Materiały źródłowe

• #1 Friction blisters. Pathophysiology, prevention and treatment – PubMed

  https://pubmed.ncbi.nlm.nih.gov/8570998/

  Blisters occur frequently, especially in vigorously active populations. Studies using respective rubbing techniques show that blisters result from frictional forces that mechanically separate epidermal cells at level of the stratum spinosum. Hydrostatic pressure causes the area of the separation to fill with a fluid that is similar in composition to plasma but has a lower protein level. About 6 hours after formation of the blister, cells in the blister base begin to take amino acids and nucleosides; at 24 hours, there is high mitotic activity in the basal cells; at 48 and 120 hours, new stratum granulosum and stratum corneum, respectively, can be seen. The magnitude of frictional forces (Ff) and the number of times that an object cycles across the skin determine the probability of blister development – the higher the Ff, the fewer the cycles necessary to produce a blister.

• #2 Friction blisters – UpToDate

  https://www.uptodate.com/contents/friction-blisters/print

  Friction blisters are intraepidermal blisters that occur when epidermal injury results from repetitive shearing forces in the skin. […] Friction blisters result from shearing forces within the epidermis rather than simple rubbing of the epidermis. The fundamental components of the mechanism of blister formation are moving bone, high friction force (the force opposing the movement of one surface against another), and repetition of the resulting shear events. […] The shearing forces produce necrosis and dissociation of keratinocytes, leading to an intraepidermal split in the stratum spinosum. Hydrostatic pressure causes the area of separation to fill with fluid similar in composition to plasma but with lower protein levels. […] The magnitude of the frictional force and the number of passes of an object on the skin determine the likelihood of blister formation. Moist skin produces higher frictional forces than dry or wet skin, increasing the risk for blistering.

• #3 Blisters: Causes, treatments, and prevention

  https://www.medicalnewstoday.com/articles/264783

  A blister is a pocket of fluid between the upper layers of skin. The blister bubble is formed from the epidermis, the uppermost layer of skin. Its purpose is to protect and cushion the layers below. Blisters can be filled with serum, plasma, blood or pus depending on how and where they are formed. […] Blisters help prevent further damage to deeper tissues. […] The most common type of blister for most individuals is the friction blister. In their most basic form, they occur due to increased shear stress between the surface of the skin and the rest of the body. The layer of the skin most susceptible to shear forces is the stratum spinosum. As this layer tears away from the tissues below, a plasma-like fluid leaks from the cells and begins to fill the gap that is created. This fluid encourages new growth and regeneration. […] Painful blisters on the palm of the hands or soles of the feet are often caused by tissue shearing in deeper layers of the skin. These layers lie next to nerve endings, thereby producing more pain.

• #4 Friction blisters – UpToDate

  https://www.uptodate.com/contents/friction-blisters

  Friction blisters are intraepidermal blisters that occur when epidermal injury results from repetitive shearing forces in the skin. The most common sites of involvement are the hands, fingers, feet, and toes. Prolonged walking or running is a common inciting activity for friction blisters on the foot, whereas use of hand tools (eg, hammers, screwdrivers, shovels, etc) are associated with blisters on the hands. Unusually severe or frequent friction blisters may occur in the setting of underlying disorders of skin fragility. […] Friction blisters result from shearing forces within the epidermis rather than simple rubbing of the epidermis. The fundamental components of the mechanism of blister formation are moving bone, high friction force (the force opposing the movement of one surface against another), and repetition of the resulting shear events.

• #5 Blister – Wikipedia

  https://en.wikipedia.org/wiki/Blister

  Friction blisters are caused by excess shear stress between the bottom and surface of the skin and the body. The strata of skin around the stratum spinosum are most susceptible to shear. As the stratum spinosum tears away from the connecting tissues below, plasma from the cells diffuses out. This plasma solution helps new cells divide and grow into new connective tissues and epidermal layers. […] The clear fluid will be reabsorbed as new cells develop and the swollen appearance will subside. Painful blisters located on hands (palmar surface) and feet (plantar surface) are due to tissue shearing deeper in the epidermis, near nerve endings. Lower tissues are more susceptible to infection.

• #6

  https://link.springer.com/article/10.2165/00007256-199520030-00002

  Blisters occur frequently, especially in vigorously active populations. Studies using repetitive rubbing techniques show that blisters result from frictional forces that mechanically separate epidermal cells at the level of the stratum spinosum. Hydrostatic pressure causes the area of the separation to fill with a fluid that is similar in composition to plasma but has a lower protein level. […] The magnitude of frictional forces (Ff) and the number of times that an object cycles across the skin determine the probability of blister development the higher the Ff, the fewer the cycles necessary to produce a blister. […] More vigorous activity and the carrying of heavy loads during locomotion both appear to increase the likelihood of foot blisters. […] Recent exposure of the skin to repeated low intensity Ff results in a number of adaptations including cellular proliferation and epidermal thickening, which may reduce the likelihood of blisters.

