examinations will help to avoid the development of odontoclasia.

K02.5 With pulp exposure

All tooth tissues are destroyed, including the pulp chamber - the partition separating dentin from the pulp (nerve). If the wall of the pulp chamber is rotten, then the infection penetrates into the soft tissues of the tooth and causes inflammation.

The patient feels severe pain when food and water enter the carious cavity. After cleansing it, the pain subsides. In addition, in advanced cases, a specific smell from the mouth appears.

This condition is considered deep caries and requires long, expensive treatment: mandatory removal of the “nerve”, cleaning of the canals, filling with gutta-percha. Several visits to the dentist are required.

Details of the treatment of all types of deep caries are described in a separate article.

Item added in January 2013.

K02.8 Another view

Another caries is a medium or deep form of the disease that develops in a previously treated tooth (relapse or re-development near the filling).

Medium caries is the destruction of enamel elements on the teeth, accompanied by attack or constant pain in the area of the lesion. They are explained by the fact that the disease has already spread to the upper layers of dentin.

The form requires mandatory dental care, in which the doctor removes the affected areas, followed by their restoration and filling.

Deep caries is a form that is characterized by extensive damage to the internal dental tissues. It affects a large area of dentin.

The disease cannot be ignored at this stage, and refusal of treatment can lead to nerve (pulp) damage. In the future, if you do not get medical help, pulpitis or periodontitis develops.

The affected area is completely removed, followed by restorative filling.

K02.9 Unspecified

Unspecified caries is a disease that develops not on living, but on pulpless teeth (those from which the nerve has been removed). The reasons for the formation of this form do not differ from standard factors. Typically, unspecified caries occurs at the junction of a filling and an infected tooth. Its appearance in other places of the oral cavity is observed much less frequently.

The fact that a tooth is dead does not protect it from developing caries. Teeth depend on the presence of sugar that enters the oral cavity along with food and bacteria. After the bacteria are saturated with glucose, acid begins to form, leading to the formation of plaque.

Caries of a pulpless tooth is treated according to the standard scheme. However, in this case there is no need to use anesthesia. The nerve that is responsible for pain is no longer in the tooth.

Prevention

The condition of dental tissue is greatly influenced by a person’s diet. To prevent caries, you need to follow some recommendations:

eat less sweets and starchy foods;
balance the diet;
monitor vitamins;
chew food well;
rinse your mouth after eating;
brush your teeth regularly and correctly;
avoid eating cold and hot food at the same time;
periodically inspect and sanitize the oral cavity.

The video provides additional information on the topic of the article.

Timely treatment will help you quickly and painlessly get rid of caries. Preventive measures prevent damage to the enamel. It is always better to prevent illness than to treat it.

If you find an error, please select a piece of text and press Ctrl+Enter.

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Other changes in teeth and their supporting apparatus

ICD-10 → K00-K93 → K00-K14 → K08.0

Exfoliation of teeth due to systemic disorders

Loss of teeth due to accident, extraction or localized periodontal disease

Atrophy of the edentulous alveolar margin

Dental root retention [retained root]

K08.8 last modified: January 2011K08.9

Changes in teeth and their supporting apparatus, unspecified

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International statistical classification of diseases and related health problems. 10th revision.

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Acute toothache - Dolor dentalis acutus

Acute toothache is understood as a sudden, sharp sensation of pain in the teeth or alveolar processes.

ETIOLOGY AND PATHOGENESIS

Pain syndrome is a constant companion to most diseases of the maxillofacial region, which is determined by the rich mixed (somatic and autonomic) innervation of this area, leading to the intensity of pain and the possibility of its irradiation to various parts of the maxillofacial region. Some somatic diseases (neuralgia and trigeminal neuritis, otitis media, sinusitis, myocardial infarction and other diseases) can simulate toothache, which makes it difficult to diagnose the existing pathology.

Acute toothache can occur when dental tissue, oral mucosa, periodontal tissue, and bone are damaged.

■ Hyperesthesia of hard dental tissues is often associated with defects of hard tissues (increased tooth abrasion, erosion of hard tissues, wedge-shaped defects, chemical damage to enamel, gum recession, etc.).

■ Caries is a pathological process manifested by damage to the hard tissues of the tooth, their demineralization and softening with the formation of a cavity.

■ Pulpitis is an inflammation of the dental pulp that occurs when microorganisms or their toxins, chemical irritants penetrate into the dental pulp (through a carious cavity, the apical foramen of the tooth root, from a periodontal pocket, hematogenously), as well as during trauma to the dental pulp.

■ Periodontitis is an inflammation of the periodontium that develops when microorganisms, their toxins, and pulp decay products enter the periodontium, as well as when a tooth is injured (bruise, dislocation, fracture).

■ Trigeminal neuralgia is a polyetiological disease, in the genesis of which disturbances in the peripheral and central mechanisms of regulation of pain sensitivity are important. With pathology of the molars, pain can spread to the temporal region, lower jaw, radiate to the larynx and ear, and parietal region. When incisors and premolars are affected, pain can spread to the forehead, nose, and chin.

CLASSIFICATION

Acute toothache is classified according to the nature of the pathological process that caused it.

■ Acute toothache caused by damage to hard tissues, dental pulp and periodontal tissues, which requires outpatient treatment by a dentist.

■ Acute toothache caused by the involvement of bone and bone marrow, which requires urgent hospitalization in a dental surgical hospital or the department of maxillofacial surgery.

CLINICAL PICTURE

Acute toothache can have a different nature and occur in different situations, which depends on what tissues are affected and how much they are affected.

The nature of pain when hard tissues are damaged depends on the depth of the pathological process.

■ With enamel hyperesthesia and superficial caries, the pain is acute, but short-lived. It occurs when exposed to exogenous (temperature and chemical) irritants and stops after the source of irritation is eliminated. Examination of teeth with superficial caries reveals a shallow carious cavity within the enamel, with uneven edges. Probing may be painful.

