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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_994_Библиотеки_им_академика_М_И_Перельмана
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104
Fig. 7.2 Patient with fat
necrosis 10 days after
injection of fat in the hips.
Drainage to solve the
problem
L. Cardenas-Camarena
treatment scheme. Drainage of the collected material will signicantly improve the
symptoms and the evolution of the clinical picture, since the permanence of necrotic
and infected material without drainage conditions a signicant worsening of the
clinical picture. This evolution without adequate management can lead to a generalized infection of the operated area and/or sepsis in the patient. That is why when we
do buttocks fat inltration, it is necessary to evaluate the patient during the rst
10days after the surgery in order to identify any eventuality with these characteristics. In our evolution of more than 25years of buttocks fat inltration, we have
almost completely eliminated this eventuality by distributing the inltrated fat more
widely [12]. Initially, by inltrating fat in the upper portion of the buttock and trying
to give greater projections in this region, our incidence of fat necrosis was higher
than now. Upon noticing this eventuality, we begin to inltrate fat enlarging the area
of inltration, which practically eliminates the fat necrosis after its injection in the
buttocks. With this process we achieve, in addition to completely eradicating fat
necrosis, also inltrate greater volumes and give better esthetic contour. Therefore,
to prevent this complication, in addition to having an excellent aseptic technique,
we must ensure proper irrigation of the inltrated fat, for which our main recommendation is to inltrate it in different subcutaneous tunnels, and properly distributed throughout the width of the buttocks region when we want to inject large
volumes.
7.3.2 Infection
An infection following buttocks fat inltration can be classied into two groups:
infections due to common microorganisms, or infections due to opportunistic
microorganisms. The usual microorganisms are usually Gram-positive or Gramnegative bacteria. The behavior is very similar to that referred to in the previous
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105
section on fat necrosis, so the clinical picture, evolution, prognosis, and treatment
will be similar to that already mentioned (Figs.7.3 and 7.4). It is important to identify the causal agent and the sensitivity by means of an antibiogram in order to carry
out an adequate and opportune management. However, infections by opportunistic
microorganisms have a relevant importance in gluteal contouring surgery secondary
to fat inltration. The main opportunistic microorganisms involved in this condition
are atypical mycobacteria, of which there are multiple types. These mycobacteria
are widely distributed in nature so that their presence in patients subjected to fat
inltration correlates with immunosuppression secondary to the surgical procedure
and to this very broad habitat in the environment. Liquids for sterilization and water
used in operating rooms, but above all, the tissue that remains trapped in the cannulas used for fat inltration have been identied as a contaminating medium, since
mycobacteria are highly resistant to sterilization processes. Mycobacteria of the
Fortuitum, Chelonae, and Abscessus type are the most commonly found in these
infectious processes. The clinical picture is very characteristic, presenting itself
after an apparently normal postsurgical evolution after a highly variable incubation
period of about several weeks. It begins with subcutaneous nodules evolving into
cellulite, painful abscesses, and spontaneous discharge of purulent material, all of
which leads to the appearance of multiple skin ulcers [13–14] (Fig.7.5). Due to the
high resistance to most antibiotics, it is necessary to carry out the identication of
the Mycobacteria and to establish its sensitivity [13–14]. A skin biopsy and the
culture of the secretion or tissue may be useful, but it is the polymerase chain
Figs. 7.3–7.4 Patient with habitual microorganism infection. Abscess drainage within a few
weeks after surgery. (Courtesy of Dr. Victor Manuel Corona Medina)
106
Fig. 7.5 Patient 5months
after surgery, with
Mycobacterium fortuitum
infection. After having
been treated with antibiotic
therapy for 3months
L. Cardenas-Camarena
reaction the most important specic test to identify the causal agent and to determine the management. Knowledge of the causal agent is one of the three parameters
for establishing the type of treatment, the other two being the patient’s immune
status and the affected body organ. Management of a Mycobacterial infection
should be both medical and surgical. Traditional antibiotics for mycobacteria are
ineffective, as are single-antibiotic treatments [13–14], so a combination of antimicrobials and a prolonged treatment over several months is required. Macrolides such
as Clarithromycin and Rifamycin derivatives such as Rifabutin are very useful medicines. Older drugs for mycobacteria such as ethambutol, rifampicin, isoniazid, and
streptomycin are generally ineffective. This is why it is important to establish sensitivity with specic tests and always be assisted by a specialist in infectious management. Surgical treatment should be carried out after the infection has been controlled,
and each case will be managed according to the needs and alterations that the infectious picture has produced. On many occasions, it will be necessary to establish a
very thorough reconstructive treatment to adequately correct the esthetic alterations
produced by the infection (Figs.7.6 and 7.7).
