Mediastinitis is a disease characterized by inflammation in the mediastinal organs, resulting in compression of blood vessels and nerves. In practical medicine, any inflammation that leads to mediastinal syndrome is called mediastinitis.
- Classification
- Causes
- Pathogenesis
- Symptoms
- Diagnostics
- Treatment
The inflammatory process is generalized due to the following conditions:
- constant volumetric and spatial movements of loose fiber
- absence of fascial barriers
According to the anatomical structure of the mediastinum, mediastinitis is divided into anterior and posterior. Each of these types can be:
- top
- median
- total
- lower
According to the course, the disease is divided into acute and chronic. Aseptic mediastinitis, which is caused mainly by nonspecific or specific microflora, is rarely recorded. It can enter in various ways, mainly through trauma to the esophagus due to diverticulum rupture, chemical burns, etc. Less commonly, the spread occurs along the fascial sheets from the neck or from adjacent tissues.
Classification
Depending on the location of the inflammation of the mediastinal tissue, mediastinitis is divided into:
- front upper
- rear lower
- rear upper
- total rear
- total front
- front upper
It is rare that the anterior and posterior mediastinum are affected simultaneously, because before this form develops, a person dies from intoxication and septic shock. The stages of development of mediastinitis, depending on the clinic, are as follows:
- serous
- purulent
Most often, mediastinal phlegmon is diagnosed, in which the mortality rate reaches from 25 to 45%. If the causative agent is anaerobic flora, then the mortality rate reaches 68-80%. A more favorable form of mediastinitis is considered to be a mediastinal abscess. With this diagnosis, there are 15-18 deaths per 100 cases.
Depending on the location of the primary source of infection, there are primary and secondary mediastinitis. The disease is considered primary if the mediastinal tissue is initially infected.
Causes
The two most common causes are median sternotomy and esophageal rupture. Esophageal rupture may be a complication of placement of a Sengstaken-Blackmore tube or Minnesota tube, as well as a complication of esophagoscopy. Also occurs with vomiting (Berhaave syndrome). Mediastinitis in 1% of cases is a complication of median sternotomy.
Chronic fibrosing mediastinitis is caused by histoplasmosis or tuberculosis, but can occur with silicosis, sarcoidosis, and fungal infections. An intense fibrotic process is typical, which leads to compression of the mediastinal structures, which can cause tracheal stenosis, superior vena cava syndrome, etc.
The cause of primary posterior mediastinitis in most cases is mechanical damage to the thoracic esophagus by foreign bodies or instruments. Causes of iatrogenic esophageal injuries may include bougienage of esophageal strictures, fibroesophagoscopy, insertion of a probe, and cardiac dilatation. In 1-2% of cases, the cause of posterior purulent mediastinitis is necrosis of the esophageal wall due to chemical burns. The cause of this form may be a spontaneous rupture of the esophagus, when, as a result of gagging or minor physical activity, a longitudinal rupture of the left wall of the esophagus is formed in the supradiaphragmatic region. Such cases are almost never diagnosed early. The reflux of stomach contents into the pleural cavity in a short time causes pleural empyema and sepsis. The mortality rate is very high, reaching from 60 to 90%.
Surgeons most often record secondary posterior mediastinitis, which is formed as a result of the spread of a purulent process from the cellular spaces of the neck. The reason is mechanical and chemical damage to the pharynx and cervical esophagus.
Possible causes of secondary posterior mediastinitis:
- odontogenic phlegmon of the floor of the mouth and submandibular spaces
- cervical adenophlegmon
- retropharyngeal abscess
- tonsillogenic phlegmon of the peripharyngeal space
Secondary posterior purulent mediastinitis develops with the participation of non-clostridial anagrobes, which settle in the gingival pockets, oral cavity and tonsil crypts. Primary anterior mediastinitis is a consequence of infection of the anterior mediastinum after sternotomy in patients with cancer or cardiac surgery, and in rare cases with a closed sternum injury, when chest fractures suppurate. The causative agents of the purulent process are gram-positive cocci (most cases), epidermal or Staphylococcus aureus.
Secondary anterior mediastinitis is caused by the spread of tonsillogenic, odontogenic phlegmon of the neck. In some cases, it is a consequence of suppuration of the soft tissues of the anterior chest wall on the anterior mediastinum. Factors that contribute to the development of the process are instability of the sternum with suppuration of the superficial layers of the wound. With inadequate drainage, wound discharge may accumulate in the anterior mediastinum, which also plays an important role in pathogenesis. Risk factors for the development of anterior mediastinitis after cardiac surgery:
- diabetes
- obesity
- use of bilateral mammary coronary bypass surgery
- long-term surgery under artificial circulation
It is generally accepted that purulent inflammation of the mediastinal tissue was first described by K. Galen [14]. In a young man with an anterior mediastinal abscess and chest wall fistula, he removed fragments of the sternum and part of the pericardium involved in the process. The postoperative wound healed successfully.
However, upon careful study of the works of A.K. Celsus [53], who lived 100 years before C. Galen, in the chapter on the signs of approaching death, we found a description of the clinical picture, which in modern language can be interpreted as odontogenic purulent mediastinitis.
Abu Ali ibn Sina [4] introduced the term, which was translated from Arabic into Latin as Inflammatio velaminis, and established that the severity of the condition and prognosis depend on the location of the “putrefactive tumor”. The term “mediastinitis” appeared in the literature in the 12th century thanks to the works of Ibn Zor, who himself suffered from this disease and recorded its clinical signs [Cit. according to 22].
All these observations concerned anterior mediastinitis, which is explained by the tendency of abscesses of this localization to break out independently and easy accessibility for emptying by trephination of the sternum.
In the Middle Ages and up to the 18th century, individual casuistic observations were described. In 1786, G. Gumet’s book “The Initial Foundations of Medical Science in the City of St. Peter” [19] appeared in Russia, where in the section “On thoracic puncture” there is a description of the inflammation of the “mid-thoracic obstruction.” A more detailed work in this area belongs to I. Bush [10], who in 1807 outlined the technique of trephination of the sternum. In subsequent years [63, 68, 79, 83], individual reports on clinical observations of anterior purulent mediastinitis were published.
