Mediastinitis

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

The absence of fascial barriers, constant volumetric and spatial movements of loose tissue caused by the pulsation of the heart and blood 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, there is anterior and posterior mediastinitis, each of which can be upper, middle, lower and total. According to the clinical course, there is acute and chronic mediastinitis.

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

Less often, the spread occurs along the fascial sheets from the neck or from adjacent tissues (bifurcation lymph nodes of the trachea, from the pleural cavity, ribs, sternum). Odontogenic infection is extremely rare.

ICD-10 code

J85.3 Mediastinal abscess

What causes mediastinitis?

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

Esophageal rupture may be a complication of esophagoscopy, installation of a Sengstaken-Blakemore tube or Minnesota hose (in case of bleeding from varicose veins of the esophagus and stomach). It may also develop with vomiting (Boerhaave syndrome).

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

Chronic fibrosing mediastinitis usually develops as a result of tuberculosis or histoplasmosis, but can also occur with sarcoidosis, silicosis, or fungal infections. It is characterized by an intense fibrotic process leading to compression of the mediastinal structures, which can cause superior vena cava syndrome, tracheal stenosis, 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 and foreign bodies. Instrumental (iatrogenic) esophageal injuries occur during fibroesophagoscopy, bougienage of esophageal strictures, cardiodilation, and tube insertion. In 1-2% of cases, posterior purulent mediastinitis occurs due to necrosis of the esophageal wall due to chemical burns. A special place in the etiology of posterior purulent mediastinitis is occupied by the so-called spontaneous ruptures of the esophagus (Boerhaave syndrome), when a longitudinal rupture of the left wall of the esophagus in the supradiaphragmatic region occurs as a result of gagging or minor physical exertion. This form of esophageal rupture is difficult for early diagnosis. Mediastinitis is the most severe. Reflux of stomach contents into the pleural cavity quickly leads to the development of pleural empyema and sepsis. Mortality reaches 60-90%.

In surgical practice, secondary posterior mediastinitis is most often detected - the result of the spread of a purulent process from the cellular spaces of the neck. The cause of purulent inflammation in the neck area is chemical and mechanical damage to the pharynx and cervical esophagus (in addition to the instrumental manipulations described above, ruptures of the pharynx and cervical esophagus can occur during attempts at endotracheal intubation).

The following diseases play a significant role in the etiology of secondary posterior mediastinitis:

• cervical adenophlegmon,
• odontogenic phlegmon of the floor of the oral cavity and submandibular spaces,
• tonsillogenic phlegmon of the parapharyngeal space,
• retropharyngeal abscess.

The spread of the listed purulent processes occurs through vascular fascial 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%, and of tonsillogenic origin - from 0.4 to 2.0% of all observations of purulent lesions of the cellular spaces of the neck.

The leading role in the development of secondary posterior purulent mediastinitis is played by non-clostridial anaerobes inhabiting the gingival pockets, tonsil crypts and oral cavity.

Primary anterior mediastinitis occurs when the anterior mediastinum becomes infected after sternotomy in patients with cardiac surgery or oncological diseases and, less frequently, when there is a closed sternum injury as a result of suppuration of chest fractures or mediastinal hematoma.

The incidence of purulent mediastinitis after transsternal access to the mediastinal organs does not exceed 1%, and mortality ranges from 10 to 47%. The causative agents of the purulent process are gram-positive cocci (75-80% of cases), Staphylococcus aureus or Staphylococcus epidermidis.

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

• obesity,
• diabetes mellitus,
• prolonged surgical intervention under artificial circulation,
• use of bilateral mammary coronary artery bypass grafting (when using both intrathoracic arteries, the sternum loses more than 90% of its blood supply).

How does mediastinitis develop?

The mediastinal tissue reacts with extensive edema within 4-6 hours after its infection. This should be classified as serous mediastinitis. The edema, spreading to the neck, to the subglottic space, epiglottis and arytenoid cartilages, leads to hoarseness, impaired breathing and swallowing. This creates certain difficulties not only during the introduction of a nasogastric tube, but also during endotracheal intubation. Edema of the mediastinal tissue leads to increasing pain in the interscapular region and behind the sternum, frequent shallow breathing and hypoxia. Acting on the interoreceptors of the aortic arch and the roots of the lungs, edema of the tissue causes difficulty in the blood flow to the right sections of the heart, an increase in central venous pressure, a decrease in stroke volume and pulse pressure, and tachycardia. Against the background of subfebrile body temperature, hyperleukocytosis with a shift in the leukocyte formula to the left, compensated metabolic acidosis are noted. The content of protein, carbohydrates and electrolytes in the blood plasma does not change significantly. With coccal microflora (anterior postoperative mediastinitis), with perforation of the esophagus, in the presence of cicatricial changes in the mediastinal tissue after previously suffered post-burn esophagitis, the serous inflammation stage can last for several days. However, with the spread of the purulent process from the neck to the unchanged tissue of the posterior mediastinum, morphological signs of phlegmonous inflammation appear after 6-8 hours.

