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Why do we use topical zinc on wounds and perilesional skin?

Elena Conde Montero
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Why do we use topical zinc on wounds and perilesional skin?

Zinc in wounds is a subject that has never lost its relevance.

Zinc is a trace element, i.e. a metal found in the body in very small amounts, but it is essential for the activity of different enzymes and transcription factors (proteins with structural domains called “zinc fingers“). Following iron, it is the most abundant trace element in the human body. The concentration of intracellular zinc is regulated by different cellular transporters.

Zinc deficiency, due to either hereditary or dietary causes, has been associated with skin alterations and delayed healing. Although dermatological disorders secondary to low levels of zinc in the body are normally resolved with oral supplements, this route of administration has not shown clear benefits in patients with wounds without this deficit. On the contrary, topical application of zinc has gained a good positioning between the alternatives of local treatment of wounds and perilesional skin.1,2

Let’s understand why.

 

What role does zinc play in wound healing?

The role of zinc in wound healing has been studied predominantly in experimental animal studies. In the skin, the highest concentration of zinc is found in the epidermis, especially in the keratinocytes closest to the basement membrane.

In the initial inflammatory phase, zinc levels rise at the edges of the wound and this concentration increases during granulation and epithelialization phase. This is due to increased expression of membrane transporters in keratinocytes, fibroblasts and macrophages. In the final stage of wound healing, these levels are reduced, with the consequent decrease in cell division..2

Although the exact action mechanism of zinc is unknown, different pathways in which it could be involved have been proposed, such as cell replication and migration (important role of zinc in the expression of the involved integrins), protein synthesis and cell repair. In addition, it has also been shown that topical zinc in wounds promotes autolytic debridement. This is due to the collagenase activity of the matrix metalloproteinases of which zinc is a cofactor. This benefit has been observed in pressure ulcers, diabetic foot and burns.1

On the other hand, zinc is also a cofactor of metalotioneins, antioxidant proteins that increase cellular resistance to apoptosis by having a protective effect against reactive oxygen species and bacterial toxins. Its anti-inflammatory effect is also associated with its regulatory action of macrophages and polymorphonuclear leukocytes.1

Although more studies are needed on its antimicrobial role, experimental studies have detected growth inhibiton of different bacterial species. However, resistance has been detected in certain strains, such as SAMR, and their ability to act on biofilms seems limited.1

The conclusion would be that, when zinc is applied directly on the wound and damaged perilesional skin, the elimination of non-viable tissue is promoted, the risk of superinfection decreases, inflammation is reduced and epithelialization is stimulated. If we take into account that these effects are what we look for in all our patients, it seems like an interesting treatment, doesn’t it?

 

What is the interest of the topical application route?

Oral zinc sulphate supplementation is essential for healing in zinc-deficient patients. If normal levels exist, the conclusion of a systemic review of six clinical trials including leg wounds (with small sample size and different limitations) is that there is no benefit over placebo.3

On the contrary, its topical application has shown improvement at experimental and clinical level in patients presenting with both deficit and normal serum levels.

 

Zinc oxide or zinc sulphate?

Although zinc oxide and low zinc sulphate concentration have anti-inflammatory effects, experimental studies comparing these two presentations have demonstrated benefit of zinc oxide in wounds. The advantages over zinc sulphate, which is a water-soluble compound, are due to the fact that it enables a sustained release of zinc avoiding cytotoxic levels. Zinc oxide appears to simulate the action of certain growth factors, in addition to increasing its release.1

It is important to emphasize the astringent effect of zinc sulfate, which we frequently use in very exudative lesions. Zinc sulphate should always be used at low concentrations, as high levels of zinc sulphate inhibit epithelialization and increase inflammation.

 

How is topical zinc absorbed?

Percutaneous zinc absorption depends on the integrity of the epidermal barrier and the amount of zinc transporters in the cell membrane of the keratinocytes. Topical application of zinc, as well as topical corticosteroids, increase the concentration of these transporters and, therefore, the absorption of zinc.

Absorption depends on the zinc concentration of the preparation and the vehicle. Zinc oxide, when in contact with a humid and acidic environment, is hydrolyzed and releases zinc ions, which are those that have biological activity (Zn 2+). These ions progressively penetrate into the deep layers of the skin. Therefore, the application of zinc oxide products with a vehicle that promotes humidity and acidity, preferably in occlusion, optimizes the absorption of this ion. This explains the interest of bandages with zinc paste (boot of Unna). On eczematous skin, a constant situation in venous ulcer patients, zinc paste bandages form a protective barrier that decreases skin inflammation.1

 

What do clinical trials conclude?

Randomised controlled experimental studies that have been conducted to assess the interest of zinc in wounds are scarce. In pressure wounds, diabetic foot wounds and burns, as mentioned above, specific studies have been carried out, which have shown their debridement role.1,2

Considering leg wounds, a randomized clinical trial with 113 patients with venous ulcers compares 3 treatment arms: zinc paste bandage, zinc stockings and a calcium alginate dressing.4 In all cases a highly elastic bandage was also used. The authors associate the faster healing obtained in the zinc bandage arm with the benefit of compression due to the stiffness of the bandage. However, the potential benefit of topical zinc cannot be excluded.

Therefore, well- designed clinical trials are needed to analyse the real clinical utility of topical zinc in patients with leg ulcers.

 

References:

  1. Lansdown AB, Mirastschijski U, Stubbs N, Scanlon E, Agren MS. Zinc in wound healing: theoretical, experimental, and clinical aspects. Wound Repair Regen. 2007 Jan-Feb;15(1):2-16. 
  2. Kogan S, Sood A, Garnick MS. Zinc and Wound Healing: A Review of Zinc Physiology and Clinical Applications. Wounds. 2017 Apr;29(4):102-106. 
  3. Wilkinson EA. Oral zinc for arterial and venous leg ulcers. Cochrane Database  Syst Rev. 2014 Sep 9;(9):CD001273. doi: 10.1002/14651858.
  4. Stacey MC, Jopp-Mckay AG, Rashid P, Hoskin SE, Thompson PJ. The influence of dressings on venous ulcer healing–a randomised trial. Eur J Vasc Endovasc Surg.  1997 Feb;13(2):174-9.

