Mediastinitis

Mediastinitis is an inflammatory process in the organs of the mediastinum, which often leads to compression of the vessels and nerves. In clinic all inflammatory processes, which in clinical practice most often determine the mediastinal syndrome, including traumatic injuries, are treated with the term "mediastinitis".

Absence of fascial barriers, constant volumetric and spatial movements of loose fiber, caused by pulsation of the heart and vessels, respiratory movements and peristalsis of the esophagus, create ideal conditions for the generalization of the inflammatory process.

According to the anatomical structure of the mediastinum, the anterior and posterior mediastinitis are distinguished, each of which can be upper, middle, lower and total in the level. The clinical course distinguishes between acute and chronic mediastinitis.

Aseptic (fibrous) mediastinitis is extremely rare, mainly inflammation caused by microflora (nonspecific or specific). Ways of penetration of microflora into the mediastinum are different: most often the cause is the trauma of the esophagus (chemical burns, ruptures, damage to the diverticulum, etc.), trachea and bronchi.

Less common is the fascial leaflet from the neck or from adjacent tissues (bifurcation lymph nodes of the trachea, from the pleural cavity, ribs, sternum). Very rarely there is odontogenic infection.

ICD-10 code

J85.3 An abscess of the mediastinum

What causes mediastinitis?

The two most common causes of mediastinitis are esophageal rupture and median sternotomy.

Esophagus rupture can be a complication of esophagoscopy, installation of a Sengstacken-Blackmore probe or a Minnesota hose (with bleeding from varicose veins of the esophagus and stomach). It can also develop with vomiting (Berhaava syndrome).

Median sternotomy is complicated by mediastinitis in approximately 1% of cases.

Chronic fibrosing mediastinitis usually develops due to tuberculosis or histoplasmosis, but is also possible with sarcoidosis, silicosis or fungal infections. An intensive fibrotic process leading to compression of mediastinal structures is characteristic, which can cause the syndrome of the inferior vena cava, stenosis of the trachea or obstruction of the pulmonary arteries or veins.

The cause of primary posterior mediastinitis in 67-80% of cases is mechanical damage to the thoracic esophagus by instruments, foreign bodies. Instrumental (iatrogenic) damages of the esophagus occur during fibroesophagoscopy, bougieirovaniya strictures of the esophagus, cardiodilation, carrying out the probe. In 1-2% of cases, the posterior purulent mediastinitis occurs due to necrosis of the esophagus wall during its chemical burns. A special place in the etiology of the posterior purulent mediastinitis is occupied by the so-called spontaneous esophageal ruptures (Burkhave's syndrome), when as a result of emetic motions or insignificant physical strain there is a longitudinal rupture of the left wall of the esophagus in the supra-diaphragmatic region. This form of esophagus rupture is difficult for early diagnosis. Mediastinitis is most severe. Throwing the contents of the stomach into the pleural cavity quickly leads to the development of pleural empyema, sepsis. The lethality reaches 60-90%.

In surgical practice, the secondary posterior mediastinitis is most often detected - the result of the spread of a purulent process from the cell spaces of the neck. The cause of purulent inflammation in the neck - chemical and mechanical damage to the pharynx and cervical esophagus (apart from the above instrumental manipulation, ruptures of the pharynx and cervical esophagus may be at attempts of endotracheal intubation).

In the etiology of secondary posterior mediastinitis, the following diseases play an important role:

• cervical adenoflegmon,
• odontogenic phlegmon of the bottom of the oral cavity and submandibular spaces,
• tonsillogenic phlegmon of the okolobloccal space,
• retropharyngeal abscess.

The distribution of these purulent processes occurs along the vascular-facial formations both in the posterior mediastinum (70-75%) and in the anterior (25-30%).

In recent years, the incidence of secondary mediastinitis of odontogenic origin has increased from 0.16 to 1.73%, tonsillogenic origin - from 0.4 to 2.0% of all observations of purulent lesion of the cellular spaces of the neck.

Leading role in the development of secondary posterior purulent mediastinitis is played by nonclostridial anaerobes inhabiting the gingival pockets, crypts of the tonsils and the oral cavity.

Primary anterior mediastinitis occurs with infection of the anterior mediastinum after sternotomy in patients with cardiosurgical or oncological diseases and less often with closed trauma of the sternum as a result of suppuration of fractures of the breast or hematoma of the mediastinum.