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

• The main links of endogenous intoxication in mediastinitis:
• massive influx of bacterial toxins into the blood and lymph directly from the purulent focus,
• the impact on organs and tissues of microbial endotoxins and biologically active substances that cause sharp disturbances in microcirculation,
• gross metabolic disorders leading to functional failure of the organs of natural detoxification (liver, kidneys), and then to PON.

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

After 3-4 days, the purulent process spreads to the pleural cavities and pericardial cavity, intoxication reaches an extreme degree. Tachycardia is over 130 per minute, rhythm disturbances often occur. The number of breaths is 28-30 per minute, hyperthermia is 38.5-39 °C. Consciousness is preserved, but the patient is inhibited, contact with him is difficult. Unfavorable prognostic signs:

• severe lymphopenia (<5%),
• sharp fluctuations in the acid-base balance.

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

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

• pleural empyema,
• purulent pericarditis,
• lung abscesses,
• subphrenic abscesses,
• septicopyemia.

Typically, esophageal-tracheal, esophageal-bronchial, mediastinopleural and mediastinopleurobronchial fistulas occur. Purulent melting of the diaphragm leads to the development of subdiaphragmatic abscesses and peritonitis, gastric and intestinal fistulas communicating with the pleural cavity. Constant hyperthermia, intensive breakdown of proteins, fats and carbohydrates against the background of large energy losses leads patients to PON and death at a later stage.

Symptoms of mediastinitis

In all cases, mediastinitis manifests itself polymorphically. The clinical picture depends on the underlying process and the level of compression, but there are also general manifestations caused by occlusion of the superior vena cava and innominate veins (superior vena cava syndrome): pain or heaviness in the chest or back, headaches, dizziness, shortness of breath, dysphagia, thickening of the neck (Stokes collar), hoarseness, puffiness of the face, cyanosis of the face, neck and arms, especially when bending the body down, dilation of the veins of the neck and chest, upper limbs, asymmetry of the chest, bulging of the tissue in the supraclavicular fossa, bradycardia, nosebleeds, hemoptysis, which manifest themselves differently in each case.

When the esophagus ruptures, the disease begins acutely, with severe chest pain and shortness of breath caused by infection and inflammation of the mediastinum.

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

Acute mediastinitis

It begins suddenly and proceeds rapidly, with a rapid deterioration of the condition due to the formation and progression of intoxication syndrome. The symptom complex of local manifestations depends on the localization and nature of mediastinitis, as well as on the degree of involvement of the mediastinal organs in the process: the esophagus, trachea, vagus, recurrent and phrenic nerves, and the sympathetic trunk. Therefore, there may be polymorphic changes that develop individually in each case, such as: dysphagia, suffocation, persistent cough, hoarseness, arrhythmia, hiccups, intestinal paresis, Bernard-Turner syndrome, etc.

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Chronic mediastinitis

Caused by a specific infection, proliferative processes in the mediastinum, can be asymptomatic for a long time: In later stages, for example, with tuberculosis, syphilis - pain in the side, cough, shortness of breath, weakness, a feeling of compression: in the chest, difficulty swallowing appear. With fibrous and proliferative mediastinitis, mediastinal tumors, signs of compression of the superior vena cava appear: puffiness of the face, swelling of the arm, cyanosis and dilation of the veins of the chest.

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Classification of mediastinitis

The trachea and pericardium separate the anterior and posterior mediastinum. In addition, the superior and inferior mediastinum are distinguished in relation to a conventional horizontal plane drawn at the level of the tracheal bifurcation. This conventional division is important for understanding the routes of infection. Depending on the localization of inflammation of the mediastinal tissue, the following are distinguished:

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

Simultaneous damage to 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 a clinical point of view, the following stages of mediastinitis development are distinguished:

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

The most common form of mediastinitis is mediastinal phlegmon, the mortality rate is 25-45%, and with anaerobic flora the mortality rate reaches 68-80%. Mediastinal abscess is considered a more favorable form of mediastinitis, the mortality rate of which does not exceed 15-18%.

