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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_511_Библиотеки_им_академика_М_И_Перельмана
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31 Complications ofFat Transfer
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Fig. 31.4 Sequential mammography images of a case with fat grafting
to the breast in a 30 year old woman. Until the rst year calcication was
not present, but at 2 years sand-like macrocalcications were clearly
detected. This indicates that calcications grow progressively at least up
to several years even with no previous noticeable lump. It is suspected
Fig. 31.5 A 34 year old woman presented with multiple oil cysts diagnosed by CT scan. She did not undergo any removal of the cysts. Between
the 3rd and 8th year the size of oil cysts did not change, but calcications
progressed during this period. Many eggshell-like calcications are shown.
(Modied from Mineda K, Kuno S, Kato H, etal. Chronic inammation
and progressive calcication as a result of fat necrosis: the worst outcome
in fat grafting. Plast Reconstr Surg 2014;133:1064–72; with permission)
that small necrotic areas become sand-like calcications, while larger
necrotic areas become oil cysts with eggshell-like calcication. (Adapted
from Mineda K, Kuno S, Kato H, etal. Chronic inammation and pro-
gressive calcication as a result of fat necrosis: the worst outcome in fat
grafting. Plast Reconstr Surg 2014;133:1064–72 [17]; with permission)
spaghetti-like technique; graft in retrograde fashion
micro-droplet; finish with gentle digital molding. The
surgeon should have complete knowledge about the
complex anatomical regions of the face, like the lower
eyelid.
When performing a fat transfer to the body, prefer 10cc
syringes, and a 2.4mm Coleman canula to transfer the fat;
perform retrograde deposits, in a cross manner.
31.9.2 How toManage Irregularities, Lumps,
andBulges?
The treatment of a lump begins with steroid injections into
the area of concern. The next step is direct excision to alleviate the contour deformity. At last, excision through a discrete
incision situated along the inferior orbital rim at the junction
of the thin lower lid skin and the thicker cheek skin may be
the last resort [14].
The management of a bulge starts with injection of
conservative amounts of triamcinolone acetonide in
increasing strengths from 5mg/mL to 40mg/mL repeated
over 1–2months. According to Rabach and colleagues,
direct liposuction of these areas has not been successful
[14].
The oil cysts are a never-ending story. If they are near the
surface, they can drain spontaneously. If deeper, a rst
approach may be to partially cut the cystic wall with a
14–18G needle and squeeze it, leading to its leakage and
phagocytosis of the oil or necrotic tissue. The placement of a
pigtail catheter is also a possible strategy [13]. Another
option is surgical resection [7].
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Fig. 31.6 A case of oil cysts in a 24-year-old woman who underwent
fat grafting for cosmetic breast augmentation 2years previously. She
recognized hardness of the entire breast at 6months and gradually recognized tenderness and abnormal sensations. (Top) She had wellprojected breasts with tight skin. The contour of the upper pole looked
similar to a breast with implant contracture. (Middle) Preoperative
computed tomography (CT) scan showed that there was a single large
calcied oil cyst under each mammary gland. It was suspected that
100–200 mL of fat tissue had been introduced in a bolus injection
before. (Bottom) Removed oil cysts were lled with muddy con- tent
caused by fat necrosis. The oil cyst wall had innermost and outermost
brous layers. (Adapted from Mineda K, Kuno S, Kato H, etal. Chronic
inammation and progressive calcication as a result of fat necrosis:
the worst outcome in fat grafting. Plast Reconstr Surg 2014;133:1064–
72; with permission)
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31.10 Scarring or Entry-Site Divot
At the donor site, the cannula’s entry point should be at concealed zones such as the umbilical fold, suprapubic area, or
inguinal fold; this offers the chance to avoid visible scars in
the case that they become hypertrophic [7]. In addition, local
wound care, detumescence, nerve nutrients, and plasma
early intervention for inhibition of scar hyperplasia and
hyperpigmentation should be performed.
Tethering or divoting at the entry site is a rare occurrence
and usually concerns more the patient at the face, since it is
a more exposed area. It manifests as a dimple at the entry site
during facial animation [14].
31.10.1 How toPrevent Scarring andEntry-
Site Divot?
An entry-site divot can easily be rectied by limited subcision using a Nokor™ needle or a standard needle across the
scar [14]. In addition, local wound care, detumescence, nerve
nutrients, and plasma are early interventions for inhibition of
scar hyperplasia and hyperpigmentation.
