Discussion
NSTIs are infectious diseases burdened with high mortality that spreads through the fascial planes and leads to connective tissue necrosis. NSTIs may occur as a complication of a variety of surgical procedures or medical conditions and it may also be idiopathic, as in scrotal or penile necrotizing fasciitis.The prevalence is higher in males and in patients aged 45 to 64 years. Physical findings may not be commensurate with the degree of patient discomfort. Early in the disease course, the patient may look misleading well; unfortunately, this may interfere with early detection, which is the cornerstone to a favorable outcome. As reported by our previous work[7], the sites from which NSTIs may originate in the cervical district are represented in order of frequency by:
odontogenic infection, peritonsillar abscess and sinusitis.
According to the depth of tissue infection and necrosis, NSTs can be classified into three forms which involve the dermis and subcutaneous tissue for necrotizing cellulitis, the fascia for necrotizing fasciitis, and the muscle layer with the intact overlying skin for necrotizing myositis [8] .
Cervical fascia is the fibrous tissue that divides structures of the neck and is divided into superficial and deep layers. The superficial layer of the deep cervical fascia envelops parotid and submandibular glands and it is the external border of the odontogenic infections of the neck [9]. Most of these infections originate from the second or third mandibular teeth infection or extraction. The roots of the second and third molars can extend up to the submandibular space and through this path the infections of this site can spread through the cervical fascia to the lateral pharyngeal space, involve the retropharyngeal space and track into the anterior or to the posterior mediastinal region with the clinical picture of mediastinitis [10]. The infection can be monomicrobial or polymicrobial. The most frequently isolated organisms in NSTI include viridans group streptococci, S. aureus, peptostreptococci, Bacteroides spp., Prevotella spp. and Fusobacterium[11]
Antibiotic therapy must be started early, must be empirical and wide spectrum in the early stages, subsequently tailored on the basis of the results obtained from cultural tests performed on biological material. Furthermore, in the choice of drugs used, other variables should be carefully considered, such as the risk factors for multidrug-resistant microorganisms. Finally, a further key point consists is the rapid antibiotic steward ship which must be based on clinical evidence and bio-humoral markers. Serum procalcitonin has been proposed as a biomarker capable of guiding the response to antibiotic therapy, allowing a rapid de-escalation. Normal serum procalcitonin concentration in a healthy individual is <0.05 ng/mL. Patients with procalcitonin concentration of <0.5 ng/mL are unlikely to have sepsis. However, this concentration does not exclude infection, because localized infections like cervical NSTI without systemic signs are still possible[12] . Regrettably, with high frequency, antibiotic therapy is started on an empirical basis without providing for targeted culture samples and subsequently followed superficially.
Cervical NSTIs uncommonly gets complicated with the involvement of muscles but when that happens, as happened in our patient, a theatre of necrotizing myositis occurs. Necrotizing myositis is a surgical emergency. It may presents without changes in the skin thus it is under appreciated and diagnosis is often delayed [13] . In our patient the entry route was through dental infection and this is in accordance with a literature review published by Pellis et al [14] , wich highlighted how the teeth are the main (65%) responsible cause of NSTIs of the cervical region. In our case infection, luckily did not involve the deep cervical fascial planes, but spread along the superficial planes and affect the subcutaneous skin and muscles of the right upper thoracic region, as evidenced by the images.
HBOT has been proposed as an adjunctive therapy for patients with NSTIs[15] . In HBOT, patients breathes 100% oxygen for a specified period of time in a pressurized chamber at pressure higher than atmospheric pressure at sea level. It causes increased blood and oxygen content in hypoxic tissues and this increased oxygen availability is responsible for multiple effects as antimicrobial activity on both aerobic and anaerobic bacteria thereby demonstrating the bactericidal and bacteriostatic effects due to enhanced mobility and bacteriophagic activity of leukocytes. Parts of the antimicrobial effects of HBOT are believed to result of both formation of reactive oxygen species (ROS)[16] and synergistic effects with some antibiotics [17]
On top HBOT promotes granulation tissue formation due to fibroblast proliferation and collagen synthesis, and improves microcirculation due to edema reduction[18] .The increase in O2 tension produced by HBOT, which persists for several hours after therapy, is responsible for angiogenic properties of HBOT [19] Hyperbaric O2 causes reduced platelet aggregation, improved tissue microcirculation, and diminished metabolic disturbances. These properties along with increased dissolved O2 in plasma lead to better oxygenation of hypoxic tissue, where red blood cells cannot reach.[20]
The hyperbaric treatment of our patient was conducted on the basis of the SIMSI guidelines [5]: in the first 3 days, we adopted the maximum oxygen dosage at 2.8 ATA (284 kPa), twice day. From the 4th day: treatments become daily with sessions at 2.5 ATA (253 kPa). The duration of each session was 80 minutes and the treatment was continued until the infection is considered to be overcome.
Absolute contraindications to HBOT are represented by non-drained pneumothorax, PaO2 / FiO2 ratio <200 assessed by blood gas analysis, seizures, claustrophobia and psychotic pictures in rupture. Our patient had none of these, he showed good compliance with the method with a good response to treatment from the third day of HBOT.