In 1952, Stanley Cohen and Rita Levi-Montalcini discovered growth factors, and this research opened the door for platelet-rich plasma (PRP). They were awarded a Nobel Prize for their work in 1986 (Santos et al, 2010). Furthermore, Cohen went on to discover epidermal growth factor (EGF) in 1962, platelet-derived growth factor (PDGF) in 1974 and vascular endothelial growth factor (VEGF) in 1989.
According to Hurjui et al (2020), the term ‘PRP’ was first used by Kingsley et al (1954) to refer to the standard platelet concentrate for transfusion (Mościcka and Przylipiak, 2021). Matras (1972) used platelets for the first time as a sealant to establish blood homeostasis during surgical procedures and Oon and Hobbs (1975) were the first scientists to use PRP in reconstructive treatments (Mościcka and Przylipiak, 2021). Furthermore, Knighton et al (1986) were the first to describe platelet concentrate protocols and referred to them as autologous platelet-derived wound healing factors (PDWHF) (Mościcka and Przylipiak, 2021). Later, Ferrari et al (1987) used PRP in heart surgery as an autologous source of transfusion, thus reducing intraoperative blood loss. Since the 1980s, PRP has been widely used in regenerative medicine. Further development in the application of PRP in dentistry occurred after Choukroun et al (2006) discovered platelet-rich fibrin (PRF), which is a type of platelet concentrate that does not use the addition of anticoagulants.
Today, PRP is at the heart of a very active field of research. Studies are being published on an almost daily basis and, at present, there are over 22000 articles on PubMed and over 40000 on Wiley Online that touch on the subject.
What is platelet-rich plasma?
PRP is an autologous concentration of human platelets in a small volume of plasma that is developed from autologous blood. This means that it is inherently safe and defined as a sample of autologous blood with concentrations of platelets in a given volume of plasma that is above the concentration found in the whole blood (Mishra, 2010).
Plasma, which is made up of 55% blood fluid, is mostly water (90% by volume), and contains dissolved proteins, glucose, mineral ions, hormones, carbon dioxide, platelets and blood cells. As PRP is a concentration of platelets, it is also a concentration of the seven fundamental protein growth factors proved to be actively secreted by platelets to initiate all wound healing. These growth factors include the three isomers of PDGF. All of these growth factors have been documented to exist in platelets, but the platelets need to be activated. On activation, they release alpha granules, within which those growth factors are stored (Kim et al, 2011).
Additionally, the activated thrombocytes have a multitude of signal molecules on their surface: CD9, CD-W17, CD41, CD42a-d, CD51, CD-W60, CD61, CD62P, CD63. As these concentrated platelets are suspended in a small volume of plasma, PRP is more than just a platelet concentrate; it also contains the three proteins in the blood known to act as cell adhesion molecules for osteoconduction and as a matrix for bone, connective tissue and epithelial migration. These cell adhesion molecules are fibrin, fibronectin and vitronectin (Everts et al, 2006).
PRP promotes soft tissue healing via growth factors released after platelet degranulation. These growth factors initiate and enhance physiological processes that contribute to tissue recovery and healing after injury.
Growth factors associated with platelets include:
- PDGF (PDGF-AA, PDGF-BB, PDGF-AB)
- Transforming growth factor-beta (TGF-b1, TFG-b2)
- Vascular endothelial growth factor (VEGF)
- Epidermal growth factor (EGF)
- Pro- and anti-inflammatory cytokines (interleukin (IL)-4), IL-8, IL-13, IL-17, tumour necrosis factor-alpha and interferon-alpha)
- Fibroblast growth factor-2 (FGF-2)
- Insulin-like growth factor (IGF)
- Fibrin, fibronectin, vitronectin, thrombin (Ranaweera, 2013).