31.11 Damage toUnderlying Structures
(Nerves, Vessels, Muscles, Glands,
Organs)
Even a blunt cannula, when inserted for removal and placement of fat, can damage underlying structures such as nerves,
muscles, glands, and blood vessels; however, permanent
injuries are extremely rare [7].
31.11.1 Nerves
So far, over the literature, most of the sensory or motor nerve
injuries along with fat grafting were temporary, due to traction with a blunt cannula; they resolve spontaneously in
about 3months. In the face, any denitive isolated sensory or
motor nerve injury has been related to the use of a sharp
needle or a pointed cannula to release a scar or adhesion.
Sensation loss happens presumably in the supraorbital or
infraorbital nerves. Coleman and Mazzola refer four injuries
of the facial nerve: two transient marginal mandibular injuries (Coleman) and one permanent (Mazzola) and one transient frontal branch injury (Coleman) [1]. The sharp needles
should be used only very supercially to avoid damage to the
nerves and intravascular injection. Care must be taken when
using a suction cannula on the face (even 2.1mm) to remove
tissue along the anterior mandibular border or an oily cystic
it is along the course of the marginal mandibular branch
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Fig. 31.7 Permanent mandibular branch injury after an attempt to
remove an oil cyst on the jawline that resulted from fat grafting to correct facial asymmetry (Coleman S, Mazzola RF. Fat Injection: From
Filling to Regeneration. second ed. NewYork: Thieme Medical; with
permission)
(Fig.31.7). The temporary injury to the frontal branch of the
facial nerve happened after placement of tissue in the temple
and pre- auricular regions and it resolved spontaneously
within 4weeks [1]. The pre-auricular region in the face is a
danger zone, regarding the parotid gland: care must be taken
to avoid perforation of the gland with a canula, which leads
to salivary stulas and parotitis. The same may happen at the
submandibular region [1]. Still, in the facial region, great
attention should be made to avoid damage to the mimic and
masticatory muscles. The same principle is valid when fat
grafting near other muscles in the body, such as the pectoralis major, rectus abdominals, gluteus maximus, and soleus.
If the surgeon considers harvesting the fat from the
abdominal region, then a pre-operative abdominal ultrasound
is advisable in order to rule out possible hernias. When performing the entry of the cannula, it is essential to pinch up
the skin to avoid perforating the gut or internal organs, which
is more likely to occur in slender patients or in those with an
undiagnosed abdominal hernia.
31.11.2 Organs
During breast fat grafting, specially while less experienced,
a surgeon may inject in a wrong plane and damage the pleura
with an injection cannula/needle. This may lead to a possible
pneumonia or pneumothorax. The rst symptoms are chest
pain the next morning after the procedure and lower oxygen
saturation. The diagnosis is conrmed by blood analysis,
chest X-ray, and/or CT scan [7]. A chest tube and hospitalization may be needed.
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31.11.3 Intravascular Injection
31.11.3.1 Fat Embolism
Fat embolism may happen by two mechanisms:
1. Fat embolism syndrome—fat droplets and lipid globules
that travel along the body and induce a systemic and pulmonary inammatory reaction resulting in reactive airway
compromise (more related to fat harvesting; more common
in the post-operative period; fat droplets will be present in
the bronchoalveolar lavage, urine, and serum) [13].
2. Macroscopic fat particles that offer mechanical obstruction
of the lung vasculature (more related to the fat grafting procedure, more common in the intra-operative period).
Mentz describes a mortality rate of 15% with fat
embolism with either mechanism [23].
Macroscopic fat particles may enter into the vascular system through the cannulation of the gluteal veins (superior or
inferior) or after a traumatic transection of the gluteal vein by
the grafting cannula. In fact, fat emboli look more probable in
individuals with varicosities of the gluteal veins [3, 23]. Wang
and colleagues recommend screening for those varicosities
[24]. Cardenas-Camarena and colleagues showed autopsy
results of a transected gluteal vein [25]. The mechanism of
entry after a transected vein is by a pressure gradient. The
high-pressure extra- vascular system (due to the introduction
of fat into the area and the overall interstitial pressure of
approximately 25mmHg) joins the low-pressure venous system. The venous system is especially at low pressure in hypovolemic intraoperative or postoperative patients [13].
31.11.3.2 Fat Embolism Syndrome (FES)
The mechanism for FES is based on fat droplets and lipid
globules entering the vasculature. This is usually related to
the fat harvesting not the fat injection portion of the procedure. FES patients have been found to have fat droplets in
bronchoalveolar lavage, urine, and serum.
How toManage FES?