An important stage in the history of mediastinitis surgery was the works of N.I. Pirogov [35], in which he cited observations of posterior mediastinitis after gunshot wounds of the esophagus and sharply criticized a certain Strohmeier, who denied the possibility of the purulent process spreading from the neck to the mediastinum. Highlighting a more benign form of mediastinitis - “abscess” (abscess) and a more dangerous one - “acute edema” (phlegmon), he pointed out the pattern of phlegmon spreading from the neck to the mediastinum and for the first time called this process “descending” (which corresponds to the modern terminology of foreign authors ).
At the same time, until the end of the 19th century, posterior purulent mediastinitis remained unstudied due to the anatomical features of this zone, which created great difficulties for surgical intervention without the help of painkillers. In 1895, the famous European surgeon G. Ziembicki [87] wrote: “Phlegmon of the posterior mediastinum is a dark spot in modern surgery.” This is confirmed by publications on fatal outcomes in the gangrenous form of posterior mediastinitis due to perforation of the esophagus [43, 44].
Progress in the surgical treatment of posterior purulent mediastinitis in these years is associated with the names of Russian surgeons. In 1888 I.I. Nasilov [30] published a short article in the journal “Vrach” in which he substantiated the possibility of posterior extrapleural access. In 1888, the text of this article appeared in the English press. Somewhat later, our foreign colleagues presented their observations of the use of this access, while some referred to the experience of I.I. Nasilova [73, 77, 81], while others do not, claiming authorship [65, 82]. Subsequently, access via I.I. Nasilova, despite its traumatic nature and the emergence of alternative developments, was used until the 60s of the 20th century [5, 78, 86].
A major step forward in the surgery of posterior mediastinitis was the development of a transcervical extrapleural approach, the author of which in Russia is considered to be V.I. Razumovsky, abroad - V. Hacker. IN AND. Razumovsky in 1897 successfully used anterior longitudinal collotomy to drain the posterior mediastinum in a 12-year-old boy with a gunshot wound. He published the surgical technique in 1899 [37]. In the same year, L. Heidenhain [74] published his observation of the use of a transverse approach in the neck. V. Hacker [73], speaking at the XXX Congress of German surgeons in 1901, reported on 3 observations known to him: V.I. Razumovsky, L. Heidenhain and his own.
However, it would be unfair to keep silent about the fact that 7 years before V.I. Razumovsky, in 1890, zemstvo surgeon V. Sheboldaev [55] successfully used longitudinal collotomy to drain the mediastinal abscess.
The first decades of the 20th century were devoted mainly to a detailed study of the anatomical formations of the mediastinum, cellular spaces and fascia, the ethnopathogenesis of various forms of purulent mediastinitis, and the ways of spread of putrefactive infection in odonto- and tonsillogenic phlegmons of the face and neck [6, 17, 51, 56].
Of great importance for understanding the ways of contact spread of odonto-, oto- and tonsillogenic phlegmons to the mediastinal tissue were the “Essays on Purulent Surgery” published in 1934 by V.F. Voino-Yasenetsky [13].
The greatest experience abroad in the 30s of the 20th century was H. Pearse [80], who published data on 64 observations of purulent mediastinitis with a mortality rate of 56.2%, as well as H. Killian [75].
The results of surgical treatment remained poor due to the ineffectiveness of drainage of narrow and upward canals using transcervical approaches. H. Lilienthal's proposal [76] to use an active drainage method with washing and aspiration did not gain popularity due to the imperfection of the equipment. According to [48], much later, in 1941, Frink published an observation of successful treatment of mediastinitis in a patient with spontaneous esophageal rupture by using aspiration through drainages of the mediastinum and pleural cavity. Another attempt to use the active drainage method was made by R. Adams [60]: in 1946, he used this method in 7 patients, all recovered, but this fact did not make an impression on the surgical community.
A major event in the first half of the 20th century in Russian surgery was the meeting of the Leningrad Society of Surgeons named after. N.I. Pirogov in 1926, in which G.F. Petrushevskaya [34] reported on the experience of using transcervical mediastinotomy in the treatment of posterior purulent mediastinitis, and V.L. Rokitsky [42] mentioned his use of a transperitoneal extrapleural approach to the posterior mediastinum in one case, without providing details.
The next stage in the development of methods for drainage of the posterior mediastinum was the work of A.G. Savinykh and B.S. Rozanova. A.G. Savinykh [46] developed in detail the method of transperitoneal sagittal diaphragmotomy for access to the lower parts of the posterior mediastinum for esophageal cancer, and B.S. Rozanov [39–41] modified this approach for drainage of the mediastinum with purulent mediastinitis, outlining the successful experience of many years of use in his monograph, which has not lost its relevance in the 21st century.
During the Great Patriotic War, the attention of surgeons was focused on the treatment of mediastinitis of gunshot origin [12, 16, 18, 23, 26, 31, 45]. In 1947 in Tomsk, at the V Plenum of the Academic Council of the Ministry of Health of the RSFSR, A.A. made reports on the main provisions of the treatment of acute purulent mediastinitis. Vishnevsky [12] and A.A. Gehrke [15].
Progress in the diagnosis of mediastinitis, starting from the first reports by O. Dehn [69], was facilitated by research into the capabilities of the x-ray method [20, 38].
In connection with the development of planned thoracic surgery in the 50s of the 20th century, the first publications appeared on the diagnosis and treatment of posterior purulent mediastinitis, which arose due to the failure of the sutures of the esophageal-gastric anastomoses [8]. At the same time, publications were published about secondary forms of mediastinitis developing with tuberculosis, tularemia, influenza, and erysipelas. The diagnosis in such cases was rarely made antemortem, and the therapeutic guidelines of that time [54] listed such signs of mediastinitis as the appearance of hyperemia and fistulas on the anterior chest wall.
In 1954, in the doctoral dissertation of A.Ya. Ivanov [22] was the first to comprehensively study the problem of purulent mediastinitis of various origins, localization and clinical course. He published the main provisions of this work in the form of a monograph [21]. In 1960, the manual of B.V. was published. Petrovsky “Surgery of the mediastinum” [33], where a separate section was devoted to purulent mediastinitis.
In the last quarter of the 20th century, the number of studies of anterior postoperative mediastinitis sharply increased due to the rapid development of cardiac surgery, which is accompanied by a high level of purulent complications [9, 28, 62]. Russian and foreign authors sound the alarm in their publications: according to [49], mortality in anterior mediastinitis reached 54.8%, according to [84] - 52%. At the same time, the not very correct term “sternomediastinitis” appeared [70]. The most fundamental work of those years on the problem under study is considered to be the manual edited by T. Salm [85].
