I. Gonzáles Alaňa; Marín De La Cruz D.; R. Palao Doménech; Barret Nerín J. P.
Department of Plastic and Reconstructive Surgery and Burns Unit, Hospital Universitario Vall d’Hebrón, Barcelona, Spain
Vyšlo v časopise:
ACTA CHIRURGIAE PLASTICAE, 49, 4, 2007, pp. 99-102
fasciitis is a progressive soft tissue infection which causes extensive
necrosis of the skin, frequently associated with septic shock (10). In two
thirds of cases it involves entry into the organism of a large variety of
microbes (defined as type I) (1, 6, 10), or one single isolated microbe, Streptococcus
pyogenes (necrotizing fasciitis type II), mainly through surgical wounds,
minor trauma, trivial wounds, ulcers and even intact skin, especially in the
lower limbs (5), but it can also present in healthy patients (3, 7).
signs and symptoms are insidious, virtually unnoticeable or non-specific in the
first 48 hours. Next, rapidly spreading necrosis of the skin develops, added to
intense pain (5, 6) and toxic syndrome.
is a combined antibiotic therapy, complete debridement of the necrotic tissue
and maintaining of haemodynamic status (3, 6, 10, 11).
despite the intensive treatment and aggressive surgery, mortality rates are
high (between 20% and 70%, depending on the series consulted) (5, 10).
reports have been found in the literature of cases of necrotizing fasciitis
following cosmetic surgery interventions, with liposuction standing out among
them (2, 4, 5, 10). Healthcare professionals must familiarise themselves with
the clinical signs and symptoms (7), since only early diagnosis and aggressive
treatment reduce the high mortality rates (5, 9).
We report of a
29-year-old female patient, with no known drug allergies or relevant medical
history, undergoing cosmetic liposuction of the torso and lower limbs at a
Centre for Cosmetic Surgery.
later, during changing of dressings, she developed hypotension, oliguria and
tachypnoea, which led to transfer to the Accident and Emergency Department of
the nearest hospital. Analysis on admission showed: creatinine 2.4 mg/dl;
leukocytes 1800.103/l; haemoglobin 6.7 g/dl; and Quick 60%.
Haematoma of abdominal wall with multiple bleeding liposuction cannula orifices
presented. CT scan revealed signs of abdominal cellulitis.
patient was admitted to Intensive Care Unit due to multiple organ failure,
requiring multiple blood transfusions, vasoactive drugs, orotracheal intubation
and mechanical ventilation. The liposuction cannula orifices began to suppurate
and Streptococcus pyogenes was cultured, sensitive to Penicillin, only
three days after the liposuction. The patient was referred to Dermatology,
where skin lesions as purpura fulminans with widespread skin necrosis (25% of
total body surface) were diagnosed, affecting anterior and posterior torso,
thighs and left arm. Due to the progression of the sepsis and the skin
necrosis, extensive debridement was carried out by General Surgery. Thirteen
days after the liposuction, Pseudomonas aeruginosa and E. coli
were isolated in the exudate from the wounds, and Candida albicans and Candida
glabrata in the urine culture and tracheal aspirate. Treatment was then
started with Piperacilin-tazobactam and caspofungin and local treatment with
normal saline and chlorhexidine.
consulting the Intensive Care Unit and Department of Plastic, Reconstructive
and Cosmetic Surgery at the Hospital Universitario Vall d’Hebron, it was
decided to transfer the patient there due to the progression of the sepsis and
the extension of the lesions. Diagnosis included septic shock, secondary to
soft tissue sepsis due to Streptococcus pyogenes, haemodynamic, renal
and respiratory failure, disseminated intravascular coagulation, pancytopenia
and purpura fulminans with extensive skin necrosis. On admission to the ICU in
our Centre, 29 days after the liposuction and 27 days after initial admission
to hospital, the wound care was changed to acetic acid every six hours and
later, silver sulphadiazine twelve-hourly, while cultures were sent which grew Acinetobacter
baumannii in wound exudates and tracheal aspirate.
ten days in the ICU and given the good progress in her general condition, the
patient was moved to the Burns Unit due to the extension of body surface
exposed. Patient was then taken to surgery on three occasions, the first two
for debridement of the granulation tissue and coverage with 1:3 skin grafts
taken from the patient’s lower limbs. At the third intervention, excision of
the dermo-epidermal separation in the dorsal area was performed with grafting of
the bloody area. The only complications presented by the patient during her
stay in the Burns Unit were a urinary infection and phlebitis, which responded
to making good progress, patient was discharged 84 days after the liposuction and after
spending 82 days in hospital. She is currently being followed up in our
Centre’s Plastic Surgery Outpatient Department. (Fig. 1–6.)
is a progressive soft tissue infection which causes extensive necrosis of the
skin, frequently associated with septic shock (10). In two thirds of cases it
involves entry into the organism of a large variety of microbes (defined as
type I (1, 6, 10), or one single isolated microbe, Streptococcus pyogenes
(necrotizing fasciitis type II), mainly through surgical wounds, minor trauma,
trivial wounds, ulcers and even intact skin, especially in the lower limbs (5).