These growth factors promote healing by:
- Attracting undifferentiated stem cells into the newly formed matrix and triggering cell division
- Suppressing cytokine release and limiting inflammation
- Attracting macrophages to improve tissue healing and regeneration
- Promoting new capillary growth (new blood vessel formation), and accelerating epithelialisation (Ranaweera, 2013).
PRP allows the body to heal faster and more efficiently, and it does this by stimulating DNA repair, which can heal wounds and remodel scars (Cervelli et al, 2009). Not only is it an effective anti-ageing treatment, but it also has wider uses within the medical profession (Amgar and Bouhanna, 2013). PRP is widely used now in several specialities, including orthopaedics, eye laser surgery, plastic surgery, cardiac surgery, dentistry, veterinary medicine and, most commonly, sports medicine (de Mos et al, 2008).
» Interestingly, the authors stated that the preparation protocols involved the withdrawal of autologous blood in the presence of anticoagulant, its centrifugation with plasma separation and the activation of platelets with calcium chloride «
Mechanism of action and clinical indications
PRP is first prepared by taking blood from the patient, then placing it in a centrifuge that spins the blood at a high speed to separate the platelets from the red blood cells. There are three layers: PRP, platelet-poor plasma (PPP) and red blood cells. The resulting small volume of fluid after the centrifugation process contains approximately five to seven times the normal volume of platelets.
After spinning, the PRP and PPP are taken from the tube and put into a syringe. The red blood cells are never injected. The PRP is injected into the patient in the area that requires treatment. Following the treatment, results are noticeable within 3–4 weeks, and, often, only one procedure is required; however, this is dependent on the kit used and the area that is treated (Sister, 2016).
PRP is an effective non-surgical treatment for facial rejuvenation, as it is natural and relatively safe, and it provides results that can last up to 12 months (Banihashemi et al, 2021). As the platelets are autologous, there is no risk of infection or rejection.
Several different PRP harvesting kits are available. However, some contain thrombin and, therefore, the end product cannot be categorised as autologous. Others use a chemical buffer to separate the plasma and red cells and, as a result, do not deliver pure PRP. Activation of the platelets is required for the release and enmeshment of growth factors, but the method of activation may influence the resulting matrix, growth factor availability and healing (Sommeling et al, 2013).
Activating the PRP prior to injecting is an interesting topic. Some PRP kits contain calcium chloride, while others do not. Many medical professionals are not aware that this is an option, which, in the author's opinion, is a result of the training that has been received and the kits that are used. Yet, there are several papers and medics that suggest activating the platelets will give better results, and, from the author's personal experience, activating the PRP yields better results. However, the author has also seen good results without activation. It must be mentioned that different PRP kits were used, which potentially may have impacted the results. In the author's opinion, this topic needs further investigation and research in the future. PRP is used to treat a variety of indications, including:
- Wound healing
- Scars and stretch marks
- Hair loss
- Facial rejuvenation
- Sports injuries
- Orthopaedics
- Vocal cord injuries
- Vagina rejuvenation (sexual dysfunction)
- Dental surgery
- Plastic surgery
- Cardiac surgery
- Respiratory conditions.
PRP can be used as a standalone treatment, but it can also be used in combination with other medical aesthetic procedures, such as dermal fillers, mesotherapy, laser, microneedling and PDO threads. PRP can be administered via modalities such as a needle, cannula or mesogun.
Safety, complications and contraindications
Many articles on PRP cover the safety of this treatment with a short paragraph on the risks, which usually include more obvious risks, such as:
- Swelling
- Bruising
- Tenderness at the injection sites
- Erythema
- Bleeding from the injection sites.
PRP is immunologically neutral and poses no danger of allergy, hypersensitivity or foreign-body reactions (Everts et al, 2020). However, in the author's opinion, PRP injections cannot be considered 100% safe due to certain factors, such as the environment in which the procedure is taking place, the safety and infection protocols used by the practitioner, the PRP kit, the centrifuge, the length of time the PRP is spun and the injection protocols used. Furthermore, the harvesting of the patient's blood is also a contributing factor. Sterility during this procedure is an important factor to prevent infection. A poor technique with a substandard kit can potentially cause issues, such as in the publicised case involving Kerry Katona in 2013 (Anisiobi, 2013).