Regarding the history of surgery for mediastinitis in Russia, one cannot fail to note the role of researchers from the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky. The pioneer in the study of this problem, starting in the 30s, was B.S. Rozanov [39-41]. In the 50s, the works of E.N. became widely known. Popova [36] and M.K. Shcherbatenko [57]. The next stage in the development of surgery for purulent mediastinitis is associated with N.N. Kanshin [24, 25], who in 1971 developed, on a fundamentally new basis, a method of active drainage of the mediastinum using flow-fractional lavage with long-term aspiration.
In the 70s, in Russia and throughout the world, the number of observations of purulent mediastinitis due to iatrogenic damage to the esophagus, associated with the widespread introduction of instrumental diagnostic and therapeutic technologies, increased sharply. During these years at the Research Institute named after. N.V. Sklifosovsky surgeons, together with specialists in maxillofacial surgery, otorhinolaryngologists, immunologists and resuscitators, developed a program for early diagnosis and surgical treatment of mediastinitis using complex intensive care, based on the experience of treating more than 500 patients with traumatic, odonto-, tonsillogenic and postoperative mediastinitis. This reduced overall mortality from 33% in 1976 to 11% in 1986 [3]. Progress in the early diagnosis of mediastinitis is associated with the introduction of X-ray computed tomography into practice [66, 67, 71]. In Russia, the results of a study of CT semiotics of various forms of purulent mediastinitis were published in 2001 [1].
However, in the 1990s the number of late admissions increased sharply. Against the backdrop of a decrease in the general immune background of the population due to the socio-economic catastrophe and the lack of opportunity in hospitals to use expensive drugs and treatment methods, mortality in purulent mediastinitis increased almost 2 times and in 2000 amounted to 18.9% [3].
In the first and second decades of the 21st century, there were no significant breakthroughs in methods of diagnosis and treatment of purulent mediastinitis. In Russia, with odonto- and tonsillogenic mediastinitis, it remains at the level of 27.5-54.5% [11, 52, 54], with perforation of the esophagus - 20.2% [32] and with anterior postoperative mediastinitis - 8.3% [ 27].
According to the European Association of Cardiothoracic Surgeons (2017), overall mortality in purulent mediastinitis continues to remain high - from 10 to 47%, depending on the form of mediastinitis [59, 64, 72]. Against this background, the International Classification of Diseases, 10th revision (ICD-10), is paradoxical, where the concepts of “mediastinitis” and “mediastinal phlegmon” are absent. A rarer and milder form of the disease is mentioned - mediastinal abscess (J 85.3), in which the mortality rate is several times lower than with putrefactive-necrotic phlegmon of the mediastinum.
Thus, completing the historical review of the difficult and unresolved problem of mediastinitis surgery, it should be concluded that significant obstacles to progress are the disunity of doctors of various specialties involved in the diagnosis and treatment of mediastinitis, the lack of uniform approaches to methods of surgical treatment, immune and antibacterial therapy, as well as the lack in some cases of economic opportunities to provide this therapy.
The author declares no conflict of interest.
The author declare no conflict of interest.
Information about authors
Abakaumov M.M.
- Doctor of Medical Sciences; prof.; https://orcid.org/0000-0001-6112-9404
Pathogenesis
After the moment of infection, the mediastinal tissue swells 4-6 hours later, which is called serous meningitis. The swelling spreads to the neck, subglottic area, epiglottis, etc. The person’s voice becomes hoarse, it becomes difficult to breathe, and the process of swallowing becomes difficult. Swelling of the mediastinal tissue causes increasing pain in the interscapular region and behind the sternum. Breathing becomes frequent and shallow, the body lacks oxygen. Blood flow to the right side of the heart becomes more difficult, central venous pressure increases, stroke volume and pulse arterial pressure decrease.
Body temperature reaches subfebrile values, hyperleukocytosis with a shift of the leukocyte formula to the left, and compensated metabolic acidosis are recorded. The content of carbohydrates, protein and electrolytes in the blood plasma remains almost unchanged. In case of perforation of the esophagus, coccal microflora, the presence of cicatricial changes in the mediastinal tissue after previously suffering post-burn esophagitis, the stage of serous inflammation can last 2-4 days. When the purulent process spreads to the unchanged tissue of the posterior mediastinum, after 6-8 hours morphological signs of phlegmonous inflammation appear.
With purulent mediastinitis, at the stage of generalization of the process, decompensated metabolic acidosis develops, and all parts of the immune system are suppressed. Severe disturbances of central hemodynamics accompany ARDS and progression of respiratory failure. After 3-4 days, the process spreads to the pleural cavities and the pericardial cavity, intoxication becomes very strong, maximum. Heart rhythm disturbances are typical at this stage of the disease. A person takes from 28 to 30 inhalations per minute, the temperature is 38.5-39 ° C. Consciousness is preserved, but the patient is noted to be lethargic.
A poor prognosis is indicated by such signs as sudden changes in CBS and severe lymphopenia (below 5%). The concentration of creatinine and urea increases, with hypoproteinemia and oliguria. If treatment is not started, death occurs within 1-3 days.
Symptoms
Symptoms of mediastinitis depend on the underlying process and the level of compression. There are also common manifestations that are caused by occlusion of the superior vena cava and innominate vein:
- feeling of heaviness and pain in the chest and back
- dizziness
- dyspnea
- headache
- neck thickening
- dysphagia
- puffiness of the face
- hoarseness of voice
- blueness of the hands, neck and face
- nosebleeds
- bradycardia
- asymmetry of the chest, etc.
When the esophagus ruptures, the disease begins acutely, starting with severe chest pain and shortness of breath, which are caused by infection and inflammation in the mediastinum.
Acute mediastinitis
Characterized by a sudden onset and rapid development. The patient's condition quickly deteriorates as intoxication syndrome forms and develops. The manifestations of this form depend on the nature and localization of mediastinitis, as well as on how involved the trachea, esophagus, sympathetic trunk, phrenic nerve, etc. are involved in the process. The following symptoms may be noted:
- suffocation
- dysphagia
- hoarseness of voice
- persistent cough
- hiccups
- arrhythmias
- Bernard-Turner syndrome
- intestinal paresis
Chronic mediastinitis
The disease is caused by proliferative processes in the mediastinum and a specific infection. For a long time there may be no manifestations at all. Later the following symptoms appear:
- cough
- pain in the side
- weakness
- dyspnea
- difficulty swallowing
- feeling of tightness in the chest
With proliferative and fibrous mediastinitis, signs of compression of the superior vena cava are revealed: puffiness of the face, swelling of the arm, cyanosis and dilation of the chest veins.