 

 

 

 

 

 

 

Why do we use so many alginate fibre sheets in our wound clinic?

Elena Conde Montero
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Why do we use so many alginate fibre sheets in our wound clinic?

The alginate fibre sheet is, without doubt, the most commonly used dressing in our wound clinic. We treat mainly leg ulcers, which are predominantly venous ulcers.

The idea of dedicating a blog post to our favourite dressing came to me during the recent 12th National Symposium on Pressure Ulcers and Chronic Wounds in Valencia (where, by the way, I enjoyed learning and sharing a lot). Many of you asked me about the dressings I usually use and I realized that our star dressing, despite being mentioned in several blog posts, was not the protagonist of any of them.

Before continuing, I would like to stress that the available evidence does not show superiority of any dressing over another in venous ulcers. Writing this entry is an opportunity to share the observations we made in our clinical practice.

Why is alginate fibre sheet our choice?

To understand this favourite condition, let’s start with some hints about biochemistry.

Alginate fibres are natural polysaccharides derived from brown algae (Phaeophyceae), formed by glucuronate and maluronate. These are biodegradable, biocompatible, non-immunogenic, non-toxic and economical biopolymers.1 Alginate has different applications in the textile, food, chemical and pharmaceutical industries due to its ability to form fibres and gels by adding calcium salts or other ions.2 Although this post is dedicated to alginate fibres in sheets or strips, this polymer can also be found among the components of other types of dressings, such as hydrogels. Its beneficial effect on healing, both haemostatic and absorbent, was discovered in the early nineteenth century, thanks to observations made by sailors, who usually used algae to cover their wounds. In fact, this practice of caring for wounds with brown algae was traditionally called “the sailor’s cure”1.

In the present day, alginate fibre dressings are widely used in very exudative wounds, as they have been shown to absorb large amounts of exudate, up to 20 times their weight.

Why do alginate fibre dressings present with absorbent and haemostatic power?

To answer this question, we must use linguistic purism. Although we usually refer to these dressings as “alginate”, the correct name would be “calcium alginate“. And these calcium ions (Ca2+), which are attached to the polysaccharide, are responsible for these two effects of the dressing.

Its high absorption power is due to the fact that the sodium ions (Na2+) present in the exudate are exchanged for calcium ions (Ca2+) from the dressing and, consequently, a sodium alginate gel is formed.2 This gel adapts to the wound surface, conveys growth factors and healing promoting cells, and continues to absorb exudate until it becomes saturated. The physicochemical properties of the formed gel depend on the proportion of glucuronate (G) and manuronate (M) contained in the alginate and the sequence of these carbohydrates in the polymer (consecutive M or G chains, or alternating MG).2 Dressings of alginate fibres rich in glucuronate make more resistant gels.

In our clinical practice, we use alginate sheets as a primary or secondary dressing. We normally cover the alginate sheets with gauze and, given that the absorption is horizontal, in very exudative wounds:

– We apply a 0.1% zinc sulphate solution (we soak compresses in this solution and keep them in the wound and perilesional skin for 10 minutes). See post “Why do we use topical zinc in perilesional wounds and skin?” 

– We place several sheets of alginate on top of each other (trying to make sure that the first ones do not exceed the surface of the wound).

– We protect the perilesional skin with a barrier cream.

– We increase the frequency of dressing changes.

The calcium present in the dressing is also responsible for its haemostatic property, as it behaves as a coagulation factor, mainly promoting platelet activation and aggregation.1

When making dressings, other ions can be added to calcium alginate fibres, such as silver, with its consequent antibacterial potential (see post: “Silver in skin wounds“).

What do the studies, guidelines and books say about the use of dressings with calcium alginate fibres?

Systematic reviews designed with the aim of comparing the benefit of different dressings in venous ulcers conclude that there is no evidence to suggest that any dressing is superior to the others in accelerating wound healing.3,4 However, the studies included in these reviews are few and of poor quality. Well-designed studies would therefore be needed to draw conclusions about the real impact of the use of the different wound dressings.

Given this lack of evidence, guidelines usually recommend that the dressing should be selected on the basis of exudate, perilesional skin, frequency of dressing changes, patient preferences and cost-effectiveness.5

And what do we find in the books? This is the most frequent list of indications for calcium alginate fibres:1

  1. Slightly bleeding wounds, due to their haemostatic power (e.g. after sharp debridement).
  2. Very exudative wounds, owing to their absorbent action.
  3. Wounds with an irregular wound bed, due to their capacity of adaption.

It is always highlighted that the frequency of dressing change will depend on the exudate. It is recommended that alginate fibres should not be used on wounds with little exudate and, if the sheet is dry and adhered to the wound bed, it should be moistened so that it gels and thus avoids a traumatic removal.

What does clinical experience tell us?

Our experience with the use of calcium alginate fibres in our clinics suggests that their interest is not limited to the indications traditionally given in the literature.

We use this dressing in any situation where we want to simulate a “physiological scab” to promote healing. More than one will be surprised by this statement, because many of you will have in mind the axiom: “scabs must always be removed”. Undoubtedly, the scab must be removed if either there is underlying pus when pressing or attempting to move the scab, or the crust is too thick and makes pressure on the wound bed or is easily detached. But wouldn´t acute wounds close with the formation of a scab that ends up coming off on its own, and if we remove it early healing may be delayed? Don’t forget that scabs are deposits of dry exudate and cellular debris that, in the absence of infection, behave like a protective layer that maintains optimal micro environmental conditions for healing.

Now we are going to talk about two applications in which daily clinical observation indicates that calcium alginate fibres are interesting:

  1. Superficial erosions and ulcers in the context of phlebolinfedema (chronic venous insufficiency and secondary lymphedema). These lesions are usually multiple and very exudative.