■ With average caries, enamel and dentin are affected; upon probing, the cavity is deeper; pain arises not only from thermal and chemical, but also from mechanical irritants, and disappears after their elimination.

■ With deep caries, when food gets into the carious cavity, a short-term, acute toothache occurs, which disappears when the irritant is eliminated. Since deep caries leaves a thin layer of dentin covering the tooth pulp, focal pulpitis may develop.

■ Pulpitis is characterized by more intense pain than with caries, which can occur for no apparent reason.

□ In acute focal pulpitis, acute toothache is localized, paroxysmal, short-term (lasts a few seconds), occurs for no apparent reason, but can be prolonged when exposed to temperature stimuli, intensifies at night. The intervals between painful attacks are long.

Over time, the pain becomes longer lasting. The carious cavity is deep, probing the bottom is painful.

□ In acute diffuse pulpitis, prolonged attacks of acute widespread toothache are noted, worsening at night, radiating along the branches of the trigeminal nerve, with short periods of remission. The carious cavity is deep, probing the bottom is painful.

□ With the development of a chronic process (chronic fibrous pulpitis, chronic hypertrophic pulpitis, chronic gangrenous pulpitis), the intensity of the pain syndrome decreases, the pain becomes aching and chronic, often occurring only when eating and brushing teeth.

■ In acute periodontal disease and exacerbation of chronic periodontitis, the patient complains of constant localized pain of varying intensity, aggravated by eating and percussion, a feeling that the tooth has “grown”, as if it has become taller. When examining the oral cavity, hyperemia and swelling of the gums and its pain on palpation are revealed. With exacerbation of chronic periodontitis, there may be a fistula tract with purulent discharge.

Percussion of the affected tooth is painful; probing may reveal an open tooth cavity. Subsequently, the general condition worsens, collateral edema of the soft tissues of the face appears, and sometimes enlarged, painful submandibular lymph nodes are palpated. With chronic periodontitis, the pain is less severe. There may be constant aching pain in the area of the affected tooth, but in some patients it is absent.

■ With trigeminal neuralgia, paroxysmal jerking, cutting, burning pains appear in a certain area of the face, corresponding to the zone of innervation of one or more branches of the trigeminal nerve.

Severe pain does not allow the patient to talk, wash, or eat for fear of provoking a new attack. The attacks occur suddenly and also stop. They may be accompanied by vegetative manifestations (hyperemia in the area of innervation of the affected branch of the trigeminal nerve, dilation of the pupil on the affected side, increased amount of saliva, lacrimation) and contraction of facial muscles. With neuralgia of the second branch of the trigeminal nerve, the pain syndrome can spread to the teeth of the upper jaw, and with neuralgia of the third branch of the trigeminal nerve - to the teeth of the lower jaw.

When palpating the zone of innervation of the corresponding branch of the trigeminal nerve, hyperesthesia of the facial skin can be detected, and when pressing on the pain points, an attack of neuralgia can be provoked. A characteristic feature of trigeminal neuralgia is the absence of pain during sleep.

The characteristics and localization of pain in diseases of the maxillofacial region are given below.

■ Superficial caries. Painful sensations can be of varying intensity and have a paroxysmal nature: short-term localized (in the area of the causative tooth) pain occurs under the action of chemical, thermal, and less often mechanical stimuli and disappears after the stimulus is eliminated.

■ Average caries. The pain is usually dull, short-term, localized in the area of the causative tooth, occurs under the action of chemical, thermal, and less often mechanical stimuli and disappears after the stimulus is eliminated.

■ Deep caries is characterized by the occurrence of acute localized (in the area of the causative tooth) intense pain when food enters the carious cavity, which disappears after the irritant is removed.

■ Acute focal pulpitis. The concern is short-term localized (in the area of the causative tooth) intense acute pain, which has a spontaneous paroxysmal nature. The pain intensifies at night.

■ Acute diffuse pulpitis. The pain is intense, long-lasting, and has an acute spontaneous nature. The pain is not localized, radiates along the branches of the trigeminal nerve and intensifies at night.

■ Acute periodontitis and exacerbation of chronic periodontitis are characterized by acute paroxysmal, pulsating, prolonged (with rare intervals of remission) pain. The pain is localized in the area of the causative tooth, has varying intensity, and intensifies with eating and percussion of the affected tooth. The patient notes the feeling that the tooth has “grown.”

■ Trigeminal neuralgia. The pain is acute, paroxysmal, and often occurs when talking and touching the skin of the face. The pain is not localized and radiates along the branches of the trigeminal nerve. The pain is intense, weakens or stops at night, and is usually short-term in nature.

DIFFERENTIAL DIAGNOSTICS

Differential diagnosis of lesions of hard tissues and dental pulp is not indicated in emergency medical care.

To resolve the issue of hospitalization of a patient at the prehospital stage, differential diagnosis of acute osteomyelitis with acute purulent periostitis and exacerbation of chronic periodontitis is important.

■ Acute periodontitis. Characterized by constant localized pain of varying intensity, aggravated by eating and percussion of the affected tooth. The patient complains of a feeling that the tooth has “grown” and sleep disturbances. During an objective examination, a deterioration in the patient’s general condition is noted, a possible increase in body temperature, and an increase in regional lymph nodes. When examining the oral cavity, hyperemia and swelling of the gum mucosa and its pain on palpation are revealed; there may be a fistula tract with purulent discharge.

Therapeutic or surgical outpatient treatment is indicated.

■ With acute purulent periostitis, severe, sometimes throbbing pain occurs. During an objective examination, an increase in body temperature, collateral edema of surrounding tissues, and enlargement of regional lymph nodes are noted. When examining the oral cavity, swelling and hyperemia of the mucous membrane of the gum edge, smoothness and hyperemia of the transitional fold are revealed. Outpatient emergency surgical treatment is indicated.