The frequency of purulent mediastinitis after transesteral access to the mediastinal organs does not exceed 1%, and the lethality varies from 10 to 47%. The causative agents of the purulent process are Gram-positive cocci (75-80% of cases), golden or epidermal staphylococcus.

Secondary anterior mediastinitis develops when the odontogenic, tonsillogenic phlegmon of the neck or suppuration of the soft tissues of the anterior thoracic wall extends to the anterior mediastinum (most often through the sternotomy wound). Predisposing factors - instability of the sternum with suppuration of the superficial layers of the wound. An important role is played by the accumulation in the anterior mediastinum of the wound detachable with inadequate drainage. Risk factors for the development of anterior mediastinitis after cardiac surgery:

• obesity,
• diabetes,
• prolonged surgical intervention under artificial circulation,
• the use of bilateral mammarocoronary shunting (with the use of both intrathoracic arteries, the sternum loses more than 90% of its blood supply).

How does mediastinitis develop?

Fetal mediastinum during 4-6 h after its infection reacts with an extensive edema. This should be qualified as serous mediastinitis. Edema, extending to the neck, into the region of the subglottic space, epiglottis and arytenoid cartilage, leads to hoarseness of the voice, violation of breathing and swallowing act. This creates certain difficulties not only with the nasogastric tube, but also with endotracheal intubation. Pulmonary edema of the mediastinum leads to increasing pain in the interblade area and behind the sternum, frequent superficial breathing and hypoxia. Acting on the interoceptors of the arch of the aorta and the roots of the lungs, the edema of the cellulose causes a difficulty in the flow of blood to the right parts of the heart, an increase in CVP, a decrease in the shock volume and pulsatile blood pressure, and tachycardia. Against the background of subfebrile body temperature, hyperleukocytosis is noted with shift of the leukocyte formula to the left, compensated metabolic acidosis. The content of protein, carbohydrates and electrolytes in blood plasma does not change significantly. In the coccal microflora (anterior postoperative mediastinitis), with perforation of the esophagus, in the presence of cicatricial alterations in the mediastinal fiber after the previous postoperative esophagitis, the stage of serous inflammation can last several days. However, when the purulent process spreads from the neck to the unaltered tissue of the posterior mediastinum, after 6-8 hours morphological signs of phlegmonous inflammation appear.

The degree of prevalence of purulent mediastinitis and the degree of purulent intoxication depend not only on the magnitude of the defect in the esophagus wall, but also on the magnitude of the so-called false course in the mediastinum made by the instrument with iatrogenic damage to the esophagus.

• The main links of endogenous intoxication with mediastinitis:
• a massive flow into the blood and lymph of bacterial toxins directly from the purulent focus,
• influence on organs and tissues of microbial endotoxins and biological active substances causing severe disturbances of microcirculation,
• gross violations of metabolism leading to functional failure of natural detoxification organs (liver, kidneys), and then to PON.

For purulent mediastinitis in the phase of generalization of the process, development of decompensated metabolic acidosis and suppression of all immunity units are characteristic. The gross violations of central hemodynamics accompany ARDS and the progression of respiratory failure.

After 3-4 days purulent process extends to the pleural cavities and pericardial cavity, intoxication reaches an extreme degree. Tachycardia over 130 per minute, often there are irregularities in the rhythm. The number of breaths is 28-30 per minute, the hyperthermia is 38.5-39 ° C. Consciousness is preserved, but the patient is inhibited, contact with it is hampered Adverse predictive signs:

• pronounced lymphopenia (<5%),
• sharp fluctuations of CBS.

There is an increase in the concentration of creatinine and urea on the background of oliguria and hypoproteinemia. Without treatment, death occurs within the next 24 hours.

If patients undergo the generalization phase (as a result of drainage of a purulent focus and antibacterial therapy), then after 7-8 days, the manifestations of secondary foci of purulent infection come to the fore:

• empyema of the pleura,
• purulent pericarditis,
• abscesses of the lung,
• sub-diaphragmatic abscesses,
• septicopyemia.