We usually apply medium strength corticoid cream on wounds and perilesional skin, covered with alginate, gauze and compressive bandage (See post “Venous insufficiency from a dermatological perspective“). If it is difficult to remove the remains of alginate fibres intermingled with the formed scabs, we leave them and wait till the next dressing change, when they are usually more easily detachable.

  1. Donor site (See post “Which dressing do I choose to cover the graft donor site?“) and punch graft recipient site (See post: “Types of grafts to cover chronic wounds: which one to choose“). In the following image I show the evolution of different wounds covered with punch grafts. Normally we space dressing changes 5-7 days. The photos of the upper row correspond to the first dressing changes and those of the lower row to the final stage of scab formation, with almost complete epithelialization.

Although these lesions can be covered with different atraumatic interfaces and alginate as a secondary dressing, experience tells us that alginate as a primary dressing is a good option from day one, since its fibres are intermingled with exudate rich in keratinocytes and growth factors, creating a scab that favours epithelialization. This yellowish-white material should not be removed between the grafts and in areas without optimal attachment. The calcium alginate sheet behaves like a matrix to convey the cells and growth factors that are present in that material. As we can see in the photos, the coloration of the grafts varies according to their attachment (the pinkish-purple ones are the ones that present greater angiogenesis). The success of the procedure lies in spacing dressing changes and cleansing the wound bed as little as possible during those changes so as not to modify the pro-healing microenvironment. Therefore, in cases of grafted wounds, the removal must be especially careful. If fibres remain adhered, we do not remove them and we wait for the formed scabs to come off in the following dressing changes.

In the following image we can see, ex vivo, an unused alginate sheet, a gelled sheet after wetting and the crusty appearance of the dressing after drying. As it is shown in the photos of the alginate sheets on the grafted wound (procedure carried out 7 days before), in order to remove the dressing adhered to the lesion, we moisten it with either faucet water or physiological serum and, once gelled, we can detach it en bloc.

If we use portable negative pressure therapy devices to promote graft attachment in complicated locations or situations (See post: “Punch grafts and negative pressure therapy: a successful couple“), we also tend to cover the grafted lesion with alginate sheets before placing the device.

Although the alginate is the protagonist of this entry, I have also mentioned the other main players in the practice, i.e., punch grafts, topical corticosteroids, negative pressure therapy and, of course, compression therapy.

References:

  1. Flanagan M. Principles of wound management. Wound healing and skin integrity. In: Flanagan M (ed) Wound Healing and Skin Integrity. Wiley-Blackwell, Oxford; 2013.
  2. Aderibigbe BA, Buyana B. Alginate in Wound Dressings. Pharmaceutics. 2018 Apr 2;10(2). pii: E42.
  3. Saco M, Howe N, Nathoo R, Cherpelis B. Comparing the efficacies of alginate,foam, hydrocolloid, hydrofiber, and hydrogel dressings in the management of diabetic foot ulcers and venous leg ulcers: a systematic review and meta-analysis examining how to dress for success. Dermatol Online J. 2016 Aug 15;22(8).
  4. O’Meara S, Martyn-St James M, Adderley UJ. Alginate dressings for venous leg ulcers. Cochrane Database Syst Rev. 2015 Aug 19;(8):CD010182.
  5. Franks, P., Barker, J., Collier, M. et al. Management of patients with venous leg ulcer: challenges and current best practice, J Wound Care, 25; 6, Suppl, 1–67.

Factitial ulcer: a silent cry for help

Elena Conde Montero
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Factitial ulcer: a silent cry for help

el grito munch

The mind and skin arise from the same embryonic layer, the ectoderm. This common origin helps to understand many skin disorders with associated psychological component, which can be classified into 3 subgroups:

  • Psychophysiological disorders: skin pathology exacerbated by psychological factors:
    • Psoriasis, atopic dermatitis, acne, urticaria, itching, alopecia
  • Primary psychiatric disorders: psychiatric syndromes with dermatological expression
    • OCD, Trichotillomania, factitial dermatitis, body dysmorphism, delirium parasitorum, glosodynia, vulvodynia
  • Secondary Psychiatric Disorders: Psychosocial impact of cutaneous disorders

In the field of skin wounds, psycho-dermatology plays an essential role.

On the one hand, the psychosocial impact of chronic skin wounds greatly limits the quality of our patients. There is a special interest in the validation of quality of life scales to quantify this impact, with the involved socio-economic costs.

On the other hand, and this is the topic on which we are going to focus today, there are the factitious lesions or dermatitis artefacta, which represent a diagnostic and therapeutic challenge, with a high consumption of time and resources.

Dermatitis artefacta includes a wide spectrum of skin lesions self-provoked by the patient, who denies his responsibility in their onset. The motivation for the production of these wounds is the satisfaction of an unconscious psychological need, usually the desire for medical care. Therefore, many times dermatitis artefacta can be framed in a Munchausen syndrome, in which the patient, repeatedly, causes lesions in different organs and seeks to be studied and treated in different hospitals. Frequently, these are patients with a history of child abuse, sexual abuse, personality disorder, depression, anxiety or impulse control disorder.

It must be differentiated from injuries produced by simulators, who also deny their authorship, but do so consciously to achieve a profit, usually economic or legal. In factitious disorders, motivation is unconscious.

There are few series in the literature on factitious dermatitis, as it is a diagnostic challenge . Available data suggest that it is more frequent in middle-aged women and patients with low sociocultural level. The clinical manifestation of these disorders varies according to the way in which the lesions are produced: excoriations (nails, cutting objects), blisters, scabs, panniculitis (injection of substances), eczema (irritants), hematomas, ulcers (sharp objects, caustic products). The attitude of the patients can give clues about the self-provocation of the lesions, from striking calm and complacency (belle indifference), to an excessive concern with angry signs.