■ In acute osteomyelitis, the patient complains of pain in the area of the causative tooth, which quickly spreads and intensifies. During an objective examination, severe intoxication, increased body temperature, chills, weakness, collateral edema of surrounding tissues, and enlarged regional lymph nodes are noted; in severe cases, pus can spread into the surrounding soft tissue with the development of phlegmon. When examining the oral cavity, hyperemia and swelling of the mucous membrane in the area of the gum edge is revealed. Urgent hospitalization and surgical treatment in a hospital followed by conservative therapy are indicated.

ADVICE FOR THE CALLER

■ If the body temperature is normal and there is no collateral edema, to alleviate the condition, the patient should be given NSAIDs (ketoprofen, ketorolac, lornoxicam, paracetamol, revalgin, solpadeine, ibuprofen, indomethacin, etc.), then be sure to consult a dentist.

■ If you have elevated body temperature and the presence of collateral tissue edema, you must urgently contact a dental surgeon.

■ In cases of high body temperature, severe intoxication, chills, collateral edema, and enlarged regional lymph nodes, urgent hospitalization of the patient in a specialized surgical department is necessary.

ACTIONS ON CALL

Diagnostics

REQUIRED QUESTIONS

■ How is the patient feeling?

■ What is your body temperature?

■ How long has the tooth hurt?

■ Have you had any attacks of acute tooth pain before?

■ Is there swelling of the gums or face?

■ What kind of pain is felt: in a specific tooth or does the pain radiate?

■ Does the pain occur spontaneously or under the influence of any irritants (food, cold air, cold or hot water)?

■ Does the pain stop when the stimulus stops?

■ What is the nature of the pain (sharp, dull, aching, paroxysmal or constant, long-term or short-term)?

■ Is it difficult to eat?

■ Does the nature of the pain change at night?

■ Are there functional disorders of the dental system (mouth opening, speaking, etc.)?

In cases where there is diffuse pain and collateral tissue swelling, the following points need to be clarified.

■ Is there any soft tissue swelling, infiltrates or pus discharge?

■ Is general weakness bothering you?

■ Has your body temperature increased?

■ Are chills bothering you?

■ How does the mouth open?

■ Is swallowing difficult?

■ Has the patient taken any medications?

■ Is the pain relieved by the drugs used (NSAIDs)?

INSPECTION AND PHYSICAL EXAMINATION

Examination of a patient with acute toothache includes several stages.

■ External examination of the patient (facial expression and symmetry, closure of teeth, skin color).

■ Examination of the oral cavity.

□ Condition of teeth (carious teeth, enamel hypoplasia, wedge-shaped defect, fluorosis, increased enamel abrasion).

□ Condition of the gum margin (hyperemia, swelling, bleeding, presence of a periodontal pocket, fistulous tract, etc.).

□ Condition of the oral mucosa.

■ Palpation of soft tissues and bones of the maxillofacial area, regional submandibular and submental lymph nodes, as well as lymph nodes of the neck and supraclavicular areas.

■ Identification of specific symptoms of neuralgia.

Determination of facial skin hyperesthesia.

Provoking an attack of trigeminal neuralgia by pressing on pain points (the first in the infraorbital region, 1 cm below the edge of the orbit along the pupillary line, the second on the lower jaw, below 4-5 teeth, in the projection of the mental foramen).

INSTRUMENTAL RESEARCH

It is not carried out at the prehospital stage.

The main task when providing emergency medical care to a patient with acute dental pain at the prehospital stage is to identify patients with acute osteomyelitis and their urgent hospitalization. NSAIDs are prescribed to relieve acute toothache.

INDICATIONS FOR HOSPITALIZATION

Patients with severe symptoms of intoxication, increased body temperature to 38 ° C or higher, chills, weakness, collateral edema of surrounding tissues, enlarged regional lymph nodes are indicated for urgent hospitalization in a surgical dental hospital or the department of maxillofacial surgery.

■ Patients with acute purulent periostitis are prescribed NSAIDs to relieve pain and antibacterial drugs and recommended to urgently consult a dental surgeon for outpatient care.

COMMON ERRORS

■ Insufficiently complete history taking.

■ Incorrect assessment of the prevalence and severity of the inflammatory process.

■ Incorrect differential diagnosis, leading to errors in diagnosis and treatment tactics.

■ Prescribing drugs without taking into account the somatic condition and the drug therapy used by the patient.

■ Unreasonable prescription of antibacterial drugs and glucocorticoids.

METHOD OF APPLICATION AND DOSES OF MEDICINES The method of administration and doses of drugs are given below. ■ Diclofenac is prescribed orally at a dose of 25-50 mg (for pain syndrome up to 75 mg once) 2-3 times a day. The maximum daily dose is 150 mg. ■ Ibuprofen is prescribed orally at a dose of 200-400 mg 3-4 times a day. The maximum daily dose is 3 g. ■ Indomethacin is prescribed orally at a dose of 25 mg 3-4 times a day. The maximum daily dose is 200 mg. ■ Ketoprofen is prescribed orally at a dose of 30-50 mg 3-4 times a day, rectally at 100 mg 2-3 times a day, intramuscularly at 100 mg 1-2 times a day and intravenously at 100-200 mg/ days The maximum daily dose is 300 mg. ■ Ketorolac: to relieve severe pain, the first dose of 10-30 mg is administered intramuscularly, then 10 mg orally 4-6 times a day. The maximum daily dose is 90 mg. ■ Lornoxicam is prescribed orally, intramuscularly and intravenously at a dose of 8 mg 2 times a day. The maximum daily dose is 16 mg. ■ Paracetamol is prescribed orally at 500 mg 4 times a day. The maximum daily dose is 4 g. ■ Revalgin* is prescribed orally at a dose of 1-2 tablets 2-3 times a day. The maximum daily dose is 6 tablets.