Homemade or cheap kits and centrifuges obtained from websites such as AliExpress, Ebay and Amazon are not safe. They are unlikely to be Conformitè Europëenne (CE)-marked or US Food and Drug Administration (FDA)-approved and are not suitable for clinical use or the reinjection of platelets into a patient.
The following medical conditions are contraindications for the use of PRP:
- Critical thrombocytopenia
- Hypofibrinogenaemia
- Haemodynamic instability
- Sepsis
- Acute and chronic infections
- Chronic liver disease
- Anti-coagulation therapy (Ranaweera, 2013).
While PRP is considered safe for most people, it is not recommended for anyone who has one of the following medical conditions:
- Hepatitis C
- Human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS)
- Any type of blood cancer
- Cardiovascular disease that requires taking a blood thinner
- Skin cancer in the area to be treated.
The reason is that these conditions affect platelets, making them unable to deliver the expected results (American Academy of Dermatology Association, 2018).
Platelet-rich plasma and blindness
According to an article by Karam et al (2020), there have been four cases of irreversible blindness caused by PRP. There were three immediate cases of blindness following injections to the glabella and one case following injections to the nasolabial folds.
The authors note that, in all of these cases, they could not obtain information about the PRP preparations, composition, technique and dosage administered to each patient. However, each of these patients described a similar PRP preparation protocol. Interestingly, the authors stated that the preparation protocols involved the withdrawal of autologous blood in the presence of anticoagulant, its centrifugation with plasma separation and the activation of platelets with calcium chloride.
Case one
The first case is of a previously healthy woman aged 61 years, who received monthly sessions of PRP injections in her hands, face and neck by a cosmetologist. During the sixth session, immediately after injection into the left glabellar region, she developed a sudden and painful loss of vision in the left eye, associated with dizziness and vomiting. On assessment the same day, her visual acuities were 20/20 with the right eye and no perception of light with the left eye. Fundus examination of the left eye showed generalised retinal whitening, segmental narrowing of the retinal arteries and white material suggestive of an embolus within the central retinal artery. The retinal veins were attenuated, and fluorescein angiography demonstrated patchy choroidal perfusion and retinal circulation blockage.
Brain magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) of the brain and neck, laboratory tests for hypercoagulability and vasculitis and cardiovascular evaluation were unremarkable.
After 3 days, there was limited and sluggish filling of the retinal arteries and late hyperfluorescence in the retinal and foveal area. Optical coherence tomography showed heightened macular retinal thickness. The patient acquired glabellar bruising and hypoaesthesia in the distribution of the first trigeminal branch on the left side.
After 1 month, the patient developed a pale left optic disc with pigment in the superior temporal region, phantom retinal vessels, pigmentation of the peripheral retinal and macular fibrosis. Fluorescein angiography demonstrated attenuated retinal vessels with hypofluorescent areas mixed with mild hyperfluorescent areas in the macula and mid-peripheral retina. Optical coherence tomography demonstrated atrophy of all retinal layers and fibrosis of the macular area.
After 4 months, the pigmentation had increased in the retina, and the optic disc remained pale. After 8 months, there was retinal detachment in the left eye.
Just following the injection, there was bruising at the injection site, and, 1 month after the injection, there was skin necrosis and ulceration of the injection area. After 4 months, this had improved, and, 8 months later, there was persistent scarring in the affected area.
