Download Necrotizing Fasciitis : Case Report and Review of Literature

Acta chir belg, 2007, 107, 29-36
Necrotizing Fasciitis : Case Report and Review of Literature
L. Smeets, A. Bous, O. Heymans
Department of plastic and reconstructive surgery, CHU Liege.
Key word. Necrotizing fasciitis.
Abstract. We report a case of necrotizing fasciitis of the lower limb. This medico-surgical emergency is a life-threatening invasive soft-tissue infection which primarily involves the fascia superficialis and rapidly extends along subcutaneous tissue with relative sparing of skin and underlying muscles. Clinical presentation includes fever, signs of systemic
toxicity and pain out of proportion to clinical findings. Paucity of cutaneous findings early in the course of the disease
makes diagnosis challenging. The confirmation of the diagnosis is often made after surgical debridement. Delay in diagnosis and/or treatment correlates with poor outcome, leading to sepsis and/or multiple organ failure. Radiologic studies
including plain radiographs, CT-scan or MRI may help to diagnose necrotizing fasciitis. Prompt surgical debridement,
intravenous antibiotics , fluids and electrolytes management and analgesia are mainstays of the therapy. Adjuvant treatments like clindamycin, hyperbaric oxygen therapy and intravenous immunoglobulins are discussed.
Introduction
Necrotizing soft-tissue infections are actually a disease
with a severe outcome characterised by a fulgurous progression of the inflammation in soft-tissue with a disastrous immediate prognosis and risk of major functional
sequellae.
Only prompt diagnosis and rapid care, including an
immediate use of appropriate antibiotherapy and extensive surgical treatment, can improve the outcome.
We report a case of limb necrotizing fasciitis. We
review diagnosis and treatment to allow fast recognition
and adequate management of this disease entity.
Case Report
An 49-year-old woman, with chronic Leriche syndrome
(aorto-iliacal arterial thrombosis) and history of drug
abuse (ethylism and heroin addiction), reported acute
right crural pain, increasing at walk. At first examination, clinical findings only included high fever, intensive
pain and a right heel phlyctena. At the third day, puncture for right knee swelling and a suspected septic arthritis remained negative. High inflammation was evidenced in routine serology. Differential diagnosis were
thrombophlebitis and osteomyelitis, but doppler and
scintigraphy remained negative. On the following day,
there was a great increase of the pain and a swelling of
the medial part of the thigh at physical examination.
Pelvic CT-scan and angioscan showed a hypodensity of
the vastus medialis without significant vascular lesions.
On the next day, infectious myositis was suspected and
the patient received 6 gr/day of Amoxicilline-clavulinate. Despite the antiobiotherapy, swelling and pain further increased. A cutaneous necrosis appeared and RMI
demonstrated an extensive muscular necrosis of the
thigh with a posteromedial collection. The patient was
immediately transferred to the university hospital. At
admission, very important swelling, necrotic phylctena
and slight hypoesthesia of the thigh were found at examination. The patient was extremely algic and anxious
with severe tachycardia and very high CRP (357 mg/ml)
and CPK level (1698 U/l). Just after initial evaluation,
the area of cutaneous necrosis extented from 10 cm2 to
400 cm2 in three hours (Fig. 1).The patient underwent
prompt surgery consisting in wide fasciotomy and
debridement of extensive necrosis of subcutaneous fat
and vastus lateralis (Fig. 2). Anatomopathogy revealed a
necrotizing fasciitis and an ischaemic muscular necrosis.
Microbiology revealed group A streptococcus and
staphylococcus. Clindamycin and Penicillin were introduced as new antibiotherapy. Despite of daily debridements of necrotic tissues and intensive supportive care,
evolution was complicated by severe acute respiratory
syndrome with septic shock treated by vasoactive
amines. The patient was maintained under respiratory
assistance during eight days. She stayed 17 days in the
intensive care unit. She was transferred to the department of plastic surgery for local wound care (Fig. 3).
Axillo-femoral by pass was later perfomed to alleviate
chronic ischaemia of the lower limbs. The extensive
tissue loss finally resulted in a high tigh amputation.
30
Fig. 1
Cutaneous necrosis just after initial evaluation in the university
hospital.