Up to 30% of factitious dermatitis present as skin ulcers. These lesions “do not heal” despite adequate treatment. The morphology of these ulcers is peculiar, frequently with geometric edges and inexplicable evolution, with worsening associated with stressful moments. Sometimes other similar lesions occur in the periphery or in other locations,  which may be more acute or chronic, and they can give us clues about the type of mechanism used for their production (for example, burn with a caustic).

However, given that this is a diagnosis of exclusion, despite strong suspicion, a complete medical history and further tests must be carried out in order to rule out other pathologies that can lead to ulcers of a similar clinical appearance.

Differential diagnosis:

  • Venous leg ulcer
  • Occlusive Vasculopathy
  • Vasculitis
  • Tumour
  • Infectious process
  • Pharmacological cause
  • Pyoderma gangrenosum

Further tests:

  • Deep incisional biopsy:
    • Inflamed edge: H-E, Gram, special stains
    • Ulcer edge: culture (including atypical mycobacteria)
  • Blood tests:
    • CBC, biochemistry, proteinogram, autoimmunity
  • Imaging tests

In many cases, diagnosis is complicated and you never discover how the injuries occur. In fact, it is not uncommon to diagnose a factitial ulcer after it has been treated as an injury of another etiology, often pyoderma gangrenosum (which is another diagnosis of exclusion). A clue for diagnosis is improvement with exclusive treatment with occlusive dressings, without the possibility of manipulation. In order to achieve a close supervision, it is sometimes necessary to admit the patient. You can find an example of this diagnosis and treatment in this article: Factitious ulcer misdiagnosed as pyoderma gangrenosum.

This pathology requires a multidisciplinary approach, with fluid communication and agreement in the management between the different professionals. Diagnosis, follow-up and treatment must be carried out jointly by dermatology and psychiatry.

It is recommended to avoid direct confrontation, establish a doctor-patient trust relationship, and explore the psychological dimension through Socratic dialogue, with open questions. It should not be forgotten that the patient consults for a problem in the skin, not mental, and can often refuse psychiatric help.

Dermatitis artefacta treatment can be frustrating for the dermatologist. Since the unconscious gain of many patients is the receipt of medical care, their goal is not to be cured. It is frequent the appearance of new lesions or worsening of the previous ones when the moment of the discharge is near. Continuous follow-up should be planned to avoid these outbreaks.

The prognosis of these patients is poor, with a high percentage of recurrences and the possibility of autolytic attempts. We cannot forget the risk of infectious complications of these lesions and the potential iatrogenia when suspecting other diseases that require aggressive treatments, such as immunosuppression in the case of pyoderma gangrenosum.

When faced with a factitial ulcer, we always have more questions than answers.

If you want to go deeper into the subject of artefactal dermatitis, I recommend that you read this interesting review, with an excellent iconography: Dermatitis artefacta: a review.

 

What if we heal with music?

Elena Conde Montero
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0
What if we heal with music?

musicoterapia

Pain in a skin wound is triggered during dressing changes, which in some cases are daily. Dressing changes can become a real stress for our patients. It is not uncommon for them to develop maladaptive coping strategies, with significant associated anticipatory anxiety. This fear of pain causes them enormous suffering, alters doctor-patient relationship and, given that it will determine the intensity of debridement, can influence  healing time.

We will dedicate another post to talk about different conventional analgesic and anaesthetic strategies that we can use to improve the tolerance of dressing changes. However, many times the pharmacological treatment is not enough and it is necessary to increase the dose, with the consequent side effects, possibility of habituation and dependence. Therefore, a comprehensive approach to pain during treatment is necessary, with special attention to the management of associated anxiety. Today we are going to talk about a less traditional technique: music therapy.

Music therapy is the use of the effects of hearing or interpretation of sounds and melodies with psychotherapeutic objectives. There are different techniques and it may have applicability in multiple fields. It is possible to work on motor, cognitive, sensory and social-emotional skills.

Pain is multidimensional, with a sensory, cognitive and affective component. This cognitive-affective dimension is highly conditioned by previous painful experiences, their interpretation and anticipation. The environment, predominantly the relationship with healthcare professionals, has a great influence. The aim of the use of music in patients who have to undergo painful interventions is to achieve adequate relaxation, stress reduction and anxiety. Music, not its distracting effect, has a potential analgesic and anxiolytic effect.

Some studies have been published on the benefits of its use to reduce pain during treatment, mainly in burn units. The results are positive, with greater relaxation and less anxiety.1-3

Most of the proposed methods are active music therapy and involve training of the nursing staff by a music therapist. This would explain how to apply and sequence the different musical protocols, in combination with the use of images and relaxation techniques to optimise the focus on the music.

Although having the help of a music therapist would be ideal, the reality is that in most cases we do not have this possibility. However, the experience is also very good in wound units that use music during dressing changes without the intervention of a specialized therapist, selected by the patient (passive music therapy).4 If we associate relaxation (breathing) and distraction (talking to the patient) techniques with ambient music, we will enhance the benefit. Nowadays we have applications that allow us to select and listen immediately to the type of music we prefer. The patient will feel more autonomous, with more control, in a safe and familiar environment, if he can select the music he likes and distracts. On the other hand, music also has a positive effect on the work of healthcare professionals.

Francisca Martín, a dermatology nurse in Hospital Universitario Gregorio Marañón and great friend, with whom I began to do my first dressing changes during my residency,is very clear about it: with music, much better. So do I.

Referencias:

  1. Fratianne RB, Prensner JD, Huston MJ, Super DM, Yowler CJ, Standley JM. The effect of music-based imagery and musical alternate engagement on the burn debridement process. J Burn Care Rehabil. 2001;22(1):47-53.
  1. Prensner JD, Yowler CJ, Smith LF, Steele AL, Fratianne RB. Music therapy for assistance with pain and anxiety management in burn treatment. J Burn Care Rehabil. 2001;22(1):83-8.
  1. Fauerbach JA, Lawrence JW, Haythornthwaite JA, Richter L. Coping with the stress of a painful medical procedure. Behav Res Ther. 2002;40(9):1003-15.
  1. Protacio J. Patient-Directed Music Therapy as an Adjunct During Burn Wound Care. Crit Care Nurse. 2010; 30:74-76.