Case two
In the second case, a previously healthy woman, aged 63 years, reported sudden, painful loss of vision in the right eye after her first PRP injection in the forehead for wrinkle treatment. Additionally, she experienced dizziness, tinnitus and acute vomiting. The patient also noted the development of iris depigmentation. At her first visit, 3 weeks after injection, her corrected visual acuities were no perception of light in the right eye and 20/20 vision in the left. Biomicroscopy showed corneal endothelial pigmentation, iris atrophy, posterior synechiae of the iris and pigment dispersion at the anterior surface of the lens. The ocular movements were normal. Following fundal examination, there was a pale right optic disc, central retinal artery occlusion and retinal haemorrhages, as well as patchy pigment dispersion and macular fibrosis. The amalric triangle sign, which indicated choroidal ischaemia, was evident in the mid-peripheral retina. Fluorescein angiography demonstrated delayed filling of the central retinal artery and impaired perfusion of the optic disc and choroid. Optical coherence tomography showed fibrosis and neurosensory retinal detachment in the macular area with an epiretinal membrane. A scar was evident in the glabellar area. Brain MRI and MRA, laboratory tests for hypercoagulability and vasculitis and cardiovascular evaluation were normal. The patient did not return for follow-up.
Case three
The third case was a previously healthy woman, aged 52 years, who, again, developed painful loss of vision in the right eye and vomiting immediately after injections of PRP in the right nasolabial fold and glabellar area. She had had many previous injections by her cosmetologist. At the first visit, after 24 hours, the visual acuities were no perception of light in the right eye and 20/20 vision in the left eye. There was an incomplete oculomotor nerve palsy (mild ptosis, restricted adduction and vertical gaze) that affected the patient's right eye. Biomicroscopy showed flare in the anterior chamber and corneal folds. The intraocular pressure of her right eye was 3 mmHg. She had a central retinal artery occlusion without a cherry red spot but had multiple retinal haemorrhages. Fluorescein angiography showed delayed filling of the central retinal artery and vein with areas of patchy choroidal non-perfusion. The patient showed bruising at the injection sites. Brain MRI/MRA, laboratory tests for hypercoagulability and vasculitis and cardiovascular evaluation were unremarkable. Although the patient did not attend for follow-up, she sent a photograph after 1 month that showed necrosis of the forehead, right periorbital region, right cheek and right nasal area.
Case four
In the fourth case, a previously healthy woman, aged 50 years, developed eye pain with transient blue vision, which was followed by vision loss in the right eye immediately after her first PRP and platelet gel injection in the forehead, glabellar and right external canthus of the eye. Furthermore, she reported a headache, nausea, urinary urgency and right ptosis. Some 3 weeks after the injection, the visual acuities were no perception of light in the right eye and 20/15 vision in the left. She had a complete right oculomotor nerve palsy. Fundal examination revealed a pale retina with a central retinal artery occlusion. Fluorescein angiography demonstrated delayed filling of the central retinal artery with areas of patchy choroidal non-perfusion. She did not return for follow-up.
Case five
During the author's research for this clinical paper, another article from Kalyam et al (2017) was found that highlighted a case of blindness in a 49-year-old woman following periocular autologous PRP treatment for skin rejuvenation. To the author's knowledge, this is the first reported case of extensive ischemia following autologous PRP therapy (APRP).
The otherwise healthy patient presented to the Yale Eye Center, US, complaining of acute loss of vision in the right eye, associated with severe nausea and eye pain. The day before, the patient underwent a APRP injection procedure by an unlicensed practitioner to reduce wrinkles in the glabellar region bilaterally. She reported that blood was taken from her antecubital region by venous puncture and centrifuged to obtain concentrated autologous plasma. Bilateral forehead rhytids injections were performed. The patient was not made aware of the details of the plasma preparation and the size of the needle that was used for injections. She tolerated the first injection on the left side well. However, during the second injection at the nasal end of right eyebrow, she felt the needle penetrate slightly deeper, accompanied by sudden pain and fullness behind her right eye with immediate visual loss over the next few minutes. She then noted transient improvement of vision in the nasal field, followed by a complete loss of vision.