Fig. 2
Extensive necrosis of subcutaneous fat and vastus lateralis
Discussion
Anatomopathology
The course and evolution of the necrotizing fasciitis
(NF) observed in our case is very pathognomic. It is an
instructive illustration of a rare disease entity. We discuss some aspects of NF, in the light of our observation.
Besides superficial skin infections such as erysipelas
and dermohypodermal infections (unfortunately named
cellulitis), there are necrotizing soft-tissue infections
also called necrotizing fasciitis. They are characterized
by a soft-tissue involment extending down to the fascia
superficialis (Fig. 4). The most difficult step is the
recognition of the deep soft-tissue infection leading to
an accurate treatment decision.
L. Smeets et al.
Fig. 3
Daily wound care in the plastic surgery departement
The common fact between these different presentations is a necrosis involving the fascia superificialis and
subcutaneous tissue, containing vessels and nerves.
Inflammation induces venous micro-thrombosis, arterial
vascularitis, local haemorrhage and secondary skin
infarctions. Edema rapidly extends as a consequence of
the release of bacterial toxins. When liquefactive necrosis of the superficial fascia and fat takes place, it
produces a watery, thin, and often foul-smelling fluid
known as “dishwater pus”.
Dermal and hypodermal tissue are severely infiltrated
by inflammatory cells (mainly neutrophils) (1). Epidermal and muscular structures are typically not involved.
However, infection can spread to underlying muscles,
resulting in myonecrosis. Haemorrhagic bullaes can
develop as infection progresses (2). In presence of
Clostridium species, gas production can be observed.
Rapid extension of the lesions is complicated by systemic disorders. As organisms and toxins disseminate
into the bloodstream, the patients develop signs and
symptoms of sepsis. Hypocalcemia can develop as a
result of extensive fat necrosis (3).
Mortality attains 30% with higher mortality in the
elderly (4). Some authors report a mortality rate as high
as 76% (5).
Microbiology and pathogenesis
NF consists in bacterial invasive infection. The clinical
presentation (including systemic disorders) changes in
function of the bacteria species involved. Guilianio suggested a classification for NF based on the wound
microbiology (6). Bruin-Dubuisson has adapted this
classification to allow a correlation of the clinical features with the bacterial etiology (Table I) (7). There are
two main categories of NF with different outcome and
therapeutic strategy.
Necrotizing Fasciitis
31
Fig. 4
Anatomy and infections of the skin
Table I
Classification , clinical aspects, anatomopathology and microbiology of Necrotizing Fasciits, Adapted from : (7)
Type
Type 1
Type 2
Clostidium fascitiis
Clostridium Myonecrosis
Pain
Cutaneous signs
+ / ++
Edema, erythema, bullae,
necrotic and ulcerated lesions
++ / +++
Edema, erythema,
necrotic bullae
+
Minor : oedema,
pale skin
+++
Pale skin, Necrotico-hemorragic
bullae, anesthesia
Systemic signs
+ to +++
+ to +++ (Toxic shock)
+
+++
Progression
Moderate (3 to 14 days)
very fast
(Toxic shock syndrom,
1-3 days)
Moderate (> 3 days)
Very Fast (1-3 days)
Gas production
+/-
-
++
+++
Deep fasciasinfection
- to ++
+ to +++
-
+++
Muscular infection
-/+ (secondary)
-/+ (secondary)
-
+++
Site of entry,
initiating factor
Wound, vascular lesion,
surgery, local infection
Trauma, surgery,
cutaneous lesion,
burn, erysipelas, varicella
Wound,
surgery
Non penetrating trauma,
limb crushing,
IM injection, sepsis
Risk factors
Diabetes mellitus
Vascular disease
Diabetes mellitus
Immunosuppression
Miocrobiology
Enterobacteraci ae, Anaerobes,
Streptococcus, Staphyloccocus
Group A
Streptococcus
C. perfingens
C. perfingens
C. septicum
Type 1
Type 1, which represents approximately 80 to 90% of all
NF cases, includes polymicrobial infection involving
non- group A streptococci plus anaerobes and/or facultive anaerobes (4). Perineal and abdominal (particulary
postoperative) fasciitis usually belong to type 1. Four to
five different bacterial species are usually found in the
same lesion but some series reported as many as 11 different organisms (6). Table II lists organisms most fre-
quently implicated in necrotizing fasciitis. Enterococci
and gram – aerobic/anaerobic enteric bacilli are the most
commonly involved species.