• #7 Friction blisters – UpToDate

  https://www.uptodate.com/contents/friction-blisters

  Effects of shearing forces on the epidermis – The shearing forces produce necrosis and dissociation of keratinocytes, leading to an intraepidermal split in the stratum spinosum. Hydrostatic pressure causes the area of separation to fill with fluid similar in composition to plasma but with lower protein levels. […] Factors influencing the likelihood of blister formation – The magnitude of the frictional force and the number of passes of an object on the skin determine the likelihood of blister formation. Moist skin produces higher frictional forces than dry or wet skin, increasing the risk for blistering.

• #8 Friction Blisters: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1087613-overview

  Friction blister formation is affected by epidermal hydration. In a study of 11 men and 11 women, the friction between the inner forearm and a hospital fabric was measured in different hydration states. Increasing skin hydration caused sex-specific changes in the mechanical properties and/or surface topography, as the friction of female skin demonstrated significantly higher moisture sensitivity. […] The influence of epidermal hydration on the friction of human skin against textiles was studied. Increasing cutaneous hydration may cause sex-specific changes in the mechanical properties and/or surface topography of human skin, leading to skin softening and increased real contact area and adhesion. […] The friction blister forms with a split in the stratum spinosum. Midepidermal necrosis is evident. The blister roof consists of normal and necrotic keratinocytes; the blister floor consists of normal, edematous, and degenerating keratinocytes. The blister cavity is filled with a clear transudate. High mitotic activity is present in the base of the blister about 30 hours after formation of the friction blister. A significant inflammatory infiltrate is not observed as long as the blister site is not secondarily infected.

• #9 Friction blisters. Pathophysiology, prevention and treatment – PubMed

  https://pubmed.ncbi.nlm.nih.gov/8570998/

  Recent exposure of the skin to repeated low intensity Ff results in a number of adaptations including cellular proliferation and epidermal thickening, which may reduce the likelihood of blisters. Clinical experience suggests draining intact blisters and maintaining the blister roof results in the least patient discomfort and may reduce the possibility of secondary infection. Treating deroofed blisters with hydrocolloid dressings provides pain relief and may allow patients to continue physical activity if necessary. There is no evidence that antibiotics influence blister healing.

• #10

  https://www.jci.org/articles/view/24855

  Knowledge of the pathophysiology of immunobullous diseases has been advanced by the demonstration that passive transfer of antibodies against skin autoantigens can induce blisters in experimental animals with clinical, histologic, and immunopathologic features similar to those seen in human patients. […] The pathophysiology of blistering diseases illustrates how impairments in epithelial adhesion lead to disorders characterized by substantial morbidity and/or mortality. Blistering diseases can be inherited or acquired; most examples of the latter are autoimmune in nature and are characterized by autoantibodies that target adhesion junctions promoting either cell-cell or cell-matrix adhesion in skin. […] Patients with bullous pemphigoid (BP) and other autoimmune subepidermal blistering diseases have autoantibodies that target autoantigens in epidermal basement membrane.

• #11

  https://www.jci.org/articles/view/24855

  Translational research over the past 25 years has demonstrated that patients with pemphigus, BP, and other autoimmune blistering diseases have autoantibodies that target specific antigens in skin; that such autoantigens often represent components of adhesion junctions; and that mutations in genes encoding such proteins are responsible for inherited diseases characterized by skin fragility, blister formation, and/or ectodermal dysplasia. […] Passive transfer of experimental IgG directed against murine homologs of 2 human epidermal BM collagens, BP180 and type VII collagen, was used to develop animal models of BP and epidermolysis bullosa acquisita (EBA), respectively. […] The finding that MMP-9-deficient mice are resistant to anti-BP180 IgG has been explained by the observation that neutrophil-derived MMP-9 inactivates 1-proteinase inhibitor, which allows unrestrained activity of neutrophil elastase that degrades BP180 and produces subepidermal blisters in this experimental model.