Kinds
According to the nature of the origin of the disease, the following are distinguished:
- Primary – caused by injury in the mediastinal organs;
- Secondary - caused by the penetration of infection into the mediastinum from other areas.
According to the clinical course of the disease, they are divided into:
Lightning;
- Spicy;
- Chronic.
According to the type of inflammation there are mediastinitis:
- Anaerobic;
- Putrid;
- Serous;
- Gangrenous;
- Tuberculosis.
The chronic type of mediastinitis can be caused by aseptic or microbial causes.
Aseptic:
- Rheumatic;
- Posthemorrhagic;
- Idiopathic;
- Adipose sclerotic.
Microbial:
- Specific;
- Nonspecific.
The disease is also distinguished by the type of localization.
Diagnostics
The high mortality rate is explained by the impossibility of early diagnosis, especially if the disease is secondary. The purulent process moves to the mediastinum. Complex instrumental examinations are carried out. A general X-ray of the chest is taken in at least two projections. Perforation of the esophagus manifests itself as follows: darkening in the posterior mediastinum in the lateral projection, the presence of air in the mediastinum, “sympathetic” pyopneumothorax.
A cavity with a horizontal fluid level is detected with a mediastinal abscess. Mediastinal emphysema can be especially extensive when the esophagus is ruptured during fibroesophagoscopy with air insufflation into the lumen of the esophagus. In some cases, a contrast study of the esophagus with a suspension of barium sulfate is relevant. Ultrasound is used extremely rarely in the diagnosis of mediastinitis. EFGS is carried out. If the method does not detect perforations, contrast radiography of the esophagus and mediastinography are performed. MRI is also valuable in establishing the diagnosis of mediastinitis.
In some cases, thoracoscopy, cavography, and bronchoscopy are relevant. Diagnosis of mediastinitis due to esophageal rupture is often based on an analysis of symptoms. CT scan detects air bubbles in the mediastinum in such cases.
Treatment
The purulent form of the pathology in question is treated with antibiotics. They are generally inclined towards de-escalation intravenous therapy with carbapenems for 7-10 days. At the same time, in case of a sutured rupture of the esophagus, in case of odontogenic, tonsillogenic infection, determining the sensitivity of the isolated microflora to antibiotics allows, in some cases, the effective use of cheaper drugs (IV generation cephalosporins, fluoroquinolones) in combination with metronidazole. This regimen gives the desired therapeutic effect if the causative agent is also coccal flora, which is typical for the postoperative anterior form of mediastinitis.
Detoxification therapy is carried out according to the same principles as for acute purulent diseases. Mediastinitis with rupture of the esophagus is treated with antibiotics administered parenterally. You can use clindamycin, which is administered intravenously every six hours at a dose of 450 mg, it is combined with ceftriaxone (2 g once a day for at least 2 weeks). In many cases, treatment requires an emergency revision of the mediastinum with primary suturing of the esophageal rupture and drainage of the pleural cavity and mediastinum.
Surgical treatment
The surgical method is the leading one in the treatment of purulent mediastinitis, since this is how complete drainage of the purulent focus is carried out. Access to the mediastinum is divided into extrapleural and transpleural. The first is resorted to in case of severe concomitant diseases, elderly patients, etc. Extrapleural approaches to the posterior mediastinum are combined with postoperative washing of the purulent focus with antiseptic solutions with aspiration of the contents in a vacuum mode in a system of the order of 10-40 cm of water. Art.
If the infected contents enter the posterior mediastinum through a defect in the pharynx, cervical, upper thoracic esophagus, then an additional drainage tube is installed with the end at the level of the perforation. The second option is suturing the defect. If gastric contents enter the mediastinum through a defect in the lower thoracic esophagus, the defect is also sutured.
Postoperative treatment
If the treatment is as intensive as possible, the treatment is successful in many cases. If this is the case, individual components of complex treatment are gradually abolished, which become irrelevant when laboratory, clinical, and instrumental manifestations return to normal.
Complex intensive treatment of mediastinitis:
- taking antibacterial drugs
- local effect on the source of purulent infection
- detoxification treatment
- immunocorrective therapy
- replenishment of the body's energy costs
Local treatment includes constant washing of the purulent focus in the mediastinum with an antiseptic solution while simultaneously using aspiration with a vacuum of about 10-40 cm of water. Art. After the cavity has collapsed and turned into a channel around the drains, the drains gradually begin to tighten and are eventually removed, replacing them with rubber outlets for several days.
If mediastinitis is a consequence of tuberculosis, appropriate anti-tuberculosis therapy is prescribed. If therapy fails, vascular stents can be installed to limit compression of some central vessels.
Mediastenitis
Classification
Mediastinitis, as well as inflammatory diseases of other localizations, are:
- acute and chronic;
- by origin: primary and secondary;
- by etiology: wound, perforation, postoperative;
- by location: anterior, posterior mediastinum;
- by prevalence: local, spilled;
- complicated and uncomplicated.
Acute suppurative processes in the mediastinum are of greatest surgical importance.
Acute mediastinitis
Acute mediastinitis, especially purulent ones, are among the most severe forms of surgical infection. Acute inflammation of the fatty tissue of the mediastinum is a severe and dangerous complication of various purulent diseases, primarily of the chest and neck organs, surgical interventions, wounds and closed injuries of the chest.
The complexity of the anatomical structure of the mediastinum, which contains a large number of vital organs, blood and lymphatic vessels, lymph nodes and nerve trunks, and the abundance of cellular spaces contribute to the rapid spread of the infectious process with a pronounced general reaction of the body against the background of severe endogenous intoxication. Continuous movement of mediastinal organs (contractions of the heart, pulsation of blood vessels, peristalsis of the esophagus, mobility of the trachea when coughing, talking, etc.) prevents the creation of conditions of rest, so necessary for the favorable course of inflammatory processes.
Etiology and pathogenesis
Causes of acute mediastinitis: open injuries; closed injury (suppuration of hematoma); perforation of the esophagus; complications of operations on the esophagus, trachea, large bronchi, mediastinoscopy, pneumomediastinography; contact spread of infection; metastatic spread of infection.