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By its biological origin, pain is a signal of danger and trouble in the body, and in medical practice such pain is often considered as a symptom of a disease that occurs when tissue is damaged due to injury, inflammation or ischemia. The formation of pain sensation is mediated by the structures of the nociceptive system. Without the normal functioning of systems that provide pain perception, the existence of humans and animals is impossible. The sensation of pain forms a whole complex of defensive reactions aimed at eliminating damage.

Pain is the most common and subjectively difficult complaint of patients. It causes suffering to many millions of people around the world, significantly worsening the human condition. Today it has been proven that the nature, duration and intensity of pain depend not only on the damage itself, but are also largely determined by unfavorable life situations, social and economic problems. Within the framework of the biopsychosocial model, pain is considered as the result of a two-way dynamic interaction of biological (neurophysiological), psychological, social, religious and other factors. The result of such interaction will be the individual nature of the pain sensation and the form of the patient’s response to pain. According to this model, behavior, emotions, and even simple physiological reactions change depending on a person's attitude to current events. Pain is the result of simultaneous dynamic processing of impulses from nociceptors and a large number of other incoming exteroceptive (auditory, visual, olfactory) and interoceptive (visceral) signals. Therefore, pain is always subjective and each person experiences it differently. The same irritation can be perceived by our consciousness in different ways. The perception of pain depends not only on the location and nature of the injury, but also on the conditions or circumstances under which the injury occurred, on the psychological state of the person, his individual life experience, culture, and national traditions.

Psychological and social problems can have a significant impact on a person's experience of pain. In these cases, the strength and duration of pain may exceed its signaling function and may not correspond to the degree of damage. Such pain becomes pathological. Pathological pain (pain syndrome), depending on its duration, is divided into acute and chronic pain. Acute pain is new, recent pain that is inextricably linked with the injury that caused it and, as a rule, is a symptom of some disease. Acute pain usually disappears when the damage is repaired. Treatment of such pain is usually symptomatic, and, depending on its intensity, either non-narcotic or narcotic analgesics are used. The course of pain as a symptom accompanying the underlying disease is favorable. When the function of damaged tissues is restored, pain symptoms disappear. However, in some patients the duration of pain may exceed the duration of the underlying disease. In these cases, pain becomes the leading pathogenic factor, causing serious disruption of many body functions and reducing the life expectancy of patients. According to the European Epidemiological Study, the incidence of chronic non-cancer pain syndromes in Western European countries is about 20%, that is, every fifth adult European suffers from chronic pain syndrome.

Among chronic pain syndromes, the most common are pain due to joint disease, back pain, headaches, musculoskeletal pain, and neuropathic pain. Doctors are faced with a situation in which identification and elimination of damage is not accompanied by the disappearance of pain. In conditions of chronic pain syndrome, as a rule, there is no direct connection with organic pathology, or this connection is of an unclear, uncertain nature. According to the definition of experts from the International Association for the Study of Pain, chronic pain includes pain lasting more than three months and lasting beyond the normal period of tissue healing. Chronic pain began to be considered not as a symptom of any disease, but as an independent disease requiring special attention and complex etiopathogenetic treatment. The problem of chronic pain, due to its high prevalence and variety of forms, is so important and significant that in many countries specialized pain centers and clinics have been created to treat patients with pain syndromes.

What underlies the chronicity of pain and why is chronic pain resistant to the action of classical analgesics? Finding answers to these questions is of extreme interest to researchers and doctors and largely determines modern trends in the study of pain.

All pain syndromes, depending on etiopathogenesis, can be divided into three main groups: nociceptive, neuropathic and psychogenic (pain of a psychological nature). In real life, these pathophysiological variants of pain syndromes often coexist.

Nociceptive pain syndromes

Nociceptive pain is considered to be pain that occurs as a result of tissue damage with subsequent activation of nociceptors - free nerve endings activated by various damaging stimuli. Examples of such pain are postoperative pain, pain during injury, angina pectoris in patients with coronary heart disease, epigastric pain in gastric ulcers, pain in patients with arthritis and myositis. The clinical picture of nociceptive pain syndromes always reveals areas of primary and secondary hyperalgesia (areas with increased pain sensitivity).

Primary hyperalgesia develops in the area of tissue damage, the zone of secondary hyperalgesia spreads to healthy (undamaged) areas of the body. The development of primary hyperalgesia is based on the phenomenon of nociceptor sensitization (increased sensitivity of nociceptors to the action of damaging stimuli). Sensitization of nociceptors occurs due to the action of substances that have a pro-inflammatory effect (prostaglandins, cytokines, biogenic amines, neurokinins, etc.) and come from the blood plasma, released from damaged tissue, and also secreted from the peripheral terminals of C-nociceptors. These chemical compounds, interacting with the corresponding receptors located on the nociceptor membrane, make the nerve fiber more excitable and more sensitive to external stimuli. The presented mechanisms of sensitization are characteristic of all types of nociceptors localized in any tissue, and the development of primary hyperalgesia is noted not only in the skin, but also in muscles, joints, bones and internal organs.

Secondary hyperalgesia occurs as a result of central sensitization (increased excitability of nociceptive neurons in the structures of the central nervous system). The pathophysiological basis for the sensitization of central nociceptive neurons is the long-term depolarizing effect of glutamate and neurokinins released from the central terminals of nociceptive afferents due to intense constant impulses coming from the area of damaged tissue. The resulting increased excitability of nociceptive neurons can persist for a long time, contributing to the expansion of the area of hyperalgesia and its spread to healthy tissue. The severity and duration of sensitization of peripheral and central nociceptive neurons directly depend on the nature of tissue damage, and in the case of tissue healing, the phenomenon of peripheral and central sensitization disappears. In other words, nociceptive pain is a symptom that occurs when tissue is damaged.