On examination, the patient's vision was no light perception in the right eye and 20/20 vision in the left eye. A pronounced right afferent pupillary defect was present. Motility of the right eye was restricted in supraduction and adduction, resulting in a right exotropia and hypotropia in primary gaze. External exam demonstrated a 1cm area of ecchymosis and induration above the right medial brow. The eyelids were soft, and there was no proptosis or resistance to retropulsion. Anterior segment exam was unremarkable in both eyes except moderate conjunctival hyperaemia in the right eye. Intraocular pressure was within normal limits bilaterally. Fundus exam of the right eye revealed profound optic disc pallor, diffuse retinal whitening (including fovea), marked attenuation of arterioles with abrupt ending of the vessels in midperiphery and central macular oedema. The absence of a cherry red spot suggested diffuse choroidal ischaemia. No Hollenhorst plaque was seen, and the left fundus exam was unremarkable.
Head and neck CT showed right subacute frontal lobe ischaemia without identifiable compromised vessels. MRI/MRA of the brain and orbit demonstrated restricted diffusion along the course of the right optic nerve and multiple subacute infarcts involving the right frontal, parietal and occipital lobes. Asymmetric abnormal FLAIR/T2 signal of the right medial rectus muscle was suggestive of ischaemia. Bone marrow oedema within the right frontal bone with irregular enhancement involving the overlying skin was also shown. MRA of the brain and neck was negative for cavernous sinus pathology, or vertebral or carotid artery dissection. CTA of the head and neck and transthoracic echocardiogram identified no embolic origin. Echocardiogram and carotid dopplers were negative. Laboratory tests revealed a mildly elevated erythrocyte sedimentation rate (26mm/h, normal 0–20) and C-reactive protein (3.8mg/L, normal 0.1–3.0) with a normal complete blood count test. Further work-up for thrombotic and arteritic processes were all negative, including PT/PTT, INR, Beta2-glycoprotein, homocysteine, protein-C and S, D-dimer, antithrombin III, cardiolipin, jak2, C3, C4, Anti-DNA ab, Lupus anticoagulant, rheumatoid factors, antineutrophil cytoplasmic antibody and haemoglobin screen.
The patient was diagnosed with acute right ophthalmic artery occlusion and brain infarction as a complication of periorbital APRP injection. Having arrived outside the window of intra-arterial tPA, she was treated with ocular massage, topical timolol 0.5% and brimonidine 0.2% and oral steroids. The patient declined anterior chamber paracentesis. She was given intravenous antibiotics for possible infectious cause of periorbital swelling and erythema. External and fundus photography taken 1 week after presentation demonstrated ecchymosis and ischaemia of the right glabellar region, as well as diffuse retinal whitening and ischaemia. Ocular motility returned to normal by week 2. Approximately 1 year after presentation, the patient's vision remained no light perception in the right eye with residual scarring and hard nodules of the right glabellar region. The patient subsequently underwent scar revision surgery of the right glabella a year later. The pathology of scar tissue showed lipid-based foreign body with giant cell reaction that was consistent with prior injection of foreign material within deep tissues.
» As there are several unanswered questions regarding the PRP kits, the centrifuge, the injection protocol and the inclusion of anticoagulant or not, it is not a certainty that the fibrin clot caused all five of these cases of blindness «
Case six
A third article (Bhalla et al, 2020) discussed the case of a 41-year-old female patient with no past medical history who presented to a private clinic with an acute reduction in her left vision immediately following an injection of PRP in her temporomandibular joint (TMJ) for temporomandibular disorder (TMD).
