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Necrotizing fasciitis is an unusual rare, progressive and life-threatening bacterial infection which spreads with frightening speed along the fascial planes and subcutaneous tissue resulting in extensive necrosis and often death. Rapidly spreading necrosis often causes systemic sepsis, toxic shock syndrome and multi organ failure. Necrotizing fasciitis of the neck is rare and commonly has a dental or pharyngeal origin. Factors affecting the success of the treatment of necrotizing fasciitis are early diagnosis, appropriate antibiotics and surgical debridement. In this article is presented a 65 years old homeless patient with necrotizing fasciitis of the neck and thorax, trigger point being an old neglected trauma with infection. Clinical features, pathogenesis and treatment of the case are discussed in the article. Rapid recovery required adequate medical treatment etiologic, also symptomatic and supportive, surgical with debridement with excision of the necrotic tissue, irrigations with antiseptics; local antibiotics early sterilization allowed adequate skin grafting with good results.
Cervical necrotizing fasciitis is a fulminate infection, with necrosis of the connective tissue that spreads with high speed along the fascial planes. It was first described by Claude Pouteau în 1783 but clinically was defined by Joseph Jones in 1871, during the U. S. Civil War, first being described in military hospitals as gangrene. In 1918, Pfanner diagnosed as necrotising erysipelas” a patient with a beta haemolytic Streptococcus infection [1-4]. Wilson introduced the term necrotizing fasciitis (NF) in 1952. In general, the isease is more common in extremities, the genital region, and the abdomen, rare in head and neck. 1-10% and is limited only at the skin and subcutaneous tissue, muscle involvement is rare. Cervical type of such an infection is infrequent and its development is determined by the complexity of anatomical planes of the neck and continuity of the fascial planes with adjacent anatomical regions, notably thorax and mediastinum . Idiopathic cases are not rare as aggressive broad spectrum antibiotic therapy may mask the primary site.
The fact that necrotizing fasciitis causes tissue necrosis and spreads rapidly along the fascial planes is due to the synergistic effect of enzymes meiped by the bacteria. The causative organism may be a single agent, commonly Group A beta haemolytic Streptococci or Staphylococccus Aureus or may be a polymicrobial infections. Polymicrobial infections are caused by mixed aerobic and anaerobic pathogens. Synergy between them contributes to the pathogenesis of polymicrobial fasciitis i.e. synergistic gangrene. Necrotizing fasciitis can be divided into 5 types [6-9]:
a) Necrotizing fasciitis Type I:Polymicrobial, is caused by non Group A streptococci and anaerobes and/or facultative anaerobes. Usually seen after trauma or surgery. There is involvement of subcutaneous fat and fascia with sparing of muscle and gas formation.
b) Necrotizing fasciitis Type II:Group A streptococcal is caused by Streptococcus pyogenes alone or associated with Staphylococcus aureus. With Streptococcal toxic shock syndrome. Predisposing factors are trauma, surgery or varicella infections.
c) Type III Clostridial myonecrosis:Gas fasciitis of the scrotum
d) Type V Lemierre’s syndrome (A. Lemierre, 1936):Gangrene is characterized by its fulminate onset. The predominant features are muscle necrosis and gas production. The commonest causative organism is Clostridium perfrigens.
e) Type IV Fournier’s gangrene (J.A. Fournier, 1883): necrotising Oropharyngeal infection with secondary thrombophlebitis of the Internal Jugular Vein and frequent metastatic infections. Caused by Fusobacterium necrophorium. In most cases, the pathogenic germs through a disruption of the skin caused by trauma or surgery
Of type I is not yet clarified possible there is a synergy between
the germs in affecting human tissues, but for sure immune status
of the host is so damaged than infection can spread very fast
Being so rare there are just a few studies on the pathogenesis
of necrotizing fasciitis. It describes a progressive liquefaction
of fat and subcutaneous connective tissue underneath the
skin of relatively normal appearance. Fascial planes decays, it
produces necrosis and release of a fat tisular liquid . Veins
placed in liquefied subdermal plane begin thrombosis and the
skin becomes congested at first and then marbled. Subsequently
arterial circulation is affected and the skin becomes pale,
leading to gangrene. The response is characterized by an intense
polymorphonuclear infiltration focal necrosis and formation
of micro-abscesses. Rapid disease progression is another
distinctive element of necrotizing fasciitis if the characteristic
clinical signs are present, the clinical diagnosis does not require
confirmations-or bacteriological examination .