A particular type of necrotizing fasciitis is caused by
the marine vibrios. The usual site of entry is a puncture
wound by a fish, a cut or an insect bite exposed to sea
water (8, 9).
Another special category must be made for type 1 NF
that develops spontaneously, without trauma or pre-
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L. Smeets et al.
Table II
Microbiology of Necrotizing fascitiis
Gram-positives
Group A streptococcus
Group AB streptococcus
Enterococcus spp
Coagulase-negative staphylococci
Staphylococcus aureus
Bacillus spp
Corynebacterium spp
Gram-negatives
Escherishia coli
Pseudomonas aeruginosa
Enterobacter cloacae
Klebsiella spp
Proteus spp
Serratia spp
Acinetobacter calcoaceticus
Citrobacter freundi
Pasteurella multicoda
Anaerobes
Bacteroides spp
Clostridium spp
Peptostreptococcus spp
Prevotella spp
Fusobacterium spp
Veilonella spp
Lactobacillus spp
Propionibacterium spp
Marine Vibrios
Vibrio vulnificus
Vibrio parahemolyticus
Vibrio Damsela
Vibrio algynolyticus
Fungi
Candida spp
Aspergillus spp
Rhizopus
streptococcal toxic shock syndrome (SST) characterised
by hypotension and multiorgan failure. Streptoccocus
seems to be responsible for fulminating presentations.
Pathogenesis of these infections has been well studied
and virulent factors identified. These include factors that
mediate attachment to host cells like protein F, lipotechoic acid and M protein.
Group A Streptococcus (GAS) also produces a
number of extracellular exotoxins that contribute to
virulence, including streptokinase, streptolysin O and S,
hyalouronidase, DNAses A, B, C and D. In addition,
certain types of GAS produce streptococcal pyrogenic
exotoxin B. This toxin is responsible for the fever and
play an important role in septic shock genesis by stimulating the production of TNF, Interleukin 1 and 6 by
mononuclear cells.
Toxins are not the only factors implicated in the
pathogenesis of streptococcal septic shock, because
Streptococcus also expresses an important number of
superantigens. Superantigens are molecules that bind
simultaneously to a class 2 MHC molecules and to the
receptor of T lymphocytes. This liaison activates a polyclonal population of T helper lymphocytes, producing an
enormous amount of cytokins that mediates systemic
toxicity. As in staphylococcal toxic shock syndrome,
streptococcal SST appears to be a superantigen mediated process (in contrast with staphyloccocus, it has been
difficult to assign an essential role to any single antigen
in the pathogenesis of the streptococcal SST).
Etiology and risk factors
existing lesions. It occurs in patients with immunodefiency or neutropenia. The diagnosis is sometimes difficult because of minor cutaneous lesions, whereas pain
and systemic toxicity signs are often important.
Enterobacteraciae (E. coli), clostridium spp and Pseudomonas are usually present.
A separate class of NF is reserved for clostridium gas
gangrene with or without myonecrosis. It is
charecterised by the production of gas in fascias and
muscles. The superficial type is associated with a blunt
trauma or a surgical intervention. The deeper type with
myonecrosis, is found after non-penetrating trauma with
crushing or intramuscular injection. As type 1-like NF, it
sometimes occurs spontaneously by hematogenous
spread of clotridium bacteria, typically in patients with
digestif neoplasia (usually C. Septicum is involved) (10).
Type 2
Type 2 necrotizing fasciitis is a monomicrobial infection
by Group A streptococcus. Necrotizing fasciitis of the
extremities and limbs is usually type 2 (11). These
lesions can be complicated by septic shock known as
Necrotizing fasciitis is caused by the spread of
pathogens in the subcutaneous tissue. Reported etiologies of soft-tissue injury leading to necrotizing fascitiis
include blunt or penetrating trauma, direct inoculation of
the subcutaneous tissue from a superficial site and
hematogenous spread from a distant site.
Occuring in any region of the body, NF most
commonly involves the abdominal wall, extremities and
perineum (Fournier gangrene). Table III lists the most
common localisations and etiologies of necrotizing
fasciitis.
Fasciitis of the face and neck is type 1 or 2 in adults,
usually following ORL or dental infection (Haemophilus influenza is also found in children). In this location,
the infection easily spreads via fascial planes into deep
cervical spaces or vascular compartments. Many complications of cervical fasciitis have been described,
including airway obstruction, jugular venous thrombosis, mediastinitis, rupture of great vessels, empyema and
lung abscess (12-14).