Being a condition that leaves important esthetic sequels as it advances in its evolution, it is of paramount importance a timely treatment and adequate prevention. It
is vital to always be careful with the material used in surgery, both in its cleaning
and in the sterilization process. Maximum care must be taken with the liquids that
are used in the different surgical processes. It is necessary to know the picture that
appears in a Mycobacterial infection, which starts several weeks after surgery with
completely normal postsurgical evolution. Knowing this, we can suspect this pathology, identify it quickly, and start pharmacological management as soon as possible.
7 Safety inGluteal Fat Inltration
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Figs. 7.6–7.7 Surgical
treatment with negative
pressure wound therapy
and direct closure after
wound cleaning
107
108
L. Cardenas-Camarena
7.3.3 Injury oftheSciatic Nerve
Although it is a rare pathology, its presence can cause important alterations and
even disabling sequels for life. Injury to the sciatic nerve is produced by injecting
directly into the nerve or in the periphery of the nerve producing axonotmesis [15].
This injury often requires surgical treatment to try and correct the problem; however, if the injury is severe, full recovery is long and difcult [15]. The sciatic nerve
is located within the deep musculature of the gluteal region, under the muscle group
of the gluteus maximus, medium, and minor, at the level of the pyriform muscle, so
its direct injury is produced when performing a fat injection in very deep planes of
the gluteal region. To avoid damaging the sciatic nerve it is imperative to avoid
going deep into the buttock when injecting the fat, which is a mistake in the surgical
technique (Figs.7.8–7.11, 7.12, 7.13–7.14, and 7.15–7.16).
Figs. 7.8–7.11 Patient with right foot mobility problems after gluteal fat lipoinjection (Courtesy
of Dr. Alexander Cárdenas-Mejia)
7 Safety inGluteal Fat Inltration
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Fig. 7.12 Approach to
explore and repair the
sciatic nerve (Courtesy of
Dr. Alexander
Cárdenas-Mejia)
109
Figs. 7.13–7.14 Fat material inside the piriformis space, adjacent to the sciatic nerve (Courtesy of
Dr. Alexander Cárdenas-Mejia)
Figs. 7.15–7.16 Fat injected into sciatic nerve. Release of affected structures (Courtesy of Dr.
Alexander Cárdenas-Mejia)
110
L. Cardenas-Camarena
7.4 Microscopic andMacroscopic Fat Embolism (MIFE
andMAFE)
Undoubtedly, the pathologies caused by the entry of fat into the bloodstream are the
most serious and dangerous eventualities that can occur when injecting fat into the
gluteal region. These pathologies have been described very broadly in recent years
and are closely related eventualities. And although the causal agent is the entry of
fat into the bloodstream, the entire clinical picture, pathophysiology, evolution,
prognosis, and treatment are totally different. The entry of fat into the bloodstream
secondary to buttocks fat inltration can occur in microscopic or macroscopic form
hence the nomenclature of both diseases (MIFE and MAFE) [16–17]. The presence
of micro-fatty emboli in the circulation activates serum lipase, which when acting
on the fatty emboli will produce free fatty acids in the circulation, which are quite
irritating and trigger a generalized systemic inammatory reaction [16]. This is the
biochemical theory that explains the appearance of the Fat Embolism Syndrome
after the entrance of fat to the circulatory torrent in diverse traumatic pathologies,
mainly in fractures of long bones. The appearance of the clinical picture is usually
2–3days after the traumatic event, which in plastic surgery the traumatic process
would be secondary to the inltration of fat into the buttocks. Signs and symptoms
are secondary to the involvement of microcirculation at three main levels of the
human body: central nervous system, respiratory system, and skin level. This causes
a series of manifestations that have been described for many years by various
authors and that have helped to establish a syndromic diagnosis of this pathology [18].
The reason why a fat embolism syndrome develops in some patients and not in
others, despite having microparticles of fat in the bloodstream, is still under study.