Streptococcus pyogenes, a catalase-negative, gram positive coccus
which occurs in chains, is a betahaemolytic-type facultative anaerobe of group
A, the pathogen group for humans (3). There are two serotypes, oropharyngeal
and cutaneous, and the sites do not interchange (3). 10% of the healthy population are
oropharyngeal carriers and 0.5–1% skin carriers, eradication not being
indicated in the absence of symptoms (3). Streptococcus pyogenes causes
secondary infections in humans (eczema, infestations, ulcers), vascular lesions
caused by circulating erythrotoxin (scarlatina), skin lesions attributed to
allergic hypersensitivity to the streptococcal antigens (erythema nodosum and
vasculitis), skin lesions apparently caused or influenced by streptococcal
infections (psoriasis, especially guttate forms) and direct infections of the
skin and subcutaneous tissue (impetigo, ecthyma, erysipelas, cellulitis or
necrotizing fasciitis) (3).
type II necrotizing fasciitis is an infection of the skin, subcutaneous tissue
and fascia, frequently associated with septic shock and multiple organ failure
and caused by Streptococcus pyogenes, the incidence of which has
increased since the 1990s (10). If it affects the underlying muscle, it is
called synergistic necrotizing cellulitis. Predisposing factors are thought to
be immunodeficiency (the very old and the very young, alcoholism, severe chronic
illness and carcinoma), peripheral vascular disease and lymphoedema, but it can
also present in healthy patients (3, 7).
mechanisms behind this disease are pressure on the tissues, vascular thrombosis
and bacterial toxins, which lead to necrosis of the skin and multiple organ
The signs and symptoms
are insidious, virtually unnoticeable or non-specific in the first 48 hours:
fever, myalgia, nausea, diarrhoea, erythema (a reddish colouring of the skin
with no clear margin, hot and painful when pressed); however intolerable pain
may be the only symptom during the initial hours (6). Generally by days 3 and 4
an extensive area of induration will appear, blisters and, at times, dark
colouring in the centre, which is a sign of poor prognosis (10). Next, rapidly
spreading necrosis of the skin develops, added to intense pain (2, 5), finally
ending up with numbness due to destruction of nerve endings, metastatic
infections and toxic syndrome, with tachycardia, respiratory distress or shock
lung, oliguria, confusion, acidosis, raised CK and falls in platelet count,
albumin, calcium, iron and clotting factors, leading to disseminated
intravascular coagulation (1, 3, 11).
Diagnosis is made by
bacteriological examination of the exudate and cultures, serological analysis
of anti-Dnase and anti-hyaluronidase (ASLO is weak and of no use for diagnosing
this disease (3)) and surgical exploration, by demonstrating that a blunt
instrument can easily be passed along the planes of the necrotic tissues (3).
However, clinical diagnosis (the identification of the skin lesions and the
changes in the patient’s general condition) is the most important element,
since it is made earlier.
Treatment is a combined
antibiotic therapy (clindamycin + penicillin G benzathine), complete
debridement of the necrotic tissue and maintaining of haemodynamic status (3,
7, 10, 11). Immunoglobulin therapy is experimental and the use of hyperbaric
oxygen has not been proven.
the intensive treatment and aggressive surgery, mortality rates are high
(between 20% and 70%, depending on the series consulted (5, 10), especially if
debridement is delayed, there are serious analytical signs, such as leukocytes
above 30,000 and creatinine over 2, or the patient has underlying heart
is a rare and aggressive condition, which can occur after surgical
interventions, including cosmetic surgery. Severe infections have been reported
following cosmetic surgery interventions, such as excisions, biopsies, grafts,
peelings, skin abrasions, resurfacing, liposuctions, blepharoplasties and
infiltrations (7). Various reports have been found in the literature of cases
of necrotizing fasciitis following cosmetic surgery interventions, with liposuction
standing out among them (2, 4, 5, 10). This is considered to be a safe
intervention (7) and has become increasingly more popular (10). Patients should
be suitably informed of the possible complications, including this serious
infection (4, 7). Likewise, in order for it to be identified rapidly,
healthcare professionals must familiarise themselves with the clinical signs
and symptoms (7), since only early diagnosis and aggressive treatment reduce
the high mortality rates (5, 9). Having said that, prevention is the
determining factor (8) since the survivors still suffer serious cosmetic
sequelae (2, 14, 10), complications all of which are unacceptable after an
elective cosmetic surgical procedure.
Adriano VI 2, 4° D
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11. Umeda T., Ohara H., Hayashi O. et al. Toxic shock syndrome after suction lipectomy. Plast. Reconstr. Surg., 106, 2000, p. 204–207, discussion p. 208–209.
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