 

Platelet Rich Plasma in wound healing

Elena Conde Montero
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Platelet Rich Plasma in wound healing

Platelet rich plasma (PRP) is a widespread technique throughout diverse fields of Medicine for improving tissue regeneration. In dermatology, the main applications during the last years have mainly been anti-aging treatments and wound healing.

PRP contains platelets in higher concentration than whole blood and, consequently, represents a growth factor pool. Chronic wounds are characterized by a prolonged inflammatory phase, involving a continuous destruction of matrix proteins and growth factors.

Growth factors promote cell migration, proliferation and differentiation, which are essential for wound healing.

In this post, I provide you a review I have recently published including principles of PRP in wound healing and an updated critical assessment of the available clinical evidence: 

The following questions are raised in the review article:

  • Role of growth factors in wound healing
  • PRP and its clinical application in wound healing
  • Safety of PRP application in wounds
  • Clinical evidence of PRP as adjunctive treatment for chronic wounds

Moreover, I suggest you a treatment algorithm that may be useful in your clinical practice. (Conde Montero E (2016) PRP in Wound Healing, In Clinical indications and treatment protocols with Platelet-rich plasma in Dermatology. Barcelona, España. Ediciones Mayo)

What is your experience with PRP in wound healing?

 

Topical corticosteroids in chronic wounds

Elena Conde Montero
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0
Topical corticosteroids in chronic wounds

Why?

Many of the uses of corticosteroids in medicine are based on their anti-inflammatory power. This effect can be harmful in those clinical situations in which the inflammatory process needs to occur, such as in the first phase of healing of an acute wound.

As mentioned in previous entries, chronic ulcers are characterized by a prolonged inflammatory phase, characterized by increased cytokines and metalloproteases, with the consequent destruction of the extracellular matrix and decreased growth factors in the wound bed. Therefore, the use of topical corticosteroids, by reducing inflammation, could be beneficial in breaking this vicious cycle. However, the potential risk of infection associated with its application in a chronic wound, which usually has a high bacterial load, should be also taken into account.

 

How?

Although the use of topical corticosteroids is a widespread practice in the management of chronic skin ulcers, it stands out the lack of clinical trials that can support their efficacy and establish their indications.

Few case series have been published on the efficacy of corticotherapy in wounds with overgranulation. One of these is a multicentre prospective study published in 2007. Of the 34 patients treated, 27 (79%), over a three-month period, had benefited from topical corticosteroid use. The outcome variables collected were healing , reduction of exudate and reduction of granulation tissue.1

A retrospective study of chronic recalcitrant skin ulcers with excessive inflammation treated with a topical preparation containing a steroid (clobetasone butyrate 0.05%), antibiotic (oxytetracycline) and antifungal (nystatin) has recently been published. Healing rates were calculated for before and during this treatment period for each patient. Of the 34 ulcers treated, 24 showed accelerated healing, 3 had no changes, while 7 suffered a slowdown of the healing process.2 Among the limitations of this study, we should highlight the lack of a control group, the etiological variability of the lesions, the subjectivity to define an ulcer with excessive inflammation (inclusion criteria) and the lack of record of other dressings or compression therapy used.

In daily practice, it is common to use a moderate-high potency corticosteroid. We regularly use betamethasone dipropionate. On a thick layer of cream, depending on the exudate and the location of the wound, we usually place an interface dressing, sheet of calcium alginate or a foam. In cases of very exudative wounds, instead of applying the corticoid in cream form, we use its presentation in aqueous suspension, which we apply by soaked gauzes in each dressing change.

 

When?

As mentioned above, there are no consensual indications for the use of topical corticosteroids in wound healing. Its occasional use in cases of overgranulation is widespread. The published case series show encouraging results to extend its use in other recalcitrant chronic ulcers, which present with clinical data of excessive inflammation.

There is one type of wound in which topical corticosteroid is one of the first line treatments. This is pyoderma gangrenosum, a rare neutrophilic dermatosis characterized by the development of ulcers mainly in areas that have suffered damage (surgery, trauma, …). It may associate systemic diseases, such as inflammatory bowel disease, but up to 50% of cases are considered idiopathic. Systemic and topical corticosteroids are first line treatments, as they decrease inflammation, which is the cause of ulcers.3 If you want to read more about pyoderma gangrenosum, go to post “Pyoderma gangrenosum: a diagnostic and therapeutic challenge”.

 

References

  1. Cohen PR. Neutrophilic dermatoses: a review of current treatment options. Am J Clin Dermatol 2009;10:301–12.
  2. Bosanquet DC, Rangaraj A, Richards AJ et al. Topical steroids for chronic wounds displaying abnormal inflammation. Ann R Coll Surg Engl 2013; 95: 291–296.
  3. Hofman D, Moore K, Cooper R et al. Use of topical corticosteroids on chronic leg ulcers. J Wound Care 2007; 16: 227–230.

 

Interest of topical corticosteroid in Martorell ulcer

Elena Conde Montero
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Interest of topical corticosteroid in Martorell ulcer

Today I am going to talk about a treatment strategy that we normally use in our wound clinic, with excellent results, in the hypertensive ischemic ulcer of Martorell: medium-high potency corticosteroid + subsequent punch grafting.

I am delighted to reflect on this topic after having attended the session “Myths and realities in chronic wound management” at the Journées Dermatologiques de Paris 2017, in which reference was made to the usefulness of this interesting therapeutic approach.

I already commented in previous posts on the benefit of early grafting of these wounds to control pain, limit necrotic spread and promote re-epithelialization in the painful and rapidly progressive Martorell ulcer.