• #12 Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome

  https://pmc.ncbi.nlm.nih.gov/articles/PMC151035/

  Bullous impetigo due to Staphylococcus aureus is one of the most common bacterial infections of man, and its generalized form, staphylococcal scalded skin syndrome (SSSS), is a frequent manifestation of staphylococcal epidemics in neonatal nurseries. […] Both diseases are mediated by exfoliative toxins (ETs), which show exquisite pathologic specificity in blistering only the superficial epidermis. […] We show that these toxins act as serine proteases with extremely focused molecular specificity to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381 between extracellular domains 3 and 4. […] The pathophysiologic basis of this specificity has been a mystery for over 30 years, even though recent crystal structure and amino acid sequences of ETA and ETB have suggested that they are atypical glutamate-specific serine proteases.

• #13

  https://www.jci.org/articles/view/15766

  Bullous impetigo due to Staphylococcus aureus is one of the most common bacterial infections of man, and its generalized form, staphylococcal scalded skin syndrome (SSSS), is a frequent manifestation of staphylococcal epidemics in neonatal nurseries. Both diseases are mediated by exfoliative toxins (ETs), which show exquisite pathologic specificity in blistering only the superficial epidermis. […] We show that these toxins act as serine proteases with extremely focused molecular specificity to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381 between extracellular domains 3 and 4. […] Thus, ETs, through specific recognition and proteolytic cleavage of one structurally critical peptide bond in an adhesion molecule, cause its dysfunction and allow S. aureus to spread under the stratum corneum, the main barrier of the skin, explaining how, although they circulate through the entire body in SSSS, they cause pathology only in the superficial epidermis.

• #14 Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome

  https://pmc.ncbi.nlm.nih.gov/articles/PMC151035/

  Here we demonstrate that ETA, ETB, and ETD act as glutamic acid-specific serine proteases with unusually focused specificity that results in a single cleavage of Dsg1, leading to its functional inactivation. […] The results we present here suggest that this border between ECs in Dsg1 is also critical for their proper function, since the cleavage of one peptide bond in this region causes dramatic dysfunction of this desmosomal cadherin. […] ETs cause blisters with pathology identical to those occurring in PF. […] Loss of function of Dsg1 by cleavage with ETs is also consistent with previous immunofluorescence experiments in which ETs cause cellular internalization and loss of cell surface staining of Dsg1. […] A major physiologic function of skin is to provide a barrier against infection. […] S. aureus, through the use of ETs, has evolved an efficient and extremely focused mechanism of proliferating and spreading under that barrier.

• #15

  https://www.jci.org/articles/view/15766

  The pathophysiologic basis of this specificity has been a mystery for over 30 years, even though recent crystal structure and amino acid sequences of ETA and ETB have suggested that they are atypical glutamate-specific serine proteases. […] Here we demonstrate that ETA, ETB, and ETD act as glutamic acid-specific serine proteases with unusually focused specificity that results in a single cleavage of Dsg1, leading to its functional inactivation. […] Taken together, the data in Figure 1 demonstrate that ETA, ETB, and ETD cleave hDsg1 at the same site, and that ETA cleaves mDsg1 at the homologous site. […] The observations that substitution of serine 195 with both cysteine and alanine inhibit cleavage, and that the mutant ETs still specifically bind Dsg1, demonstrate that serine 195 is necessary for efficient catalytic cleavage of Dsg1.

• #16

  https://www.jci.org/articles/view/15766

  ETs are serine proteases that specifically bind to and cleave Dsg1 at a unique site after a glutamic acid residue. […] The results we present here suggest that this border between ECs in Dsg1 is also critical for their proper function, since the cleavage of one peptide bond in this region causes dramatic dysfunction of this desmosomal cadherin. […] ETs cause blisters with pathology identical to those occurring in PF. Although ETs circulate throughout the body in SSSS, as do anti-Dsg1 antibodies in PF, blisters occur only in the superficial epidermis, not in the deep epidermis or in mucous membranes, identical to the findings in PF. […] Loss of function of Dsg1 by cleavage with ETs is also consistent with previous immunofluorescence experiments in which ETs cause cellular internalization and loss of cell surface staining of Dsg1. […] S. aureus, through the use of ETs, has evolved an efficient and extremely focused mechanism of proliferating and spreading under that barrier.

• #17 Signaling Dependent and Independent Mechanisms in Pemphigus Vulgaris Blister Formation | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050696

  Pemphigus vulgaris (PV) is an autoimmune epidermal blistering disease caused by autoantibodies directed against the desmosomal cadherin desmoglein-3 (Dsg3). […] Polyclonal PV IgG cause extensive clustering and endocytosis of keratinocyte cell surface Dsg3, whereas pathogenic mouse monoclonal antibodies compromise cell-cell adhesion strength without causing these alterations in Dsg3 trafficking. […] Our results reveal that the pathogenic activity of polyclonal PV IgG can be attributed to p38 MAPK-dependent clustering and endocytosis of Dsg3, whereas pathogenic monoclonal Dsg3 antibodies can function independently of this pathway. […] A major unresolved question is whether the loss of cell-cell adhesion triggered by pemphigus IgG is caused by direct inhibition of desmoglein cis or trans interactions (steric hindrance), by endocytosis of cell surface Dsg3, by the activation of cellular signaling pathways, or by some combination of these events.