Characteristic is the occurrence of esophageal-tracheal, esophageal-bronchial, mediastino-pleural and mediastinum pleura-bronchial fistulas. Purulent fusion of the diaphragm leads to the appearance of subdiaphragmatic abscesses and peritonitis, gastric and intestinal fistulas, which are connected with the pleural cavity. The constant hyperthermia, the intensive disintegration of proteins, fats and carbohydrates on the background of large energy losses leads the patients to the PON and to death in later terms.

Symptoms of mediastinitis

In all cases, mediastinitis manifests itself polymorphically. The clinic depends on the main process and the level of compression, but there are common manifestations due to occlusion of the upper vena cava and anonymous veins (upper vena cava syndrome): pain or feeling of heaviness in the chest or back, headaches, dizziness, dyspnea, dysphagia, thickening of the neck (collar of Stokes), hoarseness of voice, puffiness of face, cyanosis of the face of the neck and hands, especially when the trunk is tilted downward, the veins of the neck and chest, upper limbs, chest asymmetry, cheniya, hemoptysis, manifested in each case differently.

When the esophagus ruptured, there is an acute onset of the disease, severe chest pain and shortness of breath appear due to infection and inflammation of the mediastinum.

In the case of median sternotomy, mediastinitis usually manifests itself as the appearance of a discharge from a postoperative wound or sepsis.

Acute mediastinitis

It begins suddenly and proceeds violently, with a rapid deterioration of the state due to the formation and progression of the intoxication syndrome. Symptomatic complex of local manifestations depends on the localization and nature of mediastinitis, and also on the extent to which the mediastinum organs are involved in the process: esophagus, trachea, wandering, recurrent and diaphragmatic nerves, sympathetic trunk. Therefore, there may be polymorphic changes that develop individually in each case, can be: dysphagia, suffocation, persistent cough, hoarseness, arrhythmias, hiccoughs, intestinal paresis, Bernard-Turner syndrome, etc.

[1], [2], [3], [4], [5], [6],

Chronic mediastinitis

It is caused by specific infections, proliferative processes in the mediastinum, can be asymptomatic for a long time: In later terms, for example, with tuberculosis, syphilis - there are pain in the side, cough, shortness of breath, weakness, a feeling of constriction: in the chest, difficult swallowing. With fibrotic and proliferative mediastinitis, mediastinal tumors, there are signs of compression of the superior vena cava: puffiness of the face, swelling of the hand, cyanosis and widening of the veins of the breast.

[7], [8], [9], [10],

Classification of mediastinitis

The trachea and heart sac share the anterior and posterior mediastinum. In addition, the upper and lower mediastinum are distinguished with respect to the conventional horizontal plane, carried out at the level of the tracheal bifurcation. This conditional separation is important for understanding the pathways of infection. Depending on the localization of inflammation, the mediastinal tissue is distinguished:

• front upper,
• front lower,
• rear upper,
• rear lower,
• total front,
• total posterior mediastinitis.

Simultaneous lesion of the anterior and posterior mediastinum is rare, since such patients die before the development of this form of mediastinitis from septic shock and intoxication.

From the clinical point of view, the following stages of development of mediastinitis are distinguished:

• serous (infiltrative), which with intensive anti-inflammatory therapy may undergo reverse development,
• purulent, flowing in the form of phlegmon or mediastinal abscess.

The most common form of mediastinitis is the mediastinum phlegmon, mortality is 25-45%, and in case of anaerobic flora lethality reaches 68-80%. The mediastinal abscess is considered to be a more favorable form of mediastinitis, the lethality at which does not exceed 15-18%.

Depending on the localization of the primary focus of infection, primary (with primary mediastinal mediastinum infection) and secondary mediastinitis are distinguished (when the inflammatory process spreads from other anatomical regions).

[11], [12], [13], [14], [15]

Diagnosis of mediastinitis

One of the important causes of high mortality in mediastinitis is the difficulty of its early diagnosis, especially with secondary mediastinitis, when the purulent process spreads to the mediastinum against the background of the main suppurative focus outside the mediastinum, the clinical signs of which mask the manifestations of mediastinitis.

The complex of instrumental examination with mediastinitis is complicated. Begin with a review of chest radiographs in at least two projections. When the esophagus is perforated, the presence of air in the mediastinum, dimming in the posterior mediastinum in the lateral projection, "sympathetic" pyopneumotorax.