Based on their origin, they distinguish between primary (traumatic) and secondary mediastinitis. Primary mediastinitis occurs with wounds and closed injuries to the mediastinum and its organs, as well as after surgical and endoscopic interventions on them.
Acute primary mediastinitis with wounds of the mediastinum is rare. This is explained mainly by the relatively small number of victims with open mediastinal injuries who manage to be transported to medical institutions. Most of them quickly die at the scene due to severe combined injuries and massive blood loss. Thus, according to the experience of the Great Patriotic War and recent local military conflicts, the frequency of mediastinal wounds in relation to penetrating chest wounds in arriving wounded was only about 0.5%.
The occurrence and severity of the infectious process in the mediastinum is usually associated with the type of weapon and wounding projectile, the nature of the wound (through, blind), and the presence or absence of damage to internal organs. The progression of surgical infection is facilitated by a high level of bacterial contamination, virulence of microflora, mediastinal hematoma formed as a result of injury and traumatic necrosis of mediastinal tissue. Of great importance in the development of purulent complications is the initial state of the body at the time of injury and the decrease in its protective forces in response to acute blood loss and severe traumatic shock.
Purulent mediastinitis can be due to development reasons: wound, perforation, postoperative.
The disease most often occurs as a result of the penetration of microflora into the mediastinum from the lumen of the damaged esophagus, trachea or bronchi. Causes of esophageal perforations: bougienage due to cicatricial narrowings; foreign body; esophagoscopy (with esophagoscopy in 0.25% of cases - perforation); injuries; blunt chest trauma; chemical agents, often alkalis; inflammation of the mediastinal lymph nodes; spontaneous rupture; aortic aneurysm.
The cause of infection can be blind, usually shrapnel wounds, even without violating the integrity of the hollow organs. Metal fragments and scraps of clothing brought into the wound in this way often cause significant microbial contamination of the wound. Infected foreign bodies, located in loose mediastinal tissue, can cause necrosis with melting of surrounding tissues and the development of phlegmon or mediastinal abscesses. The inflammatory process that occurs with gunshot wounds, due to the severity of the injury, is often diffuse and affects all the posterior or anterior sections of the mediastinum. Sometimes total mediastinitis develops.
In peacetime, primary mediastinitis can occur with damage to the esophagus and trachea (instrumental and foreign bodies), open fractures of the sternum, as a result of suppuration of hematomas in closed chest injuries. Often the cause of mediastinitis is complications of surgical interventions on the mediastinal organs: failure of the sutures or necrosis of the gastric or intestinal graft during plastic surgery of the esophagus, failure of the sutures of the trachea and bronchi, suppuration of a postoperative wound or mediastinal hematoma, etc.
Secondary mediastinitis occurs 2-3 times more often than primary ones, and can occur when infection penetrates into the mediastinum through contact, hematogenous and lymphogenous routes. They can be complications of purulent and putrefactive inflammation of the tissue of the neck, diverticula and other suppurations of the walls of the esophagus, disintegrating cancer of the esophagus, osteomyelitis of the bone frame of the chest, inflammatory processes of cysts and lymph nodes of the mediastinum, suppuration of the lungs and pleura, sometimes abscesses and phlegmons of the mediastinum can be diagnosed as a manifestation septicopyemia in the presence of a primary septic focus of various locations.
The development of secondary acute mediastinitis can be caused by infectious complications of wounds of the lungs and pleura with the formation of purulent processes by contact or metastasis. A contributing factor in such cases is the accumulation of blood in the mediastinum as a result of trauma. Injuries to the neck with damage to the esophagus, larynx or trachea often lead to the formation of inflammatory foci in the mediastinum. Due to the anatomical features of this area, the conditions for the development of an infectious process in the neck with its subsequent transition to the mediastinal tissue are extremely favorable.
Sometimes the source of mediastinitis remains unidentified (so-called cryptogenic mediastinitis).
Depending on the nature of the inflammation, serous (non-purulent), purulent, putrefactive, anaerobic and gangrenous forms of acute mediastinitis are distinguished. An infectious inflammatory process in the fatty tissue of the mediastinum can be caused by various microorganisms: most often these are streptococci and staphylococci, less often - pneumococci, E. coli, Proteus, etc. A combination of purulent and putrefactive microflora is often found. Research in recent years has proven the importance of non-spore anaerobes in the development of intrathoracic infection, including mediastinitis.
The pathogenesis of abscesses and phlegmons of the mediastinum is based on the peculiarities of the interaction between macro- and microorganisms. Microbial contamination of the mediastinal tissue (in particular, during extended lung resections, resection and plastic surgery of the esophagus) does not always lead to the development of suppurative processes in it. The occurrence of purulent mediastinitis is facilitated by a decrease in the protective and reparative abilities of the body as a result of injury, surgery, blood loss, the presence of purulent intoxication, trauma and necrosis of mediastinal tissue, accumulation of blood in it, and the presence of a source of constant infection. With the formation of an abscess in the mediastinum, the pathogenetic features of the disease are due to the development of compression of the chest organs, as well as the phenomena of rapidly increasing endotoxicosis.
There are limited (abscesses) and widespread (phlegmon) forms. Among them, mediastinitis is identified anterior (upper - with the location of lesions above the level of the 3rd intercostal space; lower - downward from the 3rd intercostal space, and all anterior parts of the mediastinum), posterior (upper - with the location of the lesion above the level of the V thoracic vertebra; lower - downward from the V thoracic vertebra , and all posterior parts of the mediastinum) and total. Acute mediastinitis can have fulminant, acute and subacute forms of progression.
Clinic and diagnostics
Early recognition of primary acute mediastinitis is quite difficult. The comparative rarity of this complication in chest trauma and the lack of awareness of doctors about it often determine the late diagnosis of the disease. In cases of secondary inflammatory processes, abscesses and phlegmon of the mediastinum are masked by the manifestation of a primary purulent process in the lungs, pleura, neck tissue, etc. Unfortunately, an accurate lifetime diagnosis is made in only 20-30% of patients. However, the success of treatment of such patients and victims mainly depends on timely diagnosis and determination of the localization of the inflammatory focus in order to select a method of adequate drainage.