Neuropathic pain syndromes

Neuropathic pain, as defined by experts from the International Association for the Study of Pain, is a consequence of primary damage or dysfunction of the nervous system, however, changes were made to the definition at the 2nd International Congress on Neuropathic Pain (2007). According to the new definition, neuropathic pain includes pain resulting from direct damage or disease to the somatosensory system. Clinically, neuropathic pain is manifested by a combination of negative and positive symptoms in the form of partial or complete loss of sensitivity (including pain) with the simultaneous occurrence in the affected area of unpleasant, often pronounced pain in the form of allodynia, hyperalgesia, dysesthesia, hyperpathia. Neuropathic pain can occur both when the peripheral nervous system and the central structures of the somatosensory analyzer are damaged.

The pathophysiological basis of neuropathic pain syndromes is a violation of the mechanisms of generation and conduction of nociceptive signals in nerve fibers and the processes of controlling the excitability of nociceptive neurons in the structures of the spinal cord and brain. Damage to nerves leads to structural and functional transformations in the nerve fiber: the number of sodium channels on the nerve fiber membrane increases, new atypical receptors and zones for generating ectopic impulses appear, mechanosensitivity occurs, and conditions are created for cross-excitation of dorsal ganglion neurons. All of the above forms an inadequate response of the nerve fiber to irritation, contributing to a significant change in the pattern of the transmitted signal. Increased impulses from the periphery disorganize the work of central structures: sensitization of nociceptive neurons occurs, the death of inhibitory interneurons occurs, neuroplastic processes are initiated, leading to new interneuron contacts of tactile and nociceptive afferents, and the efficiency of synaptic transmission increases. Under these conditions, the formation of pain is facilitated.

However, damage to the peripheral and central structures of the somatosensory system, in our opinion, cannot be considered as a direct independent cause of neuropathic pain, but is only a predisposing factor. The basis for such reasoning is data indicating that neuropathic pain does not always occur, even in the presence of clinically confirmed damage to the structures of the somatosensory analyzer. Thus, transection of the sciatic nerve leads to the appearance of pain behavior in only 40-70% of rats. Spinal cord injury with symptoms of hypalgesia and temperature hypoesthesia is accompanied by central pain in 30% of patients. No more than 8% of patients who have suffered a cerebral stroke with a deficit of somatosensory sensitivity experience neuropathic pain. Postherpetic neuralgia, depending on the age of the patients, develops in 27-70% of patients who have had herpes zoster.

Neuropathic pain in patients with clinically verified sensory diabetic polyneuropathy is observed in 18-35% of cases. Conversely, in 8% of cases, patients with diabetes have clinical symptoms of neuropathic pain in the absence of signs of sensory polyneuropathy. Considering also that the severity of pain symptoms and the degree of sensitivity impairment in the vast majority of patients with neuropathies are not interrelated, it can be assumed that for the development of neuropathic pain, the presence of damage to the somatosensory nervous system is not enough, but requires a number of conditions leading to disruption of integrative processes in the field of systemic regulation of pain sensitivity. That is why in the definition of neuropathic pain, along with indicating the root cause (damage to the somatosensory nervous system), there should be either the term “dysfunction” or “dysregulation”, reflecting the importance of neuroplastic reactions affecting the stability of the pain sensitivity regulation system to the action of damaging factors. In other words, a number of individuals initially have a predisposition to the development of persistent pathological conditions, including in the form of chronic and neuropathic pain.

This is indicated by data on the existence in rats of different genetic lines of high and low resistance to the development of neuropathic pain syndrome after transection of the sciatic nerve. In addition, analysis of diseases comorbid with neuropathic pain also indicates an initial failure of the body’s regulatory systems in these patients. In patients with neuropathic pain, the incidence of migraine, fibromyalgia, and anxiety and depressive disorders is significantly higher compared to patients without neuropathic pain. In turn, in patients with migraine, the following diseases are comorbid: epilepsy, irritable bowel syndrome, gastric ulcer, bronchial asthma, allergies, anxiety and depressive disorders. Patients with fibromyalgia are more likely to suffer from hypertension, irritable bowel syndrome, osteoarthritis, anxiety and depressive disorders. The listed diseases, despite the variety of clinical symptoms, can be classified as so-called “diseases of regulation,” the essence of which is largely determined by the dysfunction of the body’s neuroimmunohumoral systems, which are unable to ensure adequate adaptation to stress.

The study of the characteristics of bioelectrical activity of the brain in patients with neuropathic, chronic and idiopathic pain syndromes indicates the presence of similar changes in the background EEG rhythm, reflecting dysfunction of cortical-subcortical relationships. The presented facts suggest that for the occurrence of neuropathic pain, a dramatic combination of two main events is necessary - damage to the structures of the somatosensory nervous system and dysfunction in the cortical-subcortical relations of the brain. It is the presence of dysfunction of the brain stem structures that will largely determine the brain’s response to damage, contribute to the existence of long-lasting hyperexcitability of the nociceptive system and the persistence of pain symptoms.

Psychogenic pain syndromes

Psychogenic pain syndromes according to the classification of the International Association for the Study of Pain include:

Pain provoked by emotional factors and caused by muscle tension;

Pain as delusions or hallucinations in patients with psychosis, disappearing with treatment of the underlying disease;

Pain due to hysteria and hypochondria, which does not have a somatic basis;

Pain associated with depression, not preceding it and not having any other cause.

In the clinic, psychogenic pain syndromes are characterized by the presence in patients of pain that is not explained by any known somatic diseases or damage to the structures of the nervous system. The localization of this pain usually does not correspond to the anatomical features of the tissues or areas of innervation, the defeat of which could be suspected as the cause of the pain. Situations are possible in which somatic damage, including disorders of the structures of the somatosensory nervous system, can be detected, but the intensity of pain significantly exceeds the degree of damage. In other words, the leading, triggering factor in the genesis of psychogenic pain is a psychological conflict, and not damage to somatic or visceral organs or structures of the somatosensory nervous system.