• #18 Signaling Dependent and Independent Mechanisms in Pemphigus Vulgaris Blister Formation | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050696

  Several observations challenge the notion that pemphigus is caused by steric hindrance alone. […] One explanation that may reconcile these disparate observations is that polyclonal patient IgG disrupts adhesion by a different mechanism than pathogenic mouse monoclonal IgG or PV mAbs cloned from patients. […] We find that the polyclonal aspect of PV patient IgG is responsible for aberrant cell surface clustering and endocytosis of Dsg3, which occur in a p38 MAPK-dependent manner. […] These findings have important implications for designing model systems to study pemphigus pathomechanisms and for developing therapies to treat this devastating disease. […] Clustering and endocytosis of Dsg3 in response to polyclonal IgG was prevented by treating with either genistein or the p38 MAPK inhibitor SB202190. […] In summary, the results presented here demonstrate that the polyclonal nature of PV IgG contributes significantly to PV pathogenicity by causing clustering and endocytosis of Dsg3 through a p38 MAPK dependent mechanism.

• #19 Epidermolysis Bullosa: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1062939-overview

  Epidermolysis bullosa is a family of bullous disorders caused by an absence of basement membrane components due to underlying gene mutations. Epidermolysis bullosa is classified into four major categories: (1) epidermolysis bullosa simplex (intraepidermal skin separation), (2) junctional epidermolysis bullosa (skin separation in lamina lucida or central BMZ), (3) dystrophic epidermolysis bullosa (sublamina densa BMZ separation, as in the images below), and (4) Kindler syndrome (extremely rare, blistering at any level). […] Many stratified squamous epithelial tissues, such as the skin and oral mucosa, contain a complex basement membrane zone (BMZ). The BMZ is composed of many specialized components that combine to form anchoring complexes. At the superior aspect of the BMZ, keratin-containing intermediate filaments of the basal cell cytoskeleton insert on basal cell plasma membrane condensations termed hemidesmosomes.

• #20 Epidermolysis Bullosa: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1062939-overview

  Type VII collagen is the primary component of anchoring fibrils. Type VII collagen contains a large N-terminal globular domain (NC-1), which interacts with laminin-332 in the lamina densa; a long collagenous domain; and a smaller C-terminal globular domain (NC-2), which is cleaved proteolytically during anchoring fibril formation. […] Junctional epidermolysis bullosa has a highly variable molecular etiology and represents a collection of different diseases. These diseases all cause blistering in the lamina lucida and variable hemidesmosomal abnormalities. […] Dystrophic epidermolysis bullosa thus far has been associated in all cases with mutations of the gene coding for type VII collagen (COL7A1). Anchoring fibrils are affected in patients with dystrophic epidermolysis bullosa, and the degree of involvement ranges from subtle changes to complete absence.

• #21 Acute edema blisters in a hereditary angioedema cutaneous attack | Allergologia et Immunopathologia

  https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-articulo-acute-edema-blisters-in-hereditary-S030105460872545X

  Numerous skin diseases are characterised by the presence of blisters. […] Most of these diseases are associated with substantial morbidity and some of them can cause death. […] Acute edema blisters rarely develop in older patients presenting with acute cardiac insufficiency or renal failure, but they have not been described in hereditary angioedema, another very uncommon cause of acute and massive edema formation. […] Blisters in the context of acute edema have been named acute edema blisters or hydrostatic bullae. […] It has been suggested that acute edema blisters develop when capillary filtration rate exceeds lymphatic drainage and where tissue compliance is low and skin is lax, like in skin folds. […] The pathogenesis of the acute edema attacks of HAE is not completely known but recent data suggest that bradykinin is the most important mediator. […] The temporal association of edema and blisters in this patient, without bulla formation outside HAE attacks supports the diagnosis of acute edema blisters. […] To our knowledge, this is the first description of spontaneous edema blisters in HAE.

• #22 Coma blisters. A key to neurological diagnosis | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-articulo-coma-blisters-a-key-neurological-S2173580820301383

  Coma blisters are bullous skin lesions appearing in patients with low levels of consciousness. They were first described in 1812 by Larrey, a surgeon serving in the French army during Napoleon Bonaparte’s rule, in soldiers with carbon monoxide poisoning. […] Coma blisters are tense blisters appearing on healthy skin and/