The treatment is somewhat similar to extensive burns. The
practice; repeated lavages debridement of the wound -dressings
made preferably in operation room. Favourable evolution
gradually appears in the depth of the wound granulation tissue
and the skin is attached to this granulation tissue, from the edges
of the wound. Antibiotic therapy can be guided by microbial
culture; hyperbaric therapy (where technical conditions permit)
can be applied, although no studies to prove its effectiveness.
Despite effective surgical and medical treatment, the
prognosis remains reserved with increased mortality. Mortality
may be due to general issues of major bleeding from about 10
days after surgery, when the infection appeared to be solved.
The main reasons for the disease are odontogenic infections,
bad oral hygiene, cavities or dental treatment. In 2/3 of cases
can fallow a skin trauma or maxillo-facial surgeries. The disease
frequently develops in individuals that have an insufficient and
low immune system, diabetes mellitus commonly seen in middle
Patient M.M, 65 years old, was referred to our emergency
department, being picked from the streets by a SMURD Unit. Our
patient without family, income leaved on the streets and was
sleeping in a sour channel. He was admitted with high fever, bad
general status, dysphagia, odinophagia, excruciating pain in the
left side of the neck and periauricular. He described a temporal
trauma 2 weeks before arrival in our department, with a small
wound in the retro auricular left area, but he neglect this trauma
till the 3rd week ,when the lesion become red ,with extension on
the latero-cervical area [11-15]. Pain became more severe day
by day, and his general status deteriorates so he fall on the street
were was discovered by the paramedics .
On presentation we discover a patient in a very bad status ,
with high fever, severe asthenia, very thin, very dirty, lice infested,
obnubilated, late reactions, responding with difficulty to the
questions. He had major pain in the cervical area, subcutaneous
oedema and a skin defect on retroauricular left area, extended
The wound appeared necrotic with a dark base and a lots of
fistulous tracts with a foul, aerated, frothy discharge . Skin
over the latero -cervical area and right thoracic wall appeared
purple discoloured, with marked oedema. Palpation revealed a
painful, infiltrated, friable area with gaseous crepitating. At the
beginning my first impression was of an Actinomycosis, maybe
a lymph nodes tuberculosis- scrofulosis so I take multiple
samples from the pus and tissue and order to the laboratory
direct examination, specific coloration-ex. Zielh-Nielsen or acid,
fast bacilli like Mycoplasma pneumoniae, for aerobic anaerobic
bacterias but also mycological examination with sensibility
to antibiotics, antifungal drugs. But when next day I remove
the dressing I was stunned by the massive extension of the
lesions on the neck and thorax so fast I ask at the lab about the
results and they confirm my suspicion of flesh eating disease.
Examination of the mouth was difficult to perform because of
the pain, revealed poor oral hygiene, multiple residues, cavities,
bad breath fetid  (Figure 1).
Imagistic:X-ray of the lungs-traces of Tuberculosis. CTneck-
thorax-superficial inflammation, necrosis, gas formation,
no extension deep or in mediastinum.
Test HIV negative, HBS Ab, Ac HBC neg, Quantiferon
Bacterial cultures from the wound showed a mixed
flora with Streptococcus pyogenes and Staphylococcus
aureus could be isolated and tested for antibiotic sensibility
Pathological examination confirmed inflammation with
tendency to abscess formation that extended between viable
muscular fibres. Fat tissue shows massive lyponecrosis with
recent thrombosis of small vessels associated to inflammatory
infiltration (Figure 2).
In ICU medical treatment with sustaining of the vital
functions, antialgics, hydratation, sustaining the general
status with parenteral nutrition-glucoses, amino-acids,
lipids, vitamins electrolytes nutrition solutions -in OR under
general anaesthesia we perform wound toilet, washing
with betadine, oxygenated water, and continue with soft
tissue debridement and resection of necrotic areas, wet
dressings soaked in betadine and antibiotic solutions,
topical application of boric acid powder iodated, hampicin, neomycin, bacitracin. This toilet was performed every day
with repeated wash outs with antiseptic solutions, sometimes
debridement and skin excision. The evolution of the process
was positive -we succeed to stop the progression of necrosis
and heal the infection, day by day general condition improves
and basis of the wound began granulation course, small
islands of epithelium appear from the edges till grafting was
possible  (Figure 3).