I would like to underline the interest of early grafting, even if the wound bed does not present with optimal characteristics (Read post: “Interest of early punch grafting in Martorell hypertensive ischemic ulcer”). Although not all punch grafts get to adhere, cells and growth factors that are released promote healing. In addition, this technique achieves pain reduction in the recipient site from the day of the procedure. It is not uncommon for us to require several sequential sessions of punch grafting until complete wound epithelialization is obtained. However, as it is a technique very well tolerated by the patient, repeated treatment does not represent a limitation in clinical practice. If you want to know more about punch grafting, go to “Types of skin grafts to cover chronic wounds: which one should you choose?”

 

And what is the role of topical corticosteroids here?

In the post “Topical corticosteroids in chronic wounds” I briefly reviewed the usefulness of topical corticoids in different clinical situations to promote healing thanks to their anti-inflammatory action. With regard to its use in Martorell ulcer, many experts recommend it, despite the scarcity of published studies to support this indication.

In 2003, a series of 7 patients admitted with Martorell ulcers in the progression phase, with necrotic wound bed and purpuric edges was published. They were treated for 1 week with a daily application of 0.05% clobetasol propionate cream on the wound bed and edges.1 The corticoid cream was applied in a thick layer and covered with petrolatum gauze. Pain was recorded using a visual analogue scale (VAS pain) during treatment and the following week. A significant pain reduction was found in the first 3 days in 5 patients, with reduction or even discontinuation of analgesic drugs in 3 of them. Within the first 15 days after beginning of treatment, the purpuric halo had faded and in 6 of them, necrosis had completely disappeared, without having performed sharp debridement.

Although this is an isolated series, with few patients and no control group, the results seem to me very interesting and coincide with our observations in our wound clinic. The application of topical corticosteroids in Martorell ulcer helps us to reduce inflammation, necrosis and allows us to improve the local conditions of the wound bed before grafting, without the need of previous aggressive surgical debridement.

 

What is your experience?

 

References:

  1. Carre D, Dompmartin A, Gislard A, Loree S, Faguer K, Verneuil L, Leroy D. [Benefit of topical steroids in necrotic angiodermatitis]. Ann Dermatol Venereol. 2003 May;130(5):547-8. 

 

 

 

Large leg wounds after mild trauma

Elena Conde Montero
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Large leg wounds after mild trauma

Large wounds secondary to mild trauma in the elderly are a frequent reason for consultation. The patient and his relatives describe very well the clinical evolution of the wound: “After a small blow with a chair … It started as a very small wound… It has grown rapidly”.

Normally these are wounds that at first have an insignificant clinical aspect, but progressively acquire a purplish or blackish colour and, in a few days, become extensive, deep and very painful wounds. In addition to age, these patients often have comorbidities such as hypertension or diabetes.

These are two wounds after mild trauma in women aged 86 and 79 respectively, both with well-controlled hypertension and diabetes.

 

 

This clinical description may have reminded you of Martorell hypertensive ischemic ulcer (See post: “Key elements to understand Martorell ulcer“). In fact, some of these post-traumatic lesions are Martorell ulcers, as they have the characteristics traditionally associated with this entity (typical lateral and posterior location on the leg, bilaterality, hypertension or diabetes mellitus). The rest of the wounds that do not meet the criteria included in the traditional Martorell definition, I like to call them “post-traumatic ulcers due to age-associated arteriolopathy”. Skin biopsy does not help to differentiate them because, if we look at them under the microscope, both types of wounds present occlusive subcutaneous arteriolosclerosis. The recent article “Cutaneous Arteriolosclerosis Is Not Specific to Ischemic Hypertensive Leg Ulcers “1 presents the results of a retrospective study comparing leg biopsy findings of patients with and without Martorell ulcer. The authors conclude that arteriolosclerosis present in both groups is associated with age and high blood pressure.

 

Let us get down to business. It seems that the available evidence suggests that the first cases described of Martorell ulcer, in patients with poorly controlled hypertension, could correspond to the pole with greater clinical (necrosis, pain and extension) and histological (arteriolosclerosis with greater hypertrophy of the wall secondary to poorly controlled hypertension) expressivity within the spectrum of “arteriolopathy ulcers in the context of age, hypertension and/or diabetes”.

Let’s clarify terminology and some physiopathology to understand what occurs under these arteriolopathic wounds.

 

What is arteriolopathy and arteriolosclerosis?

Arteriolopathy is the disease of the arterioles. Arterioles are blood vessels much smaller in diameter than the main arteries. They are found in peripheral tissues, such as the skin and subcutaneous cellular tissue, and branch out to the capillaries. They have a muscular layer that makes their lumen increase or decrease depending on the information that they receive through the autonomous innervation and molecular signals. Age, hypertension and diabetes favour the process known as arteriolosclerosis, which consists of the thickening and loss of elasticity of the arterioles walls, in some cases with the presence of calcifications, with the consequent reduction of their lumen. These findings can also occur in spite of an adequate control of arterial hypertension with pharmacological treatment.

 

What happens to the skin with arteriolopathy after trauma?

A wound secondary to trauma always has a first phase in which vasoactive substances are released to produce a vasoconstriction that limits tissue damage, bleeding and facilitates clot formation. To do this, arterioles limit the flow by contraction. After this vasoconstriction, an important vasodilation is produced with an increase in the permeability of the arterioles wall, so that cells (neutrophils, macrophages) and inflammatory molecules may reach the site of the lesion and the inflammatory phase begins.

In patients with arteriolopathy, that is to say, with less reactivity of the arterioles wall, calcifications and calibre reduction, this vasoconstriction may imply a compromise of tissue irrigation prolonged in time, with the consequent ischemia. Subsequent vasodilatation with release of inflammatory mediators increases necrosis (cell death), and here begins the vicious cycle of necrosis -inflammation.

 

What is the vicious circle of necrosis-inflammation?