Depending on the location of the primary source of infection, a distinction is made between primary (with primary infection of the mediastinal tissue) and secondary mediastinitis (with the spread of the inflammatory process from other anatomical areas).

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Diagnosis of mediastinitis

One of the significant reasons for the high mortality rate in mediastinitis is the difficulty of its early diagnosis, especially in secondary mediastinitis, when the spread of the purulent process to the mediastinum occurs against the background of the main purulent focus outside the mediastinum, the clinical signs of which mask the manifestations of mediastinitis.

The instrumental examination complex for mediastinitis is complicated. They start with a general chest X-ray in at least two projections. In case of esophageal perforation, the following is revealed: the presence of air in the mediastinum, darkening in the posterior mediastinum in the lateral projection, and "sympathetic" pyopneumothorax.

The presence of a cavity with a horizontal fluid level is characteristic of a mediastinal abscess, the presence of multiple small gas lucencies against the background of a compacted and expanded mediastinal shadow indicates mediastinal phlegmon. Mediastinal emphysema is especially extensive in cases of esophageal ruptures during fibroesophagoscopy with air insufflation into the lumen of the esophagus. In such cases, infected emphysema quickly spreads to the soft tissues of the neck, face, and chest wall.

During radiographic examination of patients with esophageal ruptures, additional information about the configuration, length of the false passage in the mediastinum, and the relationship between the esophageal wall defect and the purulent focus can be obtained using a contrast study of the esophagus with a barium sulfate suspension.

The capabilities of ultrasound in diagnosing mediastinitis are severely limited due to the screening of the mediastinum by bone structures (sternum, spine). Frequently encountered subcutaneous emphysema of the neck and chest wall also complicates diagnosis.

Then EFGS is performed. If this does not reveal perforation, the complex is supplemented with contrast, radiography of the esophagus and mediastinography. Magnetic resonance imaging provides a high diagnostic effect. The same complex is also performed for chronic mediastinitis, but supplemented with mediastinoscopy, bronchoscopy, thoracoscopy, and for fibrous mediastinitis - cavography.

Diagnosis of mediastinitis in esophageal rupture is usually based on the analysis of clinical manifestations of the disease; verification of the diagnosis is carried out by chest X-ray or chest CT, when air bubbles in the mediastinum are detected.

Diagnosis of mediastinitis following median sternotomy is based on the detection of infected fluid during sternal puncture of the mediastinum.

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

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Treatment of mediastinitis

Antibacterial therapy

The presence of purulent mediastinitis is an absolute indication for the prescription of antibacterial therapy. In the case of a comprehensive clinical picture in previously unoperated patients with late admission, it is advisable to begin antibacterial therapy during the preparation for surgery.

Taking into account the nature of the microflora, the rapid progression of purulent inflammation and the increase in intoxication against the background of suppression of the main links of the immune system, 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 new portions of microorganisms constantly entering the lesion, which is observed, for example, when it is impossible to suture a rupture of the thoracic esophagus. In these cases, microbiological examination of purulent exudate does not provide valuable reference data for prescribing drugs of a narrower spectrum.

At the same time, in case of a sutured rupture of the esophagus, in case of odontogenic, tonsilogenic infection, determination of the sensitivity of the isolated microflora to antibiotics allows in some cases to effectively use cheaper drugs (IV generation cephalosporins, fluoroquinolones) in combination with metronidazole. This combination is also effective for coccal flora, characteristic of postoperative anterior mediastinitis. Detoxification therapy.

They are carried out according to the known principles of complex treatment of acute purulent diseases; no specific features in the volume and methods of treatment are noted.

Treatment of mediastinitis due to esophageal rupture is performed by parenteral administration of antibiotics active against the microflora of the oral cavity and gastrointestinal tract, for example, clindamycin (at a dose of 450 mg intravenously every 6 hours) in combination with ceftriaxone (2 g once a day for at least 2 weeks). Many patients require emergency revision of the mediastinum with primary suturing of the esophageal rupture and drainage of the pleural cavity and mediastinum.

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Surgical treatment

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

• transpleural,
• extrapleural.

Transpleural access to the posterior mediastinum is indicated for planned intervention on the damaged thoracic esophagus (suturing of the defect, resection of the esophagus). Elderly and senile age, severe concomitant diseases, unstable hemodynamics significantly increase the risk of transpleural intervention. In addition, with this access, additional infection of the pleural cavity inevitably occurs.