The presence of a cavity with a horizontal fluid level is characteristic of the mediastinal abscess, the presence of multiple small gas enlightenments against the background of a condensed and enlarged shadow of the mediastinum indicates a medulla phlegmon. Emphysema of the mediastinum is especially extensive when the esophagus ruptures during fibroesophagoscopy with air insufflation into the lumen of the esophagus. In such cases, the infected emphysema quickly spreads to the soft tissues of the neck, face and chest wall.

When X-ray examination of patients with esophagus ruptures, additional information on the configuration, the length of the false course in the mediastinum, the relationship between the defect of the esophageal wall and the purulent focus can be obtained by contrasting the esophagus with a suspension of barium sulfate.

The possibilities of ultrasound in the diagnosis of mediastinitis are severely limited due to the screening of the mediastinum with bone structures (sternum, spine). Frequently occurring subcutaneous emphysema of the neck and chest wall also makes diagnosis difficult.

Then conduct an FGP. If this does not reveal perforation, the complex is complemented by contrast, radiography of the esophagus and mediastinography. A high diagnostic effect is produced by magnetic resonance imaging. The same complex is also performed with chronic mediastinitis, but supplemented with mediastinoscopy, bronchoscopy, thoracoscopy, and fibrous - cavografia.

Diagnosis of mediastinitis in rupture of the esophagus is usually based on the analysis of clinical manifestations of the disease; the diagnosis is verified by radiography of the chest or CT of the chest, when air bubbles in the mediastin are detected.

Diagnosis of mediastinitis due to median sternotomy is based on the detection of an infected fluid in the sternal puncture of the mediastinum.

Diagnosis of chronic fibrosing mediastinitis is based on the detection of enlarged lymph nodes of the mediastinum with CT or chest X-ray.

[16], [17], [18], [19],

Treatment of mediastinitis

Antibiotic therapy

The presence of purulent mediastinitis is an absolute indication for the purpose of antibiotic therapy. When the clinical picture is unfolded in patients who have not been operated before in case of late admission, it is advisable to start antibiotic therapy in the process of preparing for the operation.

Given the nature of the microflora, the rapid progression of purulent inflammation and the increase of intoxication against the background of oppression of the main links of immunity, the method of choice is de-escalation intravenous therapy with carbapenems for 7-10 days.

Such therapy covers the entire spectrum of not only possible pathogens and existing hospital flora, but also all new portions of microorganisms that constantly enter the focus, which is observed, for example, when the rupture of the thoracic esophagus can not be sutured. In these cases, a microbiological study of purulent exudate does not provide valuable reference data for the administration of drugs of a narrower spectrum.

At the same time, when the esophagus ruptures, with odontogenic and tonsilogenic infection, the sensitivity of the isolated microflora to antibiotics is determined in some cases, cheaper drugs (cephalosporins of the fourth generation, fluoroquinolones) in combination with metronidazole can also be used effectively. This combination is also effective in cocci flora, characteristic of postoperative anterior mediastinitis. Detoxification therapy.

Carried out according to the known principles of complex treatment of acute purulent diseases, there are no specific features in the scope and methods of treatment.

Treatment of mediastinitis with esophageal rupture is carried out by parenteral administration of antibiotics, active against microflora of the oral cavity and gastrointestinal tract, for example clindamycin (450 mg intravenously every 6 hours) in combination with ceftriaxone (2 g once daily for at least 2 weeks ). Many patients require an emergency revision of the mediastinum with primary closure of the esophagus and drainage of the pleural cavity and mediastinum.

[20], [21], [22], [23], [24], [25]

Surgical treatment

The leading role in the treatment of purulent mediastinitis belongs to the surgical method, which provides a complete drainage of the purulent focus. All existing access to mediastinum should be divided into two groups:

• Crescentral,
• extrapleural.

Crescental access to the posterior mediastinum is indicated with the planned intervention on the damaged thoracic esophagus (suturing defect, resection of the esophagus). Elderly and senile age, severe co-morbidities, unstable hemodynamics greatly increase the risk of transhexial intervention. Moreover, with this access, additional infection of the pleural cavity inevitably occurs.

Non-pleural accesses to the posterior mediastinum (from above by means of perforated mediastinotomy, from below - from the peritoneal mediastomy) and to the anterior mediastinum (from above by means of perforated mediastinotomy, from below - subxyphoid mediastinotomy) provide an adequate drainage of purulent foci, provided that in the postoperative period an active drainage method is used - washing of the purulent focus with solutions antiseptics with aspiration of the contents in a rarefaction mode in a system of the order of 10-40 cm of water. Art.