With a susceptibility to cutaneous infections, diabetics
are at high risk to develop NF. In the lower limbs, development of NF is enhanced by vascular and lymphatic
Necrotizing Fasciitis
33
Table III
Etiologic aspects of necrotizing fasciitis
Limbs and extremities
Abdominal
Genital and perineal
Face and neck
Trauma (blunt or penetrating)
Bite (animal or insects)
Drugs
Subcutaneous injection (insuline e.g)
Cutaneous infection (folliculitiis,
abcess or ulcers e.g)
Appendicitis
Colocutaneous fistula
Perforated viscus
Diverticulitis
Renal calculus
Bartholinitis
Vulvar abscess
Hysterectomy
Episiotomy
Caesarean
Salpingectomy
Coital injury
Prostatic surgery
Genitourinary infection
Pilonidal abscess
Hemorrhoidal banding
Rectal carcinoma
Cervical adenitis
Otologic infections
Peritonsillar abscess
Dental abscess
Salivary gland infection
stasis. Patients with peripheral vascular disease present a
risk of NF development. Type 1 fasciitis commonly
occurs in patients with immunosupression, as in AIDS
or after corticoid therapy, or in other situations weakening host reactions to infection ( alcohol abuse, neoplasia,
recent surgery, cardiac and pulmonary diseases, malnutrition, smoking,...). In children, varicella seems to be a
significant factor. Concurrent use of nonsteroidal antiinflammatory (NSAIDs) drugs has been incriminated,
but available prospective and retrospective studies do
not support a causal relationship (15, 16). NAIDs can
mask pain and symptoms of NF, and delay diagnosis.
The stereotypical course of NF involves a normal or
slighty inflammed soft-tissue area that suddenly progresses to overt fasciitis, accompanied by systemic
toxicity.
At this state, the local signs most commonly associated with NF are (7) :
– a rapidly progressive oedema, overstepping widely
the inflammatory area.
– bullae filled with serous fluid becoming hemorragic
or purulent, sometimes malodorous.
– blue-grey cyanotic lesions (associated with thrombosis of cutaneous perforating vessels) and pale
ischaemic areas.
– an erythema without distinct borders (in contrast to
erysipelas)
As infection extends, the overlying skin becomes
smooth, shiny and tensely swollen. Within one or two
days, lesions colour progressively changes, from red to
purple to blue and then becomes frankly gangrenous by
the fourth or fifth day, turning black. In clostridium
infection, crepitances suggest production of gas. The
infection progresses to nerve necrosis with hypoesthesic
or anaesthesic skin areas.
NF is rarely diagnosed before this stage. A series of
89 patients with NF reported a correct initial diagnosis
of NF on first presentation in only 15% of cases, with
cellulitis (59%) and abcess (18%) as the most common
misdiagnosis (17).
Signs and symptoms of systemic toxicity are capital
to orientate to diagnosis. High fever, tachycardia
(> 90/min) and tachypnea (> 20/min) are early findings.
As infection progresses, severe septic syndrome develops, with arterial pressure drop (under 90 mmHg or
diminution of 40 mmHg under the habitual pressure).
Oliguria (< 30 ml/h) and elevation of creatinine reflect
renal impairment. Pulmonary, neurologic, haematologic
and hepatic complications may be associated to initial
features, followed by severe septic shock with resistant
systemic hypotension and hypoperfusion in absence of
adequate care.
Clinical features
The early diagnosis is the major challenge in NF, due to
the paucity of cutaneous findings in the early course of
the disease. At the beginning, patients usually present
with aspecific symptoms including pain, swelling and
fever. Tenderness, erythema and warm skin are commonly the only signs of NF in its early stage.
Later, diagnosis of a necrotizing infection is based on
the association of local and systemic signs and symptoms : an exquisite pain, completely disproportionate
compaired to clinical findings, as key symptom.
The intensity of local signs can be weakened by previous antibiotherapy or in immunosuppressed patients.
Diagnosis
With an high index of suspicion (crepitus at physical
examination), a clinical diagnosis of NF can be made,
prompting early surgical exploration to confirm diagnosis (lack of resistance to dissection of normally adherent
fascia) but without soft-tissue gas. NF remains a diagnosic challenge, requiring laboratory, microbiology and
radiologic investigations.