Identifying psychogenic pain is quite a difficult task. Psychogenic pain syndromes often occur in the form of a somatoform pain disorder, in which pain symptoms cannot be explained by existing somatic pathology and they are not intentional. Patients prone to somatoform disorders are characterized by a history of multiple somatic complaints that appeared before the age of 30 and lasted for many years. According to ICD-10, chronic somatoform pain disorder is characterized by a combination of pain with emotional conflict or psychosocial problems, therefore, it is necessary to identify a psychogenic etiological factor, which can be judged by the presence of temporary connections between pain symptoms and psychological problems. To correctly diagnose a somatoform pain disorder, consultation with a psychiatrist is necessary to differentiate this condition from depression, schizophrenia and other mental disorders, in the structure of which pain syndromes may also be noted. The concept of somatoform pain disorder was introduced into the classification of mental disorders relatively recently, and to this day it causes a lot of debate.

At the same time, it must be remembered that the occurrence of pain, including psychogenic pain, is possible only if the nociceptive system is activated. If, when nociceptive or neuropathic pain occurs, direct activation of the structures of the nociceptive system occurs (due to tissue injury or damage to the structures of the somatosensory nervous system), then in patients with psychogenic pain, indirect excitation of nociceptors is possible - either through the mechanism of retrograde activation by sympathetic efferents and/or through reflex muscle tension . Prolonged muscle tension during psychoemotional disorders is accompanied by increased synthesis of algogens in muscle tissue and sensitization of nociceptor terminals localized in the muscles.

Psychological conflict is almost always also accompanied by activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, which can, through alpha2-adrenergic receptors localized on the membrane of nociceptors, contribute to retrograde excitation of nociceptors and their subsequent sensitization through mechanisms of neurogenic inflammation. Under conditions of neurogenic inflammation, neurokinins (substance P, neurokinin A, etc.) are secreted from the peripheral terminals of nociceptors into the tissue, which have a pro-inflammatory effect, causing an increase in vascular permeability and the release of prostaglandins, cytokines and biogenic amines from mast cells and leukocytes. In turn, inflammatory mediators, acting on the membrane of nociceptors, increase their excitability. The clinical manifestation of nociceptor sensitization in psychoemotional disorders will be areas of hyperalgesia, which are easily diagnosed, for example, in patients with fibromyalgia or tension headaches.

Conclusion

The presented data indicate that pain syndrome, regardless of the etiology of its occurrence, is the result of not only functional, but also structural changes affecting the entire nociceptive system - from tissue receptors to cortical neurons. With nociceptive and psychogenic pain, functional and structural changes in the pain sensitivity system are manifested by sensitization of peripheral and central nociceptive neurons, as a result of which the efficiency of synaptic transmission increases and persistent hyperexcitability of nociceptive neurons occurs. In patients with neuropathic pain, structural changes in the nociceptive system are more significant and include the formation of loci of ectopic activity in damaged nerves and pronounced changes in the integration of nociceptive, temperature and tactile signals in the central nervous system. It is also necessary to emphasize that the pathological processes observed in the nociceptive structures of the peripheral and central nervous systems are closely interrelated in the dynamics of the development of any pain syndrome. Damage to tissues or peripheral nerves, increasing the flow of nociceptive signals, leads to the development of central sensitization (long-term increase in the efficiency of synaptic transmission and hyperactivity of nociceptive neurons of the spinal cord and brain).

In turn, an increase in the activity of central nociceptive structures is reflected in the excitability of nociceptors, for example, through the mechanisms of neurogenic inflammation, as a result of which a vicious circle is formed that maintains long-lasting hyperexcitability of the nociceptive system. It is obvious that the stability of such a vicious circle and, therefore, the duration of pain will depend either on the duration of the inflammatory process in the damaged tissues, providing a constant flow of nociceptive signals into the structures of the central nervous system, or on the initially existing cortical-subcortical dysfunction in the central nervous system, due to which central sensitization will be maintained and retrograde activation of nociceptors. This is also indicated by the analysis of the dependence of the occurrence of long-term pain on age. It has been proven that the appearance of chronic pain syndrome in old age is most often caused by degenerative joint diseases (nociceptive pain), while idiopathic chronic pain syndromes (fibromyalgia, irritable bowel syndrome) and neuropathic pain rarely begin in old age.

Thus, the determining factor in the formation of chronic pain syndrome is the genetically determined reactivity of the body (primarily the structures of the central nervous system), which is, as a rule, excessive and not adequate to the damage, resulting in a vicious circle that maintains long-lasting hyperexcitability of the nociceptive system.

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M. L. Kukushkin, Doctor of Medical Sciences, Professor

Establishment of the Russian Academy of Medical Sciences Research Institute of General Pathology and Pathophysiology of the Russian Academy of Medical Sciences, Moscow

Lumbodynia is a collective pain syndrome that characterizes most diseases of the spine and is localized in the lumbar and sacrum areas. The pathology can be not only vertebrogenic or spondylogenic in nature (associated with the functional characteristics of the spine), but also be a consequence of disturbances in the functioning of internal organs: the bladder, kidneys, organs of the reproductive system and digestive tract. Regardless of the etiological factors, lumbodynia, according to the international classification of diseases (ICD 10), refers to vertebroneurological diagnoses and has a universal, single code - M 54.5. Patients with acute or subacute lumbodynia have the right to receive sick leave. Its duration depends on the intensity of pain, their effect on a person’s mobility and his ability to self-care, and the identified degenerative, deformational and dystrophic changes in the osteochondral structures of the spine.