However, the concentration of fat in the blood may be a trigger. In our experience of
more than 2000 cases of liposuction with lipoinjection, we have had only two cases
of fat embolism syndrome. These two cases were during our rst 9years as plastic
surgeon [3, 12]. In both cases, our fat injection was on an intramuscular plane and
in both cases there was severe postsurgical dehydration. Taking into account the
theory that the concentration of fatty acids in the bloodstream can be a trigger, we
started to inltrate fat in very supercial muscular planes and to have a strict control
of the patient’s hydration. In the following 20years, starting in 2009, we have not
had a single case of fatty embolism syndrome, despite the fact that we inltrate
greater amounts of fat into the buttocks and maintain the same amounts of liposuction volumes. We believe that not having had a single case of fatty embolism syndrome during this time is secondary to two factors that we changed in our surgical
technique. The rst thing is to have our patient hospitalized for 12h after the surgery when we do liposuctions greater than 500 cc, this is to maintain adequate
hydration preventing the patient from becoming dehydrated. Adequate hydration
allows for a lower concentration of free fatty acids in the bloodstream and also
favors their elimination at the renal level. And the second is to decrease the lipoinjection of fat in areas where the risk of fat particles entering the bloodstream is
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111
greater, as it would be in muscle. After the appearance of our two fat embolism
syndromes, the intramuscular fat injection reduced it signicantly, and after the
appearance of the worldwide cases of fat macro embolism, the intramuscular injection was eliminated completely. It is clear that when fat is injected into the muscle,
which is a highly vascularized area, the risk of a high volume of fat entering the
bloodstream is greater than if it is only injected subcutaneously where the vascularity is lower. If fat embolism syndrome is present, treatment should include hemodynamic and respiratory support, preferably in an intensive care unit, to help the
inammatory process subside and the patient becomes stable. With these measures,
and timely management of the problem, mortality can be less than 10%.
Currently, the most feared and serious complication secondary to fat inltration
in the buttocks is macroscopic fat embolism (MAFE). This pathology is secondary
to the entrance of fat in macroscopic form into the bloodstream [19], (Figs.7.17 and
7.18) which produces an accumulation of fat in the form of macro emboli, reaching
the heart through the venous line, producing a mechanical obstruction of the cardiorespiratory system with collapse of the heart. It is a clinical picture similar to massive thromboembolism, with many of the implications that this pathology carries
[19–20]. Macroscopic fat embolism is secondary to the rupture of the venous vessels in the deep gluteal region [19] (Fig.7.19). These venous vessels are located,
like the sciatic nerve, under the musculature of the gluteus maximus, medius, and
minor, adjacent to the pyramidal muscle. The upper gluteal vein emerges in the
Fig. 7.17 Macroscopic fat
inside inferior vena cava.
(Published in CárdenasCamarena L, Bayter JE,
Aguirre-Serrano H,
Cuenca-Pardo J.Deaths
Caused by Gluteal
Lipoinjection: What Are
We Doing Wrong? Plast
Reconstr Surg 2015)
Fig. 7.18 Macroscopic fat
in the right atrium
(Published in CárdenasCamarena L, Bayter JE,
Aguirre-Serrano H,
Cuenca-Pardo J.Deaths
Caused by Gluteal
Lipoinjection: What Are
We Doing Wrong? Plast
Reconstr Surg 2015)
112
Fig. 7.19 Gluteal vein
injury with fat entering the
bloodstream. (Published in
Cárdenas-Camarena L,
Bayter JE, Aguirre-Serrano
H, Cuenca-Pardo J.Deaths
Caused by Gluteal
Lipoinjection: What Are
We Doing Wrong? Plast
Reconstr Surg 2015)
L. Cardenas-Camarena
proximal portion of this muscle and the lower gluteal vein emerges in the distal portion accompanying the sciatic nerve. When one of these gluteal vessels ruptures, the
fat is absorbed into the bloodstream via the gluteal vein, the internal iliac vein, and
the vena cava, reaching the cardiac cavities and producing the clinical picture. It is
not necessary to go into the gluteal vein for the fat to enter the bloodstream, a rupture of the vein is more than enough since the fat is absorbed by the negative pressure exerted by the venous system at that level. The rupture is generally due to direct
injury produced by the cannula when it is inltrating; however, there is a theory that
it can also rupture due to an increase in the tension existing in the periphery of the
gluteal vessels [21]. This theory mentions that because the gluteal veins have very
little elongation capacity, as tension increases due to the injected fat, the veins can
tear and allow the fat to enter the bloodstream. Undoubtedly, there are many factors
that can cause a gluteal vessel to be injured, such as the pressure at the time of inltration, the characteristics of the cannula tip, the thickness of the cannula, the route
of approach to inltrate, movements while inltrating, and the amount of fat inltrated. However, the most important single factor that determines whether a vessel
can be injured, and a macro embolism occurs is where the fat is injected. If it is not
injected into the intramuscular plane the risk of this pathology is practically nil.