In patients with sternotomy developed after sternotomy, the sternum and ribs and anterior purulent mediastinitis for drainage use over-access. Subsequently, an extensive defect in the tissues of the chest wall is performed with a muscle tissue on the vascular pedicle or a strand of a large omentum

In addition to adequate drainage of the purulent focus, patients with mediastinitis due to perforation of the esophagus need to solve two important tasks:

• ensure the cessation of the constant receipt of infected and aggressive contents in the mediastinum (saliva, gastric juice, bile),
• ensure the possibility of prolonged enteral feeding.

The cessation of the inflow of infected contents into the posterior mediastinum through the defect of the pharynx, cervical, and upper thoracic parts of the esophagus is achieved either by suturing the defect, which is unreliable under the conditions of already developed mediastinitis, or by installing an additional drainage tube with an end at the level of the perforation, which, while ensuring a reliable permanent aspiration, the oral cavity and the esophagus into the mediastinum.

The cessation of the transfer of gastric contents into the mediastinum through the defect of the lower thoracic esophagus is also ensured by suturing the defect with diaphragmatic access and covering the seam line with the stomach bottom (Nissen fundoplication). If it is impossible to suture a high perforation, the aboral tube draining the purulent focus creates a Nissen fundoplication cuff. The presence of such a cuff prevents the transfer of gastric contents into the esophagus, allows you to permanently turn off the esophagus from the passage of food, and to provide enteral nutrition use gastrostomy. Usually apply gastrostomy according to the Kader.

In patients with odontogenic mediastinitis due to triism and in patients with mediastinitis due to rupture of the cervical and upper thoracic parts of the esophagus, enteral feeding is performed through a nasogastric tube.

In patients with tonsillogenic or anterior mediastinitis after sternotomy, problems with natural nutrition, as a rule, do not arise.

Postoperative treatment

A general approach to the treatment of mediastinitis can be successful if from the outset the treatment was as intense as possible - as with sepsis. In such cases, gradually remove individual components of complex treatment, which lose their relevance as the clinical, laboratory and instrumental survey data are normalized.

Complex intensive treatment of mediastinitis:

• local effects on the focus of purulent infection,
• antibacterial therapy,
• immunocorrecting therapy,
• detoxification therapy,
• replenishment of energy costs of the body.

Local treatment involves the constant washing of the purulent foci in the mediastinum with a solution of antiseptic with the simultaneous use of aspiration with a rarefaction of the order of 10-40 cm of water. Art.

An indispensable condition for the success of this method is the sealing of the cavity in the mediastinum (to observe the rarefaction) and constant monitoring of the healthy functioning of the entire system. Under the action of aspiration from the mediastinum, the pus and the products of tissue decay are rapidly evacuated as quickly as possible, and the absorption of toxins from the focus of purulent inflammation slows down sharply. As a result, the cavity is flattened and decreases.

After the cavity falls and turns into a channel around the drainage (this can easily be verified by filling the drains with a water-soluble contrast medium followed by X-ray diffraction), the drains gradually begin to pull up and eventually are removed, replacing them for several days with rubber graduates.

Certain difficulties arise in the local treatment of open sternal wounds after cardiosurgical interventions, especially in the presence of instability of the sternum and ribs. Dressings with sanation of a purulent foci must be performed almost daily, while providing complete anesthesia. Because of the possible development of serious complications for washing the wound, it is impossible to apply cold antiseptic solutions, as well as 3% hydrogen peroxide solution. Long, along the sternum spurs of purulent cavities are usually further drained with soft drainage tubes.

The open method of local treatment has many shortcomings. The main one is large, hard-to-repair, wound losses.

Treatment of mediastinitis due to median sternotomy is reduced to urgent surgical drainage, surgical treatment of the wound and the use of parenteral antibiotics of a wide spectrum of action. Lethality in this condition, according to some studies, is approaching 50%.

If mediastinitis develops as a result of tuberculosis, appropriate antituberculous therapy is prescribed. In the absence of the effect of therapy, it is possible to install vascular stents in order to limit the squeezing of certain central vessels.