The diagnosis of FES is based on some symptoms—rst
appear the neurologic symptoms (mild disorientation to a
coma), then respiratory symptoms (mild dyspnea to an acute
respiratory distress syndrome). About half of the patients
may reveal a petechial rash [24]. The most frequent sign,
although unspecic, is tachycardia. Wang and colleagues
published an excellent review of all the clinical and laboratory symptoms and ndings related to FES [24]. Please nd
the fat embolism syndrome diagnose criteria on Table31.6.
Table 31.6 Criteria for fat embolism syndrome diagnosis by Gurd and
Wilson [26]
Major criteria Minor criteria Laboratory ndings
Respiratory
insufciency
Cerebral
involvement
Petechial rashes
Pyrexia
Tachycardia
Retinal
changes
Jaundice
Renal
changes
Anemia
Thrombocytopenia
High erythrocyte
sedimentation rate
Fat macroglobulinemia in the
plasma
31.11.4 Embolization withInfarction (E.g.,
Retinal Artery, Ophthalmic Artery,
Anterior or Middle Cerebral Artery,
Internal Carotid Artery, Pulmonary
Arteriole, Deep Venous Thrombosis,
Skin/Mucosa/Conjunctiva Necrosis)
This is probably the most catastrophic complication that may
happen after fat grafting into the face. Conrad Miller was the
rst to warn about the dangers of intra-arterial injection of
llers in 1926 [27]. The rst report on unilateral blindness
from central retinal artery occlusion was in 1988 by
Teimourian [28]. A 2012 systematic review found 15 reports
of blindness following facial cosmetic fat grafting [29].
Beleznay et al. identied 98 cases of vision changes from
injected ller. Interestingly, the sites that were at high risk
for complications were the glabella (38.8%), nasal region
(25.5%), nasolabial fold (13.3%), and forehead (12.2%).
This highlights the importance of the knowledge of high risk
areas and the local anatomy (Figs.31.8 and 31.9) [30, 31].
Autologous fat (47.9%) was the most common ller associated with this complication, followed by hyaluronic acid
(23.5%). The most typical symptoms were immediate vision
loss and pain, especially in the rst 7h [8, 30]. The injection
of fat into an arterial lumen may travel as a column proximally and block the arterial blood ow to a particular anatomic region, which results in blindness (retinal artery,
ophthalmic artery), a stroke (anterior or middle cerebral
artery), a pulmonary embolism or others, depending on the
anatomic area being treated. What about intra-venous injection? When it happens, fat parcels probably travel to the
lungs, becoming pulmonary emboli, although it may also
result in a deep venous thrombosis.
31.11.4.1 How toPrevent Embolization?
The best weapon to avoid such kind of complications, is the
understanding of the vascular anatomy. Also the surgeon
must be aware that some particular facial areas such as the
nose, periorbital region, nasolabial fold or injection of the
b
a
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Fig. 31.8 (a) The vascular
anatomy of the face. (b) The
mechanism of fat injection
inducted blindness. (from
Beleznay K, Carruthers JDA,
Humphrey S, etal. Update on
avoiding and treating
blindness from llers: a recent
review of the world literature.
Aesthet Surg J. 2019;39
(6):670; with permission)
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Supraorbital a.
Supratrochlear a.
Dorsal nasal a.
Angular a.
Infraorbital a.
Facial a.
Central retinal a.
Ophthalmic a.
Posterior ciliary
arteries
lower lip offer higher risk [7]. Particularly in the face, where
the consequence of permanent blindness is catastrophic,
nephrine should be considered for use at the injection site for
the placement of llers.
Supratrochlear a.
Dorsal
nasal a.
Angular a.
blunt cannulas are preferred to place fat graft into the subcutaneous tissues or deeper (19–21 gauge) and 1cc Luer-Lock
syringes. The sharp needle used to open the way, should be
only applied supercially. After introducing the canula, a retrograde pull of the plunger during at least 4 seconds in order
to verify there is no intra-vascular positioning of the tip, is a
golden rule. Small aliquots of fat should be deposited, in a
retrograde fashion, which means, less than 0.1 cc in each
pass. At the periorbital region, Coleman advises aliquots of
less than 0.03 and preferably 0.02 cc. A vasoconstricted
artery is harder to cannulate than a vasodilated one, so epi-
31.11.4.2 How toManage aCentral Retinal
Artery Occlusion?