Acute purulent and putrefactive mediastinitis occurs without clearly defined symptoms against the background of an extremely difficult general condition. The severity of acute mediastinitis is explained by the presence in the mediastinum of a number of important formations - sympathetic and parasympathetic nerves, blood and lymphatic vessels, the irritation of which causes additional symptoms. As a result of damage to important nerves, the function of the organs that they innervate is disrupted - the cardiovascular system, respiration, and digestive tract. In addition, mediastinal fiber abundantly absorbs tissue breakdown products, which contributes to the development of severe endogenous intoxication. There are also symptoms of damage to the trachea and esophagus, the walls of which can be affected by the inflammatory process. These organs, in particular, can be compressed as a result of inflammatory swelling.
The disease usually begins acutely, often with chills, a significant increase in body temperature and chest pain. If acute mediastinitis occurs against the background of an already existing purulent process of another localization, then this can sometimes manifest itself as a sudden sharp deterioration in the general condition of the patient, an increase in the phenomena of purulent intoxication.
Patients complain of chest pain, increasing general weakness, malaise, and a feeling of lack of air. Noteworthy is their anxiety, sometimes with motor agitation, an increase in body temperature to 39-40 C, tremendous chills, profuse sweating, hyperemia of the skin, and shortness of breath. After a day, the picture of excitement is replaced by pronounced general depression, in some cases with confusion. Patients, as a rule, try to take a forced semi-sitting position with their head tilted to the chest, thus reducing pain and making breathing easier. Some patients experience swelling of the upper half of the torso, neck and face with dilation and tension of the superficial veins, cyanosis of the skin. Severe intoxication caused by the resorption of toxins of various origins, compression of large vessels and nerve trunks leads to noticeable disorders of the cardiovascular system. Tachycardia is always pronounced with a pulse rate of up to 110-120 per minute. As the purulent process progresses, arrhythmia appears. Blood pressure decreases, central venous pressure increases. During auscultation of the heart, dullness of tones, weakening of the first tone at the apex and the second tone at the aorta are noted. Of the local symptoms, the earliest and most persistent is intense chest pain, aggravated by swallowing and throwing the head back (Gercke's symptom). In patients with anterior mediastinitis, pain is usually localized behind the sternum, and in patients with posterior mediastinitis, pain is usually localized in the interscapular space or projected to the epigastric region. Pressing or tapping on the sternum or on the spinous processes of the vertebrae with the corresponding location of the abscesses sharply increases the pain. The progression of the inflammatory process in the mediastinum with swelling of the tissue often leads to compression of the vagus and phrenic nerves, blood vessels, and, in the presence of limited ulcers, the esophagus and trachea. As a result, dysphagia, suffocation, persistent cough, hoarseness, arrhythmias, and dysfunction of the diaphragm occur. With mediastinitis developing as a result of injury to the trachea or esophagus, as well as with anaerobic infection, mediastinal subcutaneous emphysema of the upper half of the body and neck appears. It is especially pronounced and increases rapidly when the trachea and main bronchi are damaged. Emphysema is always a very alarming sign, indicating a significant severity of the process. Anemia and high leukocytosis with a sharp shift in the leukocyte count to the left are detected in the peripheral blood. Biochemical blood tests reveal hypoproteinemia with a decrease in serum albumin, an increase in globulin levels, and a decrease in the albumin-globulin ratio.
In addition to general and local clinical signs, X-ray examination is of great importance in recognizing the inflammatory process. In this case, the expansion of the corresponding part of the mediastinum is revealed; the penetration of air leads to the appearance of horizontal levels at the border with liquid exudate accumulated in the mediastinum. A convincing sign of damage to the wall of the esophagus, incompetence of the esophagogastric or esophageal-intestinal anastomosis is the flow of contrast material beyond the contours of the organs during an x-ray examination. Sometimes these signs are combined with a picture of unilateral or bilateral pleurisy, and if the respiratory tract is damaged - pneumothorax.
To clarify the nature and extent of the pathological process in the mediastinum, computed X-ray tomography and ultrasound diagnostic methods are used; if damage to the trachea and esophagus or failure of their sutures after surgical interventions is suspected, esophagoscopy or bronchoscopy is used.
The X-ray picture of mediatinitis is characterized by: expansion of the mediastinal shadow and neck, mediastinal emphysema, subcutaneous emphysema, pneumothorax, hydropneumothorax, fluid level in the mediastinum, lung damage, esophageal fistulas.
Treatment
In case of acute purulent mediastinitis, early surgical treatment is necessary immediately upon diagnosis. The only exceptions can be cases when mediastinitis develops gradually (for example, with pinpoint perforations of the esophagus, its development from infected lymph nodes), is in the stage of serous inflammation, is limited in nature and is not accompanied by the development of a serious condition of the patient. In these cases, conservative therapy can be used, subject to dynamic monitoring of the patient in a surgical hospital.
Surgical treatment is aimed, first of all, at eliminating the cause of acute mediastinitis, opening the inflammatory focus (mediastinotomy) and its adequate drainage. Without timely surgical care, acute purulent mediastinitis almost always ends in death. Surgical assistance should be carried out even in severe general condition of the patient, after short-term preoperative intensive preparation aimed at correcting disturbances of homeostasis and eliminating disorders of vital functions.
Operations for anterior mediastinitis
For anterior limited mediastinitis that has developed as a result of injury to the sternum and mediastinal tissue, transsternal access to the mediastinal abscess with transverse sternotomy can sometimes be used. In addition to complete drainage of the abscess, the affected areas of the bones must be resected. Many types of transsternal drainage of the mediastinum have been proposed. Their main disadvantage is the risk of developing sternal osteomyelitis, so they are used exclusively for existing injuries or sternal osteomyelitis at the time of surgery.
The extrapleural parasternal access proposed by Madelung with resection of 2-3 costal cartilages has a certain practical significance. The level and side of the upcoming drainage are determined using a plain X-ray of the chest and careful intercostal-retrosternal puncture of the anterior mediastinum.
In cases of superior anterior mediastinitis, cervical mediastinotomy is used. For this purpose, a transverse incision above the manubrium of the sternum is opened and the anterior part of the upper mediastinum is drained. This method can adequately drain ulcers located above the level of the aortic arch.
For anterior inferior limited mediastinitis, extraperitoneal anterior mediastinotomy can be used. Using an incision at the level of the xiphoid process, with its resection if necessary, the diaphragm is isolated and bluntly pushed downwards. They enter the cellular layer behind the sternum, open and empty the abscess, wash the wound and drain it with silicone tubes.