Code M 54.5. in the international classification of diseases it is designated vertebrogenic lumbodynia. This is not an independent disease, therefore this code is used only for the primary designation of the pathology, and after the diagnosis, the doctor enters into the chart and sick leave the code of the underlying disease, which became the root cause of the pain syndrome (in most cases it is chronic osteochondrosis).

Lumbodynia is one of the types of dorsopathy (back pain). The terms “dorsopathy” and “dorsalgia” are used in modern medicine to refer to any pain localized in the region of the C3-S1 segment (from the third cervical vertebra to the first sacral vertebra).

Lumbodynia is called acute, subacute or recurrent (chronic) pain in the lower segment of the back - in the region of the lumbosacral vertebrae. The pain syndrome can have moderate or high intensity, unilateral or bilateral course, local or diffuse manifestations.

Local pain on one side almost always indicates a focal lesion and occurs against the background of compression of the spinal nerves and their roots. If the patient cannot accurately describe where exactly the pain occurs, that is, the unpleasant sensations cover the entire lumbar region, there can be many reasons: from vertebroneurological pathologies to malignant tumors of the spine and pelvis.

What symptoms are the basis for diagnosing lumbodynia?

Lumbodynia is a primary diagnosis that cannot be regarded as an independent disease and is used to designate existing disorders, in particular pain. The clinical significance of such a diagnosis is explained by the fact that this symptom is the basis for conducting an X-ray and magnetic resonance examination of the patient in order to identify deformities of the spine and intervertebral discs, inflammatory processes in paravertebral soft tissues, muscular-tonic status and various tumors.

The diagnosis of “vertebrogenic lumbodynia” can be made either by a local therapist or by specialists (neurologist, orthopedic surgeon, vertebrologist) based on the following symptoms:

severe pain (stabbing, cutting, shooting, aching) or burning in the lower back with transition to the tailbone area, located in the area of the intergluteal fold;
impaired sensitivity in the affected segment (feeling of heat in the lower back, tingling, chills, tingling);
reflection of pain in the lower limbs and buttocks (typical for a combined form of lumbodynia - with sciatica);
decreased mobility and muscle stiffness in the lower back;
increased pain after physical activity or exercise;
easing of pain after prolonged muscle relaxation (at night).

In most cases, an attack of lumbodynia begins after exposure to any external factors, for example, hypothermia, stress, increased stress, but in an acute course, a sudden onset for no apparent reason is possible. In this case, one of the symptoms of lumbodynia is lumbago - acute lumbago in the lower back, occurring spontaneously and always having a high intensity.

Reflex and pain syndromes with lumbodynia, depending on the affected segment

Despite the fact that the term “lumbodynia” can be used as an initial diagnosis in outpatient practice, the clinical course of the pathology is of great importance for a comprehensive diagnosis of the condition of the spine and its structures. With lumbarization of various segments of the lumbosacral spine, the patient experiences a decrease in reflex activity, as well as paresis and reversible paralysis with various localizations and manifestations. These features make it possible, even without instrumental and hardware diagnostics, to assume in which part of the spine degenerative-dystrophic changes have occurred.

Clinical picture of vertebrogenic lumbodynia depending on the affected spinal segment

Affected vertebrae	Possible irradiation (reflection) of lumbar pain	Additional symptoms
Second and third lumbar vertebrae.	Area of the hips and knee joints (along the front wall).	Flexion of the ankles and hip joints is impaired. Reflexes are usually preserved.
Fourth lumbar vertebra.	Popliteal fossa and shin area (mainly on the front side).	Extension of the ankles becomes difficult, abduction of the hip provokes pain and discomfort. Most patients have a pronounced decrease in the knee reflex.
Fifth lumbar vertebra.	The entire surface of the leg, including the legs and feet. In some cases, pain may be reflected in the first toe.	It is difficult to bend the foot forward and abduct the big toe.
Sacral vertebrae.	The entire surface of the leg from the inside, including the feet, heel bone and phalanges.	The Achilles tendon reflex and plantar flexion of the foot are impaired.

Important! In most cases, lumbodynia is manifested not only by reflex symptoms (this also includes neurodystrophic and vegetative-vascular changes), but also by radicular pathology that occurs against the background of pinched nerve endings.

Possible causes of pain

One of the main causes of acute and chronic lumbodynia in patients of various age groups is osteochondrosis. The disease is characterized by degeneration of the intervertebral discs, which connect the vertebrae to each other in a vertical sequence and act as a shock absorber. The dehydrated core loses its elasticity and elasticity, which leads to thinning of the fibrous ring and displacement of the pulp beyond the cartilaginous end plates. This shift can occur in two forms:

Neurological symptoms during attacks of lumbodynia are provoked by compression of nerve endings that extend from nerve trunks located along the central spinal canal. Irritation of the receptors located in the nerve bundles of the spinal nerves leads to attacks of severe pain, which most often has an aching, burning or shooting character.

Lumbodynia is often confused with radiculopathy, but these are different pathologies. (radicular syndrome) is a complex of pain and neurological syndromes caused by direct compression of the nerve roots of the spinal cord. With lumbodynia, the cause of pain can also be myofascial syndromes, circulatory disorders or mechanical irritation of pain receptors by osteochondral structures (for example, osteophytes).

Other reasons

The causes of chronic lower back pain may also include other diseases, which include the following pathologies:

diseases of the spine (vertebral displacement, osteoarthritis, osteosclerosis, spondylitis, etc.);
neoplasms of various origins in the spine and pelvic organs;
infectious and inflammatory pathologies of the spine, abdominal and pelvic organs (spondylodiscitis, epiduritis, osteomyelitis, cystitis, pyelonephritis, etc.);
adhesions in the pelvis (often adhesions form after difficult childbirth and surgical interventions in this area);
injuries and damage to the lower back (fractures, dislocations, bruises);
Swelling and bruising are the main symptoms of a lower back injury
pathologies of the peripheral nervous system;
myofascial syndrome with myogelosis (formation of painful compactions in the muscles due to inadequate physical activity that does not correspond to the age and physical training of the patient).