Her vision dropped to no perception of light. Upon examination, the patient had a textbook central retinal artery occlusion. Due to the delayed presentation to an ophthalmologist, all acute treatments were futile. Urgent neuroimaging was requested, as there was a concern of retropulsion of the PRP solution into the intracranial arterial system. Fortunately, this did not show any acute intracranial vascular events. As a last resort, the patient underwent an emergency pars plana vitrectomy, an intraocular procedure where the vitreous is removed, in the hope that mechanical disruption of the intraocular anatomy would dislodge the emboli and regain some perception of light. However, this also proved to be unsuccessful. The patient was transferred to an NHS ophthalmology clinic for management of potential sequelae of arterial occlusion. She subsequently developed iris neovascularisation, which put the patient at risk of developing a painful blind eye that can only be treated with enucleation. She currently remains under close monitoring with regular topical guttate atropine 1% and guttate dexamethasone 0.1% drops to keep the eye painless and cosmetically functional.
Discussion
It is important to note that, in the first two articles (cases 1–5), the authors state that PRP is being used as a cosmetic filler.
Karam et al (2020) stated: ‘PRP has become one of the world's most widely used facial cosmetic fillers’, while Kalyam et al (2017) said that, ‘recently, physicians and cosmetologists across the country have been exploring its use as cosmetic filler for skin augmentation’.
This is not the case in true PRP, as it is a liquid. It stimulates collagen but does not add volume, so it is not a filler. The authors use the word ‘filler’ often, so it could be their terminology, rather than implying that a dermal filler was added to the PRP. Kalyam et al (2017) wrote that ‘some practitioners deliberately modify these products before injection, including mixing the PRP with fillers’. They also stated that, to their knowledge, there have been no reports of vision loss associated with APRP when used as a filler. Their 49-year-old patient declined to disclose the contact information of the practitioner who performed her treatment, but it is documented that they were unlicensed. It is also noted that she was not aware of the PRP preparation, or the size of the needle used. They mention the injection of a platelet clot.
None of the Karam et al's (2020) patients discuss dermal filler being added to the PRP, and some had these treatments before. In case three, the patient had five previous treatments at monthly intervals, so it is highly unlikely that a dermal filler was added to the PRP in each of these repeated treatments. In case four, it states that the patient had platelet gel injected with PRP. Therefore, this is a fibrin clot.
In the third article (case six), Bhalla et al stated: ‘The composition of PRP is serous; however, practitioners are known to mix the solution with hyaluronic acid (HA), which helps mimic the physiological microenvironment of the synovial joint. The PRP stimulates cell proliferation and production of cartilage matrix whereas HA provides visco supplementation. The injection is normally guided into the upper mandibular joint space, and this can be determined by the extent of mandibular movement during the procedure by the injector. The maxillary and superficial temporal arteries are at risk of infiltration during the procedure due to their proximity near the TMJ’.
It is unclear what this patient had administered, but the authors discussed PRP and HA. They cited that this was the first reported ocular complication in TMJ injections, and they hope that this case highlights the importance of clear anatomical understanding to all practitioners who administer PRP and HA. The author contacted them to see if this was a non-crosslinked or crosslinked HA or whether it was PRF. Without the necessary information, it is hard to know for certain what was injected. In this case, until proven otherwise, the author believes that this was a combination of PRP and HA.
Two articles mention fillers being injected into blood vessels and the complications associated with fillers. They also talk about necrosis of the skin, which was seen in a few of these cases. The author believes that this is used to highlight the complications of injections, particularly in the glabella and nasolabial fold areas. Both articles cite literature regarding vascular occlusions. The author is of the opinion that, in cases 1–5, a dermal filler was added to the PRP, but, again, this is unclear. However, it is now known that case four was a fibrin clot, so the rest may have been also.
Two of the articles mention that cosmetologists administered the treatments. Who are cosmetologists? This does not mean that they were lay injectors. In other parts of the world, they use the term cosmetologist to describe licensed practitioners. However, both articles stated that these treatments should only be performed by highly experienced cosmetologists. Again, without the necessary information regarding the experience and qualifications of these injectors, we cannot comment on their techniques or skills.
In regard to the fibrin clot, the author conducted an experiment. It is known that PRP is liquid and will integrate into the tissues; however, PRF is a gel, and the kit used, the centrifuge and the time its spun will depend on the thickness of the thrombin clot.