The patient experienced excruciating pain accompanied by
immediate and permanent loss of vision in one eye [7]. This
is as emergency situation. Any minutes of retinal anoxia will
result in permanent retinal degeneration with blindness. All
the treatments have the objective to dislodge the embolus to
a more peripheral location in the retina, so it mitigates its
damage to maximum a partial blindness. Here are some
immediate measures of supportive care to keep in mind [1]:
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Lateral nasal a.
Dorsal nasal a.
Marginal
alar rim a.
Ophthalmic a.
Dorsal nasal a.
Angular a.
Lateral nasal a.
Marginal
alar cartilage a.
Oblique alar a.
S. Santareno et al.
artery. The difference here is that the pressure applied on the
plunger by the surgeon is higher, which forces the column
back into the internal carotid artery. From here, the fat graft
can travel anywhere into the brain and lead to a stroke. One
of the most dramatic cases happened in 2010, with an
18years old patient, that had a fat graft into the posterior and
lateral pharyngeal walls to treat a velopharyngeal incompetence [32]. Another case happened in a 22years old girl that
had a fat graft for aesthetic purposes [33].
The surgeon must have a high index of suspicion when
performing the fat transfer—the literature reports an acute
onset of symptoms, within minutes or hours. Early recognition (tomography angiography or MRI can help in diagnosis
and follow-up) and early supportive therapy are key [33].
This includes mannitol, steroids, antiplatelet agents, and possibly hyperbaric oxygen. Neurologic function has been
reported to improve over time [8].
Columellar a.
labial a.
Fig. 31.9 The vascular anatomy of the nose and midface. (from
Tansatit T, Apinuntrum P, Phetudom T.Facing the worst risk: confronting the dorsal nasal artery, implication for non-surgical procedures of
nasal augmentation. Aesth Plast Surg. 2017;41:193; with permission)
Facial a.Superior
– Immediate cessation of the fat graft if periocular pain
develops.
– Digital globe pressure (may dislodge the embolus).
– Make the patient rebreathe air into a paper bag (it will
level up the carbon dioxide level, creating immediate
vasodilation of the retina).
– Oral acetazolamide or dorzolamide—eye drops (carbonic
anhydrase inhibitors that will reduce the resistance of the
central retinal artery).
– Steroids, antiplatelet agents, hyperbaric oxygen [8].
– Paracentesis of the globe (is a last resort to reduce the
intraocular pressure).
Additional medical treatments may be performed in order
to improve microcirculation, reduce swelling, nourish the
nerve, rehydrate, and to correct electrolyte disorders.
31.11.5 Stroke or Neurologic Decits
The mechanism of this complication is basically the same
that happens when an emboli is sent to the central retinal
31.11.6 Skin, Mucosa, or Conjunctiva
Necrosis
Tissue necrosis may also happen from fat embolism to terminal arterioles and perforasomes—the arterial supply of the
skin, mucosa or conjunctiva. Unlike the hyaluronic acid,
there is no reversal agent for the fat graft, so supportive therapy is recommended [8].
Velilla’s skin necrosis protocol is summarized on
Table31.7; it is based on some experimental studies [34, 35].
Local anesthetics and nitroglycerin interfere with the necrosis
induced inammation, plasma extravasation and the release
and synthesis of several mediators (prostaglandins, histamine). The effect of vasodilators on the vascular tone, may
inhibit leukocyte adherence to the endothelium of the injured
vessels and its migration into the injured tissues; it probably
Table 31.7 Skin necrosis management protocol by Velilla
Immediate approach
Topical nitroglycerin
2% every 3h
Topical Lidocaíne
4% every 3h
Topical Arnica
Montana every 3h
Pentoxifylline
400mg per os twice
daily
Manual stimulation
Direct oxygen
injection
Therapeutic
ultrasound twice
daily
Secondary approach (when
skin necrosis is
maintained)
Local dressings
Intralesional
triamcinolone
Fraxel laser
Tertiary
approach (after
3months)
Surgical
revision of
scars
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inhibits as well the release of toxic lysozymes, oxygen free
radicals, and histamine [34]. In another study is postulated
that the inhibition of burn edema by local anesthetics in conjunction with the anti-thrombotic effects of these agents,
account for the prevention of progressive burn ischemia [35].
On the recipient site, hyaluronidase may redistribute the fat
grafts in order to decrease local tissue pressure by breaking
apart the collagen matrix within the recipient site [8].
The most common symptom is pain followed by tissue
loss. The immediate aspect of skin necrosis after an abdominal liposuction is shown on Figs.31.10 and 31.15. The evolution of skin necrosis with the immediate approach of the
referred protocol is presented in Figs.31.10, 31.11, 31.12,
31.13, and 31.14. Another case that did not respond to the
immediate approach is shown (Figs. 31.15, 31.16, 31.17,
31.18, 31.19, and 31.20). Skin necrosis management proto-
col by Velilla is presented on Table31.7.