Therefore, at present, the injection of fat into the muscle should be totally outlawed.
Currently, there is also a theory that it is not necessary to inject in deep intramuscular planes to produce rupture or tearing of the gluteal vessels, and when large volumes are injected in supercial intramuscular planes, the fat is displaced to the
depth of the intramuscular space, increasing tension and producing rupture [21].
That is why we must be especially careful not to produce disruption in the muscle
fascia when injecting in a subcutaneous plane since this fascia acts as a safety barrier avoiding the fat to enter in deeper planes. The clinical picture of the macroscopic fat embolism is very characteristic. Unlike the microscopic fat embolism,
which appears some days after the surgery, the macroscopic fat embolism starts at
the moment of the fat inltration or some minutes later [16, 19–20]. Secondary to
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113
the entry of fat into the bloodstream and its displacement in the form of macro
emboli into the cardiac chambers, the patient presents three pathognomonic data of
the problem: bradycardia, hypotension, and hypoxemia [20]. These signs appear
suddenly and are secondary to the heart not being able to pump blood properly and
the blood not reaching the lung circuit. When blood cannot be pumped out, blood
pressure and heart rate decrease and when blood does not reach the lungs, oxygen
saturation also decreases. That is why in the presence of this characteristic triad we
must immediately think about the pathology and try to solve the problem.
Unfortunately, the appearance of this complication is almost always fatal, so we
must act quickly, performing CPR maneuvers in an aggressive manner. With aggressive resuscitation maneuvers, the fatty embolus in the heart can be dislodged, displacing it towards the rest of the body’s economy and solving the most serious
condition [22]. These maneuvers will condition the fat to pass to other organs, converting a picture of macroscopic fat embolism into one of microscopic fat embolism, which, although also serious, does not have the same high mortality as the rst
one [22]. The clinical characteristics and differences between MIFE and MAFE are
described in Table7.2.
With the evidence found by multiple scientic studies over the past 5years, we
can emphasize that intramuscular fat injection is not an appropriate method to seek
buttock augmentation by fat injection. It is not necessary to inject large quantities
for the problem to occur [19–20], simply that it coexists with injury to the gluteal
vessels is enough. The injection of subcutaneous fat is a very safe procedure so its
application in this plane should be the element of choice when deciding to inject fat
Table 7.2 Clinical characteristics and differences between MIFE and MAFE
Micro fat embolism (MIFE) Macro fat embolism (MAFE)
Causal agent Microscopic fat, usually liquid, which can
form micro emboli
Physio
pathology
Beginning 24 and 72h after surgery Immediately, during surgery
Clinical
presentation
Diagnosis CLINICAL, CT with pleural effusion and
Prognosis Mortality of 10–30%, depends on timely
Treatment Cardiorespiratory and hemodynamic
Prevention – Avoid injecting “liquid fat”
Lipase acts on micro emboli releasing
fatty acids and irritating alveoli and
capillaries (biochemical effect)
Affectation of the microcirculation of the
nervous, pulmonary, and cutaneous
system (criteria of Gurd)
frosted glass image
treatment
support in ICU
– Adequate hydration
– Avoid injecting into vascularized areas
Macroscopic fat that can be
grouped forming macro emboli
Emboli obstructing large vessels
and heart (mechanical effect)
Heart failure, similar to pulmonary
thromboembolism
CLINICAL, suddenly, usually
when the fat is injected
Almost 100% mortality
There is currently no specic
aggressive cardiovascular support
and reanimation
Embolectomy, Rosuvastatin?
– Avoid intramuscular injection
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