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.