Routine laboratory, including white blood cell count
and C-reactive protein level, may distinguish NF from
non-necrotic soft tissue infection. CPK concentration is
also useful as marker of muscular necrosis. WONG et al.
34
have recently developed a Laboratory Risk Indicator for
necrotizing fasciitis (LRINEC). A score was assigned
from a combination of values for C-reactive protein,
white blood cell count, hemoglobin, serum sodium and
glucose (18), parameters with an early change in the
infection. A low score (< 6) was associated with a less
than 50% probability of having NF, and a high score
(> or equal to eight) with a greater than 75% probability
of NF. This model has not been prospectively analysed.
Hemoculture and aspirates of cutaneous lesions or
bullae with a thin needle are often sterile, due to a prior
antibiotherapy. Peroperatorive culture with antibiogram
leads to bacterial species identification and to adequate
antibiotic treatment. Biopsy is also helpful as an alternative diagnostic method.
Radiologic studies are also contributive but should
never delay appropriate surgical treatment of highly suspicious cases. Radiographies are more sensitive to detect
gas than physical examination (19). Unfortunately, the
production of gas is highly variable and tend to appear
late in the course of NF. Presence of gas excludes a type
2 fasciitis.
CT scanning is more accurate in detecting gas tracking along fascial planes than plain radiographies (20).
CT scan identifies subcuteaneous and fascial thickening,
foreign bodies and focal fluid collection (abscess). It
also delineates the spread of infection, especially in cervical fasciitis. However, oedema of soft-tissue can lead
to overestimation of lesions. Finally, CT scan sometimes
does not adequately differentiate between severe cellulitis and NF, and cases of NF with negative CT findings
have been reported (21).
Magnetic resonance imaging has the highest sensitivity (93-100%) for diagnosing NF. NF exhibits high signal intensity on T2-weighted images by MRI with
hyperintense signal corresponding to fluids associated
with NF. Using MRI, RAHMOUNI et al. were able to separate necrotizing soft-tissue infections which warrant
immediate surgical intervention from non-necrotizing
cellulitis, which can be treated medically (22). However,
hyperintense signal can be seen in other diseases with
fascial edema without necrosis as cellulitis, abscess,
lymphatic obstruction, rheumatic disease, recent surgery
or passive oedema (congestive heart failure, cirrhosis).
In Fournier gangrene, scrotum ultrasonography has
been used to reveal skin thickening and swelling, with
subcutaneous, hyperechoic foci representating gas (23).
The role of ultrasonography in the evaluation of NF in
other areas of the body is less evident.
Treatment
Treatment modalities include aggressive surgical debridment, broad-spectrum antibiotics, haemodynamic support and general cardiorespiratory supportive care to
L. Smeets et al.
maintain vital organ functions. Hyperbaric oxygen and
immunoglobulins do not have firm evidence supporting
their use. WONG et al. (17) analysed factors correlated
to adverse outcome. Three factors were found to affect
survival : advanced age, presence or two or more
associated comorbidities, and delay from admission to
operation of more than 24 h.
Surgery
The first choice treatment of NF remains surgery including early debridment of all necrotic tissues and drainage
of involved fascia planes via extensive fasciotomy.
Prompt surgery has been associated with improved survival, compared to delayed intervention (5, 24). Surgery
should be performed within 24 h of presentation as the
mortality rate significantly increases beyond this period (17). Wide resection of all devitalized tissues is the
key of adequate surgery. Limited resection or drainage
are inappropriate. Re-exploration and further debridements are often required to achieve control of the necrotizing process. Repetitive interventions are the rule and
survival has been documented after excision of as much
as 45% of a patient’s surface area (25). Surgical wounds
must be frequently reevaluated for evidence of disease
extension. In perineal NF, diverting colostomy and/or
urinary diversion are often needed to control infection.
Amputation of extremities is sometimes necessary,
particularly in patients with diabetes and/or peripheral
vascular disease. Reconstructive procedures, including
skin grafting, flap or free flap are often required.
Antibiotics
Parenteral antimicrobial therapy must assure broad coverage for a wide range of pathogens including aerobic
gram-positive, gram-negative organisms and anaerobes.