In the author's experiment, a basic vial was used, and anticoagulant was not added to it. The vials were spun for a few minutes, and the fibrin clot was a very fine gel consistency with some liquid PRP. It was then spun it for a few more minutes and it became a thicker gel until, at the end, it was like rubber.
Conclusion
Karam et al (2020) cited Bosetti et al and the fact that lysophosphatidic acid is produced by the platelets once they are stimulated by a prothrombotic agent in the bloodstream, which could be an important development of arterial occlusion. They also stated that one could speculate that there could be a potential reaction with the calcium chloride during the activation of PRP. This is a possibility, but we would expect to see and hear about a lot more cases if this was indeed the case. As with all aspects of PRP and PRF, much more research is required.
Kalyam et al (2017) hypothesised that the injection technique used may have contributed to the visual complications. The injection site was close to the superior orbital artery and superior trochlear artery, which presumably caused inadvertent injection of PRP into the artery. The pressure from the syringe likely resulted in retrograde flow of the platelet clot. The authors also concluded that the syringe was not drawn back prior to injection, so the placement of the needle was not known, and this may have led to the intra-arterial injection.
Bhalla et al (2020) also looked into the case of the 49-year-old female patient described by Kalyam et al (2017), and they hypothesised that the PRP solution was likely to have been injected into either the temporal or maxillary artery at high pressure to overcome normal arterial flow. This likely caused a retrograde propulsion of the solution into the external carotid artery, which then occluded the ophthalmic and retinal-end arteries, leading to irreversible sight loss. In these cases, the best chance of recovery often means prompt recognition and referral to an ophthalmologist (within 240 minutes) for urgent treatment to give the patient some chance of visual potential. While neither of these articles used the term PRF, they did mention PRP gel and platelet clot. As there are several unanswered questions regarding the PRP kits, the centrifuge, the injection protocol and the inclusion of anticoagulant or not, it is not a certainty that the fibrin clot caused all five of these cases of blindness. As previously stated, the importance of using the correct medical devices for this treatment, as highlighted in the publicised case of Kerry Katona, is crucial. The training and experience of the practitioners involved must also be taken into consideration and examined.
So, the question still remains: is PRP completely safe? While several medics around the world will argue that it is, these six cases of blindness following PRP injections cannot be ignored. In the grand scheme of things, this is a very low number. Additionally, it can be argued that the authors used the term PRP wrongly, as they did not mention the possible addition of dermal fillers, but the bottom line remains that no medical aesthetic procedure is completely safe. All procedures come with a risk.
The author believes that anyone offering this procedure should ensure best practice in clinical settings to ensure patient safety and correct protocols should be followed using CE-marked licenced PRP devices and not making up your own kits. This can cause issues with retrieving the PRP and potentially retrieving a fragment of the gel substance separating the platelets. Injecting slowly and knowing the anatomy of the face is crucial. The most important thing to remember is that injections into the glabella and nasolabial folds come with a higher risk and, whether it is PRP/PRF or a dermal filler, the risks are still the same. From the author's own experiment, it is clear that PRF could cause issues, in particular, with the spinning of the vials for longer periods of time to get thicker fibrin clots. The author believes that this is an easier way for lays or medics to make their own cheap kits without the use of an anticoagulant in a cheap centrifuge that is not compatible for this treatment.
Key points
- Platelet-rich fibrin is a second generation platelet concentrate that is anticoagulant-free
- Platelet-rich plasma (PRP) can be used as a standalone procedure or used in combination with other medical aesthetic procedures
- PRP is an autologous concentration of human platelets in a small volume of plasma
- Safe injection techniques are crucial in high-risk areas
- There are six reported cases of blindness associated with PRP.
CPD reflective questions
- When were growth factors first discovered, and by whom?
- What are the contraindications for the use of platelet-rich plasma (PRP)?
- What is used to activate PRP?