Extrapleural approaches to the posterior mediastinum (from above by transcervical mediastinotomy, from below by transperitoneal mediastomy) and to the anterior mediastinum (from above by transcervical mediastinotomy, from below by subxiphoid mediastinotomy) ensure adequate drainage of purulent foci, provided that an active drainage method is used in the postoperative period - washing the purulent focus with antiseptic solutions with aspiration of the contents in a vacuum mode in the system of about 10-40 cm of water.

In patients with osteomyelitis of the sternum and ribs and anterior purulent mediastinitis that developed after sternotomy, transsternal access is used for drainage. Subsequently, an extensive defect in the chest wall tissue is made with muscle tissue on a vascular pedicle or a strand of the greater omentum

In addition to adequate drainage of the purulent focus, in patients with mediastinitis due to esophageal perforation, it is necessary to solve two important problems:

• to ensure the cessation of the constant flow of infected and aggressive contents into the mediastinum (saliva, gastric juice, bile),
• provide the possibility of long-term enteral nutrition.

Stopping the flow of infected contents into the posterior mediastinum through a defect in the pharynx, cervical, and upper thoracic esophagus is achieved either by suturing the defect, which is unreliable in conditions of already developed mediastinitis, or by installing an additional drainage tube with the end at the level of the perforation hole, which, while ensuring reliable constant aspiration, prevents the contents of the oral cavity and esophagus from flowing into the mediastinum.

Stopping the reflux of gastric contents into the mediastinum through a defect in the lower thoracic esophagus is also ensured by suturing the defect through the diaphragmatic approach and covering the suture line with the stomach bottom (Nissen fundoplication). If it is impossible to suture a high perforation aboral to the tube draining the purulent focus, a Nissen fundoplication cuff is created. The presence of such a cuff prevents the reflux of gastric contents into the esophagus, allows the esophagus to be excluded from the passage of food for a long time, and a gastrostomy can be used to provide enteral nutrition. Kader gastrostomy is usually used.

In patients with odontogenic mediastinitis due to trismus and in patients with mediastinitis due to rupture of the cervical and upper thoracic esophagus, enteral nutrition is carried out through a nasogastric tube.

Patients with tonsillogenic or anterior mediastinitis after sternotomy, as a rule, do not have problems with natural nutrition.

Postoperative treatment

A general approach to the treatment of mediastinitis can be successful if the treatment was maximally intensive from the very beginning - as in sepsis. In such cases, individual components of the complex treatment are gradually discontinued, losing their relevance as the clinical, laboratory and instrumental examination data normalize.

Complex intensive treatment of mediastinitis:

• local impact on the focus of purulent infection,
• antibacterial therapy,
• immunocorrective therapy,
• detoxification therapy,
• replenishment of the body's energy expenditure.

Local treatment includes continuous rinsing of the purulent focus in the mediastinum with an antiseptic solution while simultaneously using aspiration with a vacuum of about 10-40 cm H2O.

An essential condition for the success of this method is the sealing of the cavity in the mediastinum (to maintain vacuum) and constant monitoring of the proper functioning of the entire system. Under the action of aspiration, pus and tissue decay products are evacuated from the mediastinum as quickly as possible, and the absorption of toxins from the site of purulent inflammation is sharply slowed. As a result, the cavity flattens and decreases.

After the cavity has collapsed and turned into a channel around the drains (this can be easily checked by filling the drains with a water-soluble contrast agent and then taking an X-ray), the drains are gradually tightened and eventually removed, replacing them with rubber drains for a few days.

Certain difficulties arise in the local treatment of open sternal wounds after cardiac surgery, especially in the presence of instability of the sternum and ribs. Dressings with sanitation of the purulent focus have to be performed almost daily, while providing full pain relief. Due to the possible development of serious complications, cold antiseptic solutions and 3% hydrogen peroxide solution cannot be used to wash the wound. Long spurs of purulent cavities running along the sternum are usually additionally drained with soft drainage tubes.

The open method of local treatment has many disadvantages. The main one is large, difficult to replace, wound losses.

Treatment of mediastinitis following median sternotomy involves emergency surgical drainage, surgical wound treatment, and the use of broad-spectrum parenteral antibiotics. Mortality in this condition, according to some studies, approaches 50%.

If mediastinitis develops as a result of tuberculosis, appropriate anti-tuberculosis therapy is prescribed. If therapy is ineffective, vascular stents may be installed to limit compression of some central vessels.