At first, the extent of cell death depends on the duration and intensity of the ischemia during that initial vasoconstriction. Damaged cells release molecules that alert the body that an injury has occurred. These signals are pro-inflammatory, which intensify the first phase of the healing process (the inflammatory phase).2 This phase, characterized by hyperemia, plasma protein output from the capillaries and recruitment of leukocytes, is essential to ensure cleansing and protection against different pathogens (see post “Brief overview of wound healing“). However, if maintained over time, inflammatory mediators and cells produce uncontrolled destruction of cells (necrosis) and tissue (proteolytic activity) that promote wound chronicity. Therefore, it seems logical to think that in older patients in whom a rapid extension of the wound is observed after trauma, initial necrosis by prolonged vasoconstriction stimulates the inflammatory phase. Necrosis secondary to this inflammation would maintain the pro-inflammatory mediators with the consequent extension of the wound.

 

How do we stop this vicious cycle?

In order to stop the pathological cycle of necrosis-inflammation, an anti-inflammatory and neo-angiogenic strategy is ideal, so that tissue destruction is stopped and more oxygen may be provided to the wound. Topical corticosteroids and early punch grafting, which we commonly use in our clinical practice, could fulfill these functions. The benefit of both treatments has been published in Martorell hypertensive ischemic ulcer (See post: “The interest of the topical corticosteroid in Martorell’s ulcer“, “The interest of early punch grafting in Martorell ulcer“). Considering that Martorell ulcer and age-associated post-traumatic arteriolopathy share clinical aspects and both present arteriolosclerosis, lesions in the same spectrum could be considered to benefit from the same treatment.

After cleansing and debridement of the bed, in order to favour graft taking, we frequently use a single-use negative pressure therapy device (See post: “Punch grafting and negative pressure therapy: a successful couple“).

This is the evolution of the two progressive post-traumatic wounds with which we have begun this post. In the first case, after topical corticosteroid application and autolytic and sharp debridement, the wound was treated with punch grafts and negative pressure. Coverage with grafts was performed in two sessions, separated by one week (the central photo was taken after the second procedure), with complete epithelialization in less than 7 weeks. 

 

 

We did not wait until we had the optimal bed for grafting because, although in the first procedure there was no punch grafting, the pain decreased, necrosis was limited, the wound contracted and granulation tissue improved. With this improvement of the bed, the second procedure was able to be performed in better conditions in order to favour punch grafting and rapid complete epithelialization.

In the second case, the clinical appearance of the wound bed observed on the left image was obtained after the failure of an initial punch grafting procedure. After the second application of grafts and negative pressure therapy, we achieved complete graft taking. The third photo shows the clinical appearance 7 days after the procedure.

Before starting interventions to promote epithelialization, chronic venous insufficiency or peripheral artery disease must be ruled out. Whenever there is no contraindication, compression therapy, due to its anti-gravity and anti-inflammatory effect, will promote healing of these lesions.

Finally, it should be pointed out that in the case of a black-purplish wound in an older patient, which progresses rapidly, deep dissecting hematoma must be ruled out. As you can read in the post “Wounds secondary to dermatoporosis or chronic cutaneous insufficiency“, this hematoma, which is the most serious stage of skin fragility, requires drainage as early as possible to prevent the progression of necrosis secondary to ischemia.

 

References

  1. Monfort JB, Cury K, Moguelet P, Chasset F, Bachmeyer C, Francès C, Barbaud A, Senet P. Cutaneous Arteriolosclerosis Is Not Specific to Ischemic Hypertensive Leg Ulcers. Dermatology. 2018 Sep 10:1-4.
  2. Rock KL, Kono H. The inflammatory response to cell death. Annu Rev Pathol. 2008;3:99-126.

Pyoderma gangrenosum: a diagnostic and therapeutic challenge

Elena Conde Montero
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Pyoderma gangrenosum: a diagnostic and therapeutic challenge

Pyoderma gangrenosum is an inflammatory disease that leads to skin ulcers and its diagnosis and treatment can represent a real challenge for healthcare professionals.

Although it is not an infectious disease, the name pyoderma is maintained for historical reasons, since the hypothesis to explain the first cases described was that the lesions were secondary to an infection by organisms that produced pus (bacterial infection). The adjective gangrenous refers to the necrotic and destructive progression of the lesions.

And why is it a challenge? Essentially because we do not know many clues to understand the behaviour of this disease, it remains a diagnosis of exclusion and may be resistant to treatment.

As in order to diagnose a disease, clinical suspicion is the first step. Here we go!

Pyoderma gangrenosum typically occurs with the onset of single or multiple erythemato-violaceous pustules that rapidly progress to necrotic ulcers with an infiltrated purpuric rim. It can arise anywhere on the body. It may appear spontaneously or triggered by minor trauma or surgery.

Worsening of lesions following skin biopsy or surgical debridement of necrotic tissue is also typical. This hyper-reactivity is called pathergy phenomenon.

 

pioderma gangrenoso pierna

 

pioderma gangrenoso abdomen

It’s a rare disease. It is more frequent in middle-aged patients, 30-50 years, with a slight female predominance. In addition to the classic form, ulcerative, pyoderma gangrenosum may have a bullous, pustular or vegetative presentation.

Pyoderma gangrenosum is an entity characterized by uncontrolled activity of the immune system cells, predominantly neutrophils, with production of necrosis and skin ulcers. Therefore, it is included in the group of neutrophilic dermatoses. In up to 50% of cases there may be associated systemic involvement, such as inflammatory bowel disease, arthritis or lymphoproliferative syndromes.

 

Regarding differential diagnosis, it is necessary to consider other diseases that may have a similar clinical presentation. Although pyoderma gangrenosum has typical histological findings (neutrophilic inflammatory infiltrate), they are not pathognomonic and may vary depending on the evolution of the lesion over time. It is therefore a diagnosis of exclusion. This implies that misdiagnosis may occur with other diseases (it is estimated that this occurs in 10% of cases).

Although wound progression may occur after biopsy, this procedure is needed to rule out other aetiologies that require management other than pyoderma gangrenosum.

 

Pyoderma gangrenosum is treated with immunosuppressive drugs.

Prognosis is generally good, but recurrences are not uncommon.