However, there are no guidelines for specific initial
antibiotic therapy. Despite appropriate and early antibiotic use, infection may progress because of thrombosis
of superficial vessels precluding effective antibiotic penetration. In this case, the main goal of antibiotherapy is
infection control, avoiding hematogenous dissemination, while waiting surgical intervention.
A beta-lactam/beta-lactamase combinaison such as
ampicillin/sulbactam, piperacillin/tazobactam or ticarcillin/clavulinate are reasonable empiric choices despite
increasing resistance of enteric pathogens. For penicillinallergic patients, clindamycin and aztreonam association
is an acceptable alternative. Third or fourth-generation
cephalosporins with metronidazole or clindamycin for
anaerobe coverage are also recommended. Antimicrobial
therapy should be tailored to culture and susceptibility
results. Extended coverage with vancomycin has to be
added for nosocomial infections (Pseudomonas spp,
highly resistant gram-postive bacteria) or surgical wound
contamination.
Necrotizing Fasciitis
For type 2 fasciitis, high-dose penicillin remains the
best option. Animal and human studies suggest beneficial effects of adding clindamycin in type 2 NF because
clindamycin may suppress production of exotoxins
and/or virulence factors and enhance phagocytosis by
inhibiting M-protein synthesis (26). Retrospective data
suggest a benefit of clindamycin in invasive group A
streptococci disease. In Clostridium fasciitis, penicillin/clindamycin is also the treatment of choice.
Supportive care
35
mortality (30-33). Several mechanisms of actions are
proposed, including direct opsonization, antagonization
of bacterial superantigens and modulation of immune
cytokine responses through unidentified pathways. This
treatment remains expensive and without consensus
on the optimal dose. Risks associated to their use are
renal failure and anaphylaxis (in patients with IgA
deficiency).
Conclusion
After initial debridement, the cooperation of intensivists,
surgeons and infectious disease specialists is crucial for
optimal care. Patients require early intensive care for
metabolic and haemodynamic support. Adequate nutritional support improves survival (4, 27). As in burn victims, patients may loss fluids, proteins and electrolytes
from a large surgical wound. Fluid and electrolyte resuscitation and analgesia are the mainstays of support for
patients with advanced sepsis usually combined with
vasoactive amines associated with mechanic ventilation.
With persistant inflammation and intravascular coagulation, patients are at high risk of thrombosis. As
thrombo-embolic complications are the second cause of
mortality (7), appropriate anticoagulation therapy is
needed. Equilibration of diabetes, correction of metabolic acidosis and renal failure are also an important part of
management.
Despite antibiotic therapy and surgical intervention, the
mortality and morbidity of NF remain high. Only early
identification of the necrotizing process can improve the
outcome of this life-threatening disease. NF should be
suspected in every skin infection with fever, signs of
systemic toxicity and severe pain. An adequate use of
radiologic procedures should not delay surgical debridement. Future diagnostic clues, including transcutaneous
oxymetry, might advance our ability to provide prompt
therapy. New potential treatments for group A streptococci NF could be vaccines, new antibiotics and superantigen directed therapies such as neutralization and
inhibition of production of super-antigens by streptococci.
Adjuvant therapy
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Use of hyperbaric oxygen (HBO) is based on animal
studies, case reports, and retrospective studies (28). The
physiologic effects of HBO have been shown to include
increased killing ability of leukocytes, reduction of
oedema, promotion of angiogenesis and wound healing.
Direct effects on anaerobes are caused by elevation of
oxydoreduction potential producing NADPH and
NADH consumption, and production of free radicals
enhancing bacterial death.
Retrospective analyses suggest benefits both in
mortality and in morbidity for HBO in the setting of NF
but these results have not been prospectively validated.
However, HBO use in anaerobic infection such as
clostridial gangrene is supported by experimental data
and should be instituted before surgical intervention
(29). In NF, if HBO therapy is available, it should be
considered as additional treatment but should never
preclude nor postpone early surgical debridement.
Free radical production is a physiologic complication
of HBO with pulmonary oxygen toxicity (edema and
sometimes evolution to fibrosis) and reversible myopia
(up to 20%). Barotrauma complications (pneumothorax,
otobarotrauma, tympanic rupture, etc) are exceptional.
Perfusion of immunoglobulins is another adjunctive
treatment in streptococcal NF which could reduce
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L. Smeets
Department of Plastic and Reconstructive Surgery
CHU Liège