31.11.7 Death
The focus has intensied due to the increase in the number
of reported deaths secondary to fat grafting into the but-
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Fig. 31.10 The aspect of skin necrosis on day 1 after abdominal liposuction (courtesy of Velilla)
Fig. 31.11 The aspect of skin necrosis on day 3, under the immediate
approach protocol from Velilla
tocks. This has also raised the awareness in the media,
which has led to increased attention by the plastic surgery
community. An ASAPS Task Force survey evaluated 25
deaths related to gluteal fat grafting and Cardenas-
Camarena evaluated 22 deaths from Mexico and Columbia
[25]. The ASAPS survey included Mexico and Columbia, so
presumably some of these deaths that are reported may be
reported in both studies. In 2015 several plastic surgeons
both from Mexico and Colombia referred about 13 deaths
in Mexico and 9in Colombia in the rst 24 hours after the
fat grafting into this particular body area. The pathological
reports referred globules of fat in the superior gluteal vein
and macroscopic fat in the inferior vena cava, right atrium,
right ventricle, and lungs [25, 32]. Also, in 2015 a death
during lipoinjection to the buttocks was reported; the
autopsy revealed small vessels of both lungs with multiple
grossly plugs and adipose tissue—the hypothesis of gluteal
varicose veins as a possible conduit for the emboli to enter
the venous system was initiated (Figs.31.21, 31.22, 31.23,
and 31.24).
Based on these studies, a few important concepts and rec-
ommendations must be highlighted [36]:
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Fig. 31.12 The aspect of skin necrosis on day 5, under the immediate
approach protocol from Velilla
1. The volume of fat does not correlate with risk of fat
embolism.
2. Location of fat grafting seems to correlate with risk of
fat embolism. The deep gluteus maximus should be
avoided. Presumably, because that is where the veins are
located, they are at greater risk for transection.
3. Injection of grafted fat should be limited to the super-
cial muscle and subcutaneous tissue.
4. Injection cannula size should be 4.1mm or greater, sin-
gle hole.
5. The cannula should be kept parallel to the plane of the but-
tock to avoid inadvertent deep intramuscular injection.
6. Maintain constant 3-dimensional awareness of the can-
nula tip.
7. Only inject when cannula is in motion.
8. Consider pulmonary fat embolism in unstable intra- and
postoperative patients.
9. Review gluteal vascular anatomy.
10. Include the risk of fat embolism and surgical alternatives
in the informed consent process.
Fig. 31.13 The aspect of skin necrosis on day 10, under the immediate
approach protocol from Velilla
This risk of death has been calculated to be approximately 1:3000 [18]. The ASAPS Task Force stressed that
this is an inexact estimate due to the numerous limitations
of the methodology of the study. They believe, however,
that the estimate is signicantly higher than for the other
aesthetic procedures. For comparison, the overall mortality in an American Association for Accreditation of
Ambulatory Surgery Facilities facility for any aesthetic
procedure is 1:55,000 and many orders of magnitude
higher than an abdominoplasty, which has been shown to
be 1:135,000 [36]. The Multi-Society Task Force for
Safety in Gluteal Fat Grafting released a practice advisory
regarding gluteal fat grafting in 2018 and a second practice
advisory in August 2019 [37]. In 2021, the Aesthetic
Surgery President commissioned a “Practice Advisory on
Gluteal Fat Grafting” [37]. Recently, the American Society
of Plastic Surgery (ASPS) published a comment following
the workshop for Regulation 64B8-9.009 in 2022 that hap-
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Fig. 31.14 The aspect of skin necrosis after 1month, under the immediate approach protocol from Velilla
Fig. 31.15 First local signs of probable skin necrosis following liposuction of the abdomen (courtesy of Velilla)
Fig. 31.16 The 30th day aspect of a skin necrosis managed with local
dressings and supportive care (courtesy of Velilla)
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Fig. 31.17 The 40th day aspect of a skin necrosis managed with local
dressings and supportive care (courtesy of Velilla)
Fig. 31.18 After 4months; the wound was managed with 3 series of
intralesional triamcinolone and Fraxel laser (courtesy of Velilla)
Fig. 31.19 The aspect 2weeks after the surgery review of the skin
necrosis (courtesy of Velilla)
Fig. 31.20 One year after the surgical review of the skin necrosis
(courtesy of Velilla)
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