The diffuse anterior phlegmon of the mediastinum is drained using a combination of supra- and substernal approaches.
Operations for posterior mediastinitis
For upper posterior mediastinitis, the method proposed by V.I. Razumovsky (1899) is used to drain the mediastinum. The technique of the operation is as follows. The patient lies on his back with a cushion placed under his shoulders, his head is turned to the right. From an incision along the anterior edge of the left sternocleidomastoid muscle, the skin, subcutaneous tissue, superficial and second fascia of the neck are dissected in layers. Together with the muscle, the neurovascular bundle is retracted outward. Using a finger, a canal is carefully created, penetrating deep and down behind the esophagus, towards the posterior mediastinum. The abscess is opened, the wound is washed and drained.
For lower posterior mediastinitis, transdiaphragmatic mediastinotomy is performed according to Savinykh-Rozanov. With this method, the abdominal cavity is opened with an upper-middle incision. The triangular ligament of the liver is dissected and its left lobe is retracted downwards and to the right, exposing the esophageal opening of the diaphragm. The abdominal cavity is limited with gauze pads. A sagittal diaphragmotomy is performed. Using a finger, they separate the fiber and penetrate up along the esophagus, reaching the cavity of the abscess. After removing the pus and introducing drainage, the diaphragm incision around it is carefully sutured to create a seal around the purulent cavity. The subphrenic space is drained.
To this day, the “classical” method of posterior mediastinotomy according to I.I. Nasilov (1888) also retains its significance, although the method itself is quite traumatic, and the postoperative wound is too deep and does not always provide sufficient drainage. During the operation, the patient lies on his stomach. According to the localization of the abscess on the posterior surface of the chest, a rectangular flap in the form of a leaf is cut out, with the base facing laterally. They fold it outward and separate the long back muscles. 2-4 ribs are resected subcutaneously over a distance of 5-7 cm. The remaining intercostal soft tissues are crossed, and bleeding from the intercostal arteries and veins is carefully stopped. The pariental pleura is peeled outward, following the parapleural tissue. They find a purulent focus, empty it and wash it with an antiseptic solution. To access the lower parts of the esophagus, I.I. Nasilov recommended making an incision to the right of the spine.
In the case of diffuse mediastinitis, which developed as a result of late recognized injury to the esophagus, transpleural mediastiotomy is used according to V.D. Dobromyslov (1900). The technique of the operation is as follows. A lateral thoracotomy is performed in the 5th-6th intercostal space on the side of the injury. The lung is moved anteriorly. The suspected site of injury to the esophagus is isolated with napkins and the mediastinal pleura is widely dissected. If there is a wound defect in the esophagus, it is hermetically sutured with the suture line covered with a mediastinal pleura flap. The pleural cavity is thoroughly washed with an antiseptic solution and drained. A double-lumen drainage tube is installed along the esophagus in the mediastinum, which is removed through a separate incision to the anterior chest wall along the slope of the diaphragm. The thoracotomy wound is sutured.
The difficulties of surgical treatment of purulent mediastinitis are due to the difficulty of creating conditions for adequate drainage. In recent decades, the method of hermetic drainage of the mediastinum with constant washing of the abscess with antiseptic solutions and active aspiration of the contents, proposed by N.N. Kanshin (1973), has received great recognition. The drainage method consists of using silicone double-lumen drainage tubes inserted through extrapleural access, followed by active aspiration of pus while simultaneously washing the cavity with antiseptic solutions and solutions of proteolytic enzymes. With an average infusion rate of 2-3 ml of antiseptic per minute, from 3 to 5 liters of solutions are consumed per day. It is very important to create a sealing of the cavity, which is achieved by using narrow drainage channels. Aspiration is achieved by creating a constant vacuum of 50-100 cm of water column. According to the author himself, the use of this drainage method made it possible to reduce mortality in acute purulent mediastinitis by 3 times.
In case of damage to the esophagus and the development of diffuse mediastinitis (usually in combination with purulent pleurisy), we adhere to active tactics. The time since the injury is not an argument for refusing thoracotomy and complete drainage of the mediastinum and esophageal suture. Our experience has shown that late admission (time from injury to hospitalization more than 6 hours) is not a correlating factor affecting mortality. Short-term intensive preoperative therapy, thoracotomy with wide dissection of the mediastinal pleura, careful sanitation, suture of the esophagus, intraoperative intravenous administration of 4 grams of kefzol, rational drainage of mediastinal tissue with two silicone tubes followed by round-the-clock lavage, give a better chance than “blind” drainage of the damaged area. The pleural cavity is drained with a separate silicone tube. If the lower third of the esophagus is damaged, to prevent reflux of gastric contents, we suggest applying a purse-string suture with catgut to the mucous membrane of the esophagus in the zone of transition of the latter to the stomach. A purse string suture is performed with a nasogastric silicone tube with a diameter of 0.5 cm installed. The advantage of this technique is seen in the following: minimal disruption of the blood supply to the esophagus, provision of nutrition through a nasogastric tube, the ability to independently restore patency of the esophagus.
Considering the significant severity of purulent mediastinitis in the pre- and postoperative periods, it is necessary to use all means of intensive conservative therapy. An important role in the treatment of patients belongs to massive general antibacterial, detoxification and infusion therapy, parenteral and enteral (tube) nutrition. Feeding patients through a tube with damage to the esophagus begins when congestion in the stomach is eliminated and intestinal motility is restored. In the absence of esophageal injury, enteral nutrition begins the next day after surgery. The combination of enteral and parenteral nutrition in patients with acute mediastinitis makes it possible to provide the energy and plastic needs of the body.
Acute mediastinitis remains today one of the most difficult to diagnose and severe diseases. Mortality with it continues to remain quite high and reaches 26-40%.
Chronic mediastinitis
Chronic mediastinitis can be aseptic and microbial. Aseptic mediastinitis includes:
- idiopathic;
- posthemorrhagic;
- coniose;
- lipophagic;
- rheumatic;
- adipose sclerotic.
Microbial chronic mediastinitis is divided into nonspecific and specific (syphilitic, tuberculous, mycotic).
Aseptic mediastinitis . Common to all types of such mediastinitis, in addition to the absence of microbial agents in the tissues involved in the inflammatory process, is the predominantly productive nature of inflammation with the development of more or less pronounced sclerosis of the mediastinal tissue.