Patient was referred to the plastic surgery Clinic was the
skin defect was covered. All skin grafts survived and patient
had a swift recovery being discharged after an additional
postoperative week. Early postoperative functional results are
very good with no limitations in movements, while cosmetic
aspects are acceptable. A psychiatric examination revealed a
Dementia probably alcohol induced -we insist on this because
our patient was completely amnesic, could not remember his
name, or were his house, wife or children . We contact the
police and social department but were impossible to discover
a relative, so, when we discharge the patient completed healed
social worker assistant help him to obtain a place in a social
shelter also recuperate his ID, retirement pension. He is still
coming every month to check -up and is in good health.
Cervical necrotizing fasciitis is an infection that rapidly
progresses on the fascial planes, even if cases are rare. It
comprises 2.6% of all head and neck infections. It is more
common in middle aged males. The cause it is the most
frequently dental pathology, followed by parapharyngeal and
peritonsillar infections. Surgeries and traumatic lacerations may
be considered possible causes. Necrotizing fasciitis is
an insidiously advancing soft tissue infection characterized
by widespread fascial necrosis. Organisms spread from the
subcutaneous tissue along the superficial and deep fascial
planes, presumably facilitated by bacterial enzymes and toxins.
This deep infection causes vascular occlusion, ischemia, and
tissue necrosis. In most cases aetiology is plurimycrobial.
(Type I necrotizing fasciitis) and this form may initially
be mistaken for wound cellulites more so when toxicity is not
obvious. Type II is a streptococcal infection also called “flesh
eating infection” and type III is a gas gangrene with myonecrosis.
The case presented in this paper was a typical type II infection
with infection spreading on fascial planes and association with
vascular thrombosis a super infection after an initial traumatic
wound. The disease starts suddenly and violently with a high
temperature. The infection causes necrosis in subcutaneous
tissue as a result of intense lymphocytic infiltration, vascular
thrombosis, and oedema as it spreads . The disease
progresses more rapidly in patients with diabetes, chronic kidney
failure, insufficient immune systems, or have undergone surgery,
trauma, and radiotherapy previously. Our patient was a chronic alcoholic men living in poor conditions; with malnutrition, toxic
hepatophaty, also sign of dementia.
Suitable radiological examinations should be requested
as soon as possible in order to determine the extent of the
disease, and to correctly evaluate the airway of the patient. The
CT enables us to see the formation of subcutaneous gas and
abscess. Even though the CT image does not illustrate significant
pathology, it helps guide surgical intervention. Hyperbaric
oxygen and intravenous immune globulin treatment decreases
the mortality rate. The key in management is early recognition
and early debridement. Of course resuscitation is to be started
immediately and empirical antibiotics commenced even before
the first surgical gesture, with later tailoring according to in vitro
Aggressive surgery implies to remove all non-viable tissue,
without concern for further reconstruction preserving nonviable
structures for a future cosmetic result is responsible
for continuous toxicity and infection progression beyond
the healthy margins. Repeated debridements are required
as lesion may progress away from apparent viable limits of
resection. Bleeding can be a problem mostly if associated with
intravascular coagulation, but in most cases bleeding from small
vessels is a sign of adequate resection. Complex anatomy of the
neck allows progression along superficial as well as deep fascial
structures [8,20]. Continuity of the neck fascia with mediastinum
and thoracic wall structures favors progression towards these
anatomic areas. Appropriate surgical management of deep neck
infections is predicated on a comprehensive understanding of
the anatomy of the head and neck.
All infected spaces should be readily opened and drained.
One should take into account possible spreading to these
spaces and the pictures we present clearly demonstrate the
importance of adequately debridement fascia in these spaces.
Reconstruction should be decided together by ENT surgeon
in charge and the plastic surgeon but early grafting should be
delayed until bacteriological eradication. A good level of trust
and communication between the two specialties will speed up
the procedure. Mortality in cervico-facial fasciitis is almost 40%.
Necrotizing fasciitis is rarely seen in the head and neck
region, but the clinician must be aware that the illness may occur
and capable to applied a good clinical examination, a make a
correct empiric antibiotic selection, and an appropriate surgical
intervention. The management of necrotizing fasciitis affecting
cervical spaces continues to be a challenge and require surgical
skills and courage to insure an early aggressive debridement.
Rapid and suitable medical and surgical treatment, applied
before the disease spreads, and before mortality-increasing
complications arise, increases the rate of success.