Article UFEK2023
Article UFEK2023
Article UFEK2023
https://doi.org/10.1007/s00266-023-03722-3
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Included items in green, excluded items in red. VAE vascular adverse event
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HYAL can be advantageous due to its edema-reducing not included because of secondary effects but may be
effects, decreasing occluding vessel pressure [16]. considered [34]. Pentoxifylline is also included because of
The estimated dose of HYAL varies depending on the its beneficial effect on improving ischemic symptoms [35].
thickness and number of areas involved; based on the old In late vascular occlusion, application of clostridium A
treatment protocol, proper HYAL dose is approximately collagenase ointment once daily has been demonstrated to
300–600 units of HYAL, whereas if we base it on the new enhance wound healing by selectively removing necrotic
modality of ‘‘high-dose pulsed HYAL’’, it is approximately tissue without affecting healthy skin [36].
500 units, every hour, for each localized affected area as Occlusion of the ophthalmic artery occurs because of
described by deLorenzi [17]. Reevaluation and reinjection HA embolism via retrograde from the supratrochlear,
are performed until perfusion returns to normal. Ultrasound supraorbital, and dorsal nasal artery [37]. In this case,
(US)-guided HYAL injection has been shown to be more vasodilators could be useful since they could move the
effective [18, 19]. embolus to a more distal branch, causing less ischemic
Two variations to this posology are the nose, where 900 damage [38], although this is not proven. To improve
units are used, and in the case of blindness, where retrob- ocular perfusion and dislodge the embolus, it is important
ulbar HYAL injection should be considered. However, there to decrease intraocular pressure [8, 39]. With this purpose,
is no consensus about retrobulbar HYAL injection in cases triple topical hypotensive therapy (timolol, brimonidine,
of blindness, with some articles in favor [20–23] and some and brinzolamide), oral acetazolamide, and intravenous
articles against it [24–26]. Proper retrobulbar HYAL injec- mannitol are included.
tion dosage is estimated to be approximately 800 units [26], Vascular occlusion can compromise blood flow and
although more units have been applied in some cases [27]. nutrient supply to the affected area, which weakens the
Regarding antiplatelet and anticoagulant treatment, it is immune system and increases invasive infection [40].
important to consider terminal artery embolization and Polymicrobial (staphylococci, streptococci, enterococci,
vascular tree vasospasm as the causative agents of arterial E. coli, and other gram-negative bacteria) infections are
occlusion [28]. The skin does not contain terminal arteries; common, with Staphylococcus aureus being the most fre-
instead, the flow is controlled by compensation mechanisms quently implicated pathogen in vascular occlusion-related
of small vessels that are closed or have low flow in the basal infections [40]. Based on its broad spectrum coverage,
state and increase their flow according to the needs of the amoxicillin-clavulanate would be indicated for empiric
supplied territory [29]. These vessels are called choke ves- treatment, and in cases of suspected methicillin-resistant S.
sels [28] and provide double protection against arterial filler aureus (MRSA), vancomycin should be considered [41]. In
occlusion: (1) some choke vessels of the ischemic area will early vascular occlusion, which is considered to be diag-
dilate, compensating for the blood supply, and (2) vasos- nosed and resolved at the moment of intervention, no
pasm occurs in vessels acting as a barrier and preventing the ambulatory antibiotic is needed.
embolus from arriving at a terminal artery [18]. What trig- Decreasing the inflammatory component with systemic
gers vasospasm in choke vessels is unknown [30], but HA corticosteroids is recommended in emergent cases
has been shown to be a strong inflammatory response [16, 42, 43]. Intramuscular (IM) administration is supposed
inductor within blood vessels [31]. This new concept of to result in fast and complete absorption with high absolute
choke vessel spasm is the major determinant of the location bioavailability [44], so it is indicated for emergent com-
and extent of tissue necrosis following inadvertent hya- plications. Intravenous (IV) hydrocortisone will be added
luronic acid intraarterial injection [29]. in anaphylaxis [45]. For ambulatory treatment in late
As the choke vessel mechanism causes ischemia within occlusion, we included prednisolone tablets [9].
the vascular territory but also blocks HA embolus, pre- Anaphylaxis is a life-threatening type I hypersensitivity
venting irritation spread to other territories, the use of reaction [45]. The first step in anaphylaxis cases is to
vasodilators such as nitroglycerin, phosphodiesterase inhi- administer IM adrenaline. Apart from the IV corticos-
bitors or prostaglandin analogs is not included in early teroids mentioned, antihistamines and salbutamol should
occlusion treatment [29]. However, an antiplatelet agent be considered [45].
such as acetylsalicylic acid (AAS) is included in the kit, as We present a revised application kit protocol, specifying
blood fluidization improves perfusion in the affected each scenario: acute vascular occlusion, late vascular
territory. occlusion, blindness, and anaphylaxis:
In late occlusions, vasodilators should be considered
after HYAL treatment and positive pinprick test results or Acute Vascular Occlusion
HA embolus dilution confirmed by ultrasound [32, 33]. In
the UFEK, calcium channel blockers, such as diltiazem, are Stop the injection immediately once signs of vascular
considered vasodilators. Phosphodiesterase inhibitors are occlusion appear, which include pain, pallor, or blanching
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