Idiopathic chronic mediastinitis (mediastinal fibrosis, fibrous mediastinitis) has the greatest surgical significance. The reasons for its occurrence are not completely clear. It is characterized by the progressive growth of dense connective tissue along the mediastinal tissue, with the gradual involvement of blood vessels, nerve trunks and mediastinal organs (with the exception of the myocardium) in the cicatricial process. The anterior parts of the mediastinum are predominantly affected. There are generalized and localized forms. General signs of inflammation in idiopathic fibrous mediastinitis are usually absent; the leading clinical signs of the disease are symptoms associated with compression of the mediastinal organs.
The prognosis for a rapidly progressing generalized form of mediastinitis is usually unfavorable. No pathogenetic therapy has been developed. Radiation therapy and the use of corticosteroids have some effect. Surgical treatment is palliative in nature and is used mainly for localized forms and to reduce compression of organs or perform plastic surgery (esophagoplasty, bypass of the superior vena cava, etc.).
Posthemorrhagic chronic mediastinitis occurs after a chest injury due to the organization of a hematoma infiltrating the mediastinal tissue. However, in these cases, the scarring process does not reach the same extent as in idiopathic fibrous mediastinitis. Cicatricial degeneration of organs, vessels and nerve trunks of the mediastinum does not develop, but compression syndrome is expressed to varying degrees.
Coniotic chronic mediastinitis is associated with secondary damage to the regional lymphatic system and mediastinal tissue in silicosis or anthracosis of the lungs. Fiber scarring mainly develops in the affected areas of the lymph nodes. Clinically, superior vena cava syndrome may manifest itself as asthmatic attacks, hoarseness, and Horner's syndrome.
Lipophagic chronic mediastinitis practically does not occur at present. Its occurrence is associated with the penetration of paraffin into the mediastinum, used for extrapleural collapse therapy for pulmonary tuberculosis.
Rheumatic chronic mediastinitis occurs as a consequence of rheumatic pericarditis. The process is local in nature; as a rule, the pericardial tissue is affected. Treatment is antirheumatic medication, and if indicated, pericardiectomy.
Adipose sclerotic chronic mediastinitis is associated with excessive deposition of fatty tissue in the mediastinum and the development of degenerative and sclerotic processes in it. Occurs with obesity, in severe cases it can lead to compression of the superior vena cava and its branches.
Chronic nonspecific mediastinitis . There are primary and secondary chronic microbial nonspecific mediastinitis.
Primary chronic nonspecific mediastinitis arises from the same reasons as acute mediastinitis, but, bypassing the acute stage of purulent inflammation, the process immediately becomes chronic. Often, primary chronic mediastinitis is observed with tumors and cysts of the mediastinum, especially infected, purulent lymphadenitis, delimited by a dense fibrous capsule. A similar situation can be observed with non-through or point injuries of the esophagus, when a powerful limiting connective tissue capsule has time to develop and a chronic abscess is formed, often communicating with the esophageal cavity. At the site of damage, in the wall of the esophagus, an inflammatory process develops, which can lead to the development of a cicatricial stricture of the esophagus.
Secondary chronic nonspecific mediastinitis is usually the outcome of acute mediastinitis, which, due to one reason or another, has taken a chronic course. This may be facilitated by the presence of a residual purulent cavity, often with the development of external fistulas, the development of purulent chondritis of the costal cartilages, osteomyelitis of the sternum, foreign bodies remaining after injuries, etc.
A characteristic morphological sign of chronic nonspecific microbial mediastinitis is the presence of an abscess limited by a connective tissue capsule, the development of a more or less pronounced reactive scar process in the mediastinum. In other cases, chronic inflammation and the development of scar connective tissue may be a consequence of lymphangitis, when infection spreads from adjacent organs (esophagitis due to cardiospasm, burns of the esophagus, etc.).
The clinical picture of chronic nonspecific mediastinitis is characterized by prolonged low-grade fever with periodic increases and decreases to normal levels, weakness, sweating, and chest pain. Due to compression of the mediastinal organs and the development of inflammatory changes in them, shortness of breath, cough, dysphagia, and hoarseness may occur. Patients are usually pale and have poor nutrition. There may be fistulas on the chest wall with purulent discharge. When examining peripheral blood, anemia, leukocytosis with a slight shift of the leukocyte formula to the left, lymphopenia, and accelerated ESR are noted.
Treatment of chronic nonspecific mediastinitis without the presence of an encysted abscess in the mediastinum consists of eliminating the cause that supports the inflammatory process (cardiospasm, reflux esophagitis, esophageal stenosis, etc.) and conducting antibacterial anti-inflammatory therapy. In the presence of an encysted mediastinal abscess, purulent chondritis, or sternal osteomyelitis, surgical treatment is indicated. It consists of opening, sanitation and drainage of the purulent cavity, through an access corresponding to its location. A limited abscess that has a dense capsule and is not connected to the lumen of the esophagus or trachea can be excised en bloc along with the capsule. In the presence of chondritis or osteomyelitis, resection of areas of costal cartilage and sternum within healthy tissue is indicated.
Specific chronic mediastinitis
Chronic specific mediastinitis is most often associated with tuberculosis infection. Syphilitic mediastinitis, actinomycosis, mediastinal histoplasmosis, etc. are extremely rare.
Tuberculous mediastinitis develops in connection with specific inflammation in the lymph nodes of the mediastinum, as well as with pericarditis of tuberculous etiology. The tissue of the anterior and middle parts of the mediastinum is most often affected. The posterior, as well as the posterior part of the upper mediastinum is affected mainly in spinal tuberculosis. Typically, around a package of lymph nodes containing tuberculous mycobacteria and specific granulomatous tissue, more or less pronounced nonspecific periadenitis occurs, followed by the development of scar connective tissue, which, depending on the location, can cause compression of various organs and anatomical formations of the mediastinum. Breakthrough of caseous masses from the affected lymph node into the mediastinal tissue is very rare and, as a rule, without the development of purulent mediastinitis.
The clinical picture of the disease is determined mainly by the severity and course of the tuberculosis process. Developing scar-sclerotic changes in the tissue of the mediastinum can cause compression syndrome of the superior vena cava, esophagus, large nerve trunks with the development of corresponding clinical signs.