Provoking factors that increase the risk of lumbodynia may be obesity, abuse of alcoholic beverages and nicotine, increased consumption of caffeine-containing drinks and foods, and chronic lack of sleep.

Factors in the development of acute shooting pain (lumbago) are usually strong emotional experiences and hypothermia.

Important! Lumbodynia during pregnancy is diagnosed in almost 70% of women. If the expectant mother has not been diagnosed with abnormalities in the functioning of internal organs or diseases of the musculoskeletal system that can worsen under the influence of hormones, the pathology is considered physiologically determined. Lower back pain in pregnant women can occur as a result of irritation of the nerve endings by the enlarging uterus or be the result of edema in the pelvic organs (swelling tissue puts pressure on the nerves and blood vessels, causing severe pain). There is no specific treatment for physiological lumbodynia, and all recommendations and prescriptions are aimed primarily at correcting nutrition, lifestyle and maintaining a daily routine.

Is it possible to get sick leave for severe lower back pain?

Disease code M 54.5. is the basis for opening a sick leave due to temporary disability. The duration of sick leave depends on various factors and can range from 7 to 14 days. In especially severe cases, when pain is combined with severe neurological disorders and prevents the patient from performing professional duties (and also temporarily limits the ability to move and fully self-care), sick leave can be extended to 30 days.

The main factors influencing the duration of sick leave for lumbodynia are:

intensity of pain. This is the main indicator that a doctor evaluates when deciding on a person’s ability to return to work. If the patient cannot move, or movements cause him severe pain, the sick leave will be extended until these symptoms resolve;
working conditions. Office workers usually return to work earlier than those performing heavy physical work. This is due not only to the characteristics of the motor activity of these categories of employees, but also to the possible risk of complications if the causes of pain are not completely relieved;
the presence of neurological disorders. If the patient complains of any neurological disorders (poor sensitivity in the legs, heat in the lower back, tingling in the limbs, etc.), the sick leave is usually extended until the possible causes are fully clarified.

Patients who require hospitalization are issued a sick leave certificate from the moment of admission to the hospital. If it is necessary to continue outpatient treatment, the temporary disability certificate is extended for the appropriate period.

Important! If surgical treatment is necessary (for example, for intervertebral hernias larger than 5-6 mm), a sick leave certificate is issued for the entire period of hospital stay, as well as subsequent recovery and rehabilitation. Its duration can range from 1-2 weeks to 2-3 months (depending on the main diagnosis, the chosen treatment method, and the speed of tissue healing).

Limited ability to work with lumbodynia

It is important for patients with chronic lumbodynia to understand that closing sick leave does not always mean complete recovery (especially if the pathology is caused by osteochondrosis and other diseases of the spine). In some cases, with vertebrogenic lumbodynia, the doctor may recommend light work to the patient if the previous working conditions may complicate the course of the underlying disease and cause new complications. These recommendations should not be ignored, since vertebrogenic pathologies almost always have a chronic course, and heavy physical labor is one of the main factors in the exacerbation of pain and neurological symptoms.

Typically, people with limited ability to work are recognized as representatives of the professions listed in the table below.

Professions that require easier working conditions for patients with chronic lumbodynia

Professions (positions)	Causes of limited ability to work
	Forced inclined position of the body (impairs blood circulation in the lumbar region, increases muscle tension, increases compression of nerve endings).
	Lifting heavy objects (can cause an increase in hernia or protrusion, as well as rupture of the fibrous membrane of the intervertebral disc).
	Prolonged sitting (increases the intensity of pain due to severe hypodynamic disorders).
	Staying on your feet for a long time (increases tissue swelling, contributes to increased neurological symptoms in lumbodynia).
	High risk of falling on your back and spinal injury.

Is it possible to serve in the army?

Lumbodynia is not included in the list of restrictions for military service, however, a conscript may be declared unfit for military service due to an underlying disease, for example, grade 4 osteochondrosis, pathological kyphosis of the lumbar spine, spondylolisthesis, etc.

Treatment: methods and drugs

Treatment of lumbodynia always begins with the relief of inflammatory processes and the elimination of painful sensations. In most cases, anti-inflammatory drugs with an analgesic effect from the NSAID group (Ibuprofen, Ketoprofen, Diclofenac, Nimesulide) are used for this purpose.

The most effective regimen of use is considered to be a combination of oral and local dosage forms, but for moderate lumbodynia, it is better to avoid taking tablets, since almost all drugs in this group negatively affect the mucous membranes of the stomach, esophagus and intestines.

Back pain bothers most people, regardless of their age and gender. For severe pain, injection therapy may be performed. We recommend reading, which provides detailed information about injections for back pain: classification, purpose, effectiveness, side effects.

The following can also be used as auxiliary methods for the complex treatment of lumbodynia:

medications to normalize muscle tone, improve blood flow and restore cartilaginous nutrition of intervertebral discs (microcirculation correctors, muscle relaxants, chondroprotectors, vitamin solutions);
paravertebral blockades with novocaine and glucocorticoid hormones;
massage;
manual therapy (methods of traction, relaxation, manipulation and mobilization of the spine;
acupuncture;

If there is no effect from conservative therapy, surgical treatment methods are used.

Video - Exercises for quick treatment of lower back pain

Lumbodynia is one of the common diagnoses in neurological, surgical and neurosurgical practice. Pathology with severe severity is the basis for issuing a certificate of temporary incapacity for work. Despite the fact that vertebrogenic lumbodynia has its own code in the international classification of diseases, treatment is always aimed at correcting the underlying disease and may include medications, physiotherapeutic methods, manual therapy, exercise therapy and massage.

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