Oral prednisone is considered the first line treatment. In cases requiring high doses of corticosteroids, or which do not respond satisfactorily, cyclosporine is recommended. In resistant lesions despite these immunosuppressive treatments, tumour necrosis factor alpha inhibitors (anti-TNF) may be an effective treatment alternative.

Now let´s go to the crucial point, how do we manage these wounds locally?

As in any wound, the use of dressings that promote healing in a moist environment is essential to facilitate autolytic debridement of necrotic and slough tissue, decrease pain, and enhance healing.

Treatment with local immunosuppressive drugs (corticoids or topical tacrolimus) will be indicated in superficial lesions or in patients with multiple comorbidities to avoid the risks of systemic immunosuppressive therapy. We already commented on this indication in the post “The role of topical corticosteroids in chronic skin wounds“.

Surgical debridement is contraindicated in these patients. However, when inflammatory activity has been controlled with adequate immunosuppressive therapy and the lesions are extensive, surgical debridement and skin graft coverage may be considered.

What is your experience with wounds secondary to pyoderma gangrenosum? Do you also consider it a diagnostic and therapeutic challenge?

 

Reasons for the hyaluronic acid boom in wound healing

Elena Conde Montero
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0
Reasons for the hyaluronic acid boom in wound healing

Hyaluronic acid is in vogue in the world of wound healing. And it seems that this privilege position will last long time. The key to understanding the beneficial role of this molecule in wound closure is given by the analysis of the foetal healing process. In the foetus, healing generally involves tissue regeneration, not tissue repair. The process is rapid, with no inflammatory phase and no scarring. This absence of inflammation is influenced by the composition of the extracellular matrix of the foetus, which is different from that of the adult. Hyaluronic acid, which is abundant in the foetal dermis because it degrades to a lesser extent. By inhibiting platelet aggregation, it produces a decrease in growth factors and inflammatory mediators in the wound.

In addition, hyaluronic acid plays an essential role in cell migration, proliferation and differentiation. Interesting, isn’t it? Let’s learn more about this promising molecule.

What is hyaluronic acid?

Hyaluronic acid is a polysaccharide found in different human tissues, including skin and soft tissues. It is a molecule with a high capacity to absorb water (hygroscopy) and form gels. Since the discovery in the 90s that the esterification (union with an alcohol) of hyaluronic acid helped to preserve its characteristics, it has been possible to design dressings that contain it in different presentations (gel, cream, sheet, matrix). The objective is that the products applied topically maintain the activity of hyaluronic acid, avoiding rapid enzymatic degradation in the wound bed. This high concentration of hyaluronic acid would simulate the environment of foetal healing, in which it is maintained at high levels until complete healing.

Role of hyaluronic acid in wound healing

In the proliferation phase to form granulation tissue, hyaluronic acid synthesized mainly by fibroblasts allows, within the framework of a temporary extracellular matrix, the diffusion of nutrients and the elimination of waste products. Hyaluronic acid facilitates the migration and proliferation of fibroblasts and keratinocytes, and represents a reservoir of growth factors. This is due to the ability of hyaluronic acid to absorb water, maintain wound moisture and limit cellular adhesion to extracellular matrix molecules. This matrix and fibroblasts maintain a bidirectional interaction, since fibroblasts participate in the synthesis and remodelling of the extracellular matrix and this modulates the activity of these cells. In addition, it has been demonstrated that degradation products of hyaluronic acid are pro-angiogenic. Subsequent remodelling of granulation tissue involves lowering hyaluronic levels and increasing the proportion of other proteoglycans and collagen to improve tissue resistance and elasticity.1

What do studies conclude about its benefit in wounds?

Different studies have shown, in vitro and in vivo, the beneficial role of hyaluronic acid in wound healing. In 2012, a systemic review2 was published, which collected clinical trials on the usefulness of hyaluronic acid derivatives in the treatment of a wide variety of wounds: burns (including radiodermitis), superficial surgical wounds (dermabrasion) and chronic wounds (venous ulcers and diabetic foot). Of the nine included clinical trials, which registered either complete healing or percentage wound size reduction, eight found differences in favour of hyaluronic acid compared with conventional therapies. The remaining study, which included 11 patients with wounds produced with dermatome to obtain a partial skin graft, found faster healing in wounds treated with pure glycerine than with hyaluronic acid. The wide range of n (sample size) of the studies analysed in the review (10-160 patients included), the variability of the product used and how it was applied, and the combination with other procedures (skin grafting) should be noted. In subgroup analysis according to wound aetiology, a significant acceleration of healing was detected in neuropathic ulcers treated with hyaluronic compared to other aetiologies.

It is important to point out that this review does not include studies evaluating the benefit of hyaluronic acid in combination with other active principles, which may also be interesting.

If we consider that a non-healing wound is a stagnant lesion in an abnormally prolonged inflammatory phase, it is interesting to continue researching and optimizing preparations with hyaluronic acid, for its known modulating action on inflammation in the normal healing process. But WATCH OUT! Like any local wound treatment, it must always be framed in a holistic anti-inflammatory strategy, in which the fundamental pillar is the appropriate etiological approach.

The surfing inspiration comes from Biarritz, one of my favourite destinations and where I have written this post.

 

References:

  1. Price RD, Myers S, Leigh IM, Navsaria HA. The role of hyaluronic acid in wound healing: assessment of clinical evidence. Am J Clin Dermatol. 2005;6(6):393-402.
  2. Voigt J, Driver VR. Hyaluronic acid derivatives and their healing effect on burns, epithelial surgical wounds, and chronic wounds: a systematic review and meta-analysis of randomized controlled trials. Wound Repair Regen. 2012;20(3):317-31. 

 

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About me

I'm from Coruña, although I live in Madrid, and I discovered my passion for wound healing during my Dermatology residency. I have trained in phlebology and geriatrics in Paris, focusing on leg wounds. I hope the information you find on the blog feels relatable, simple, and useful. I am very grateful for the trust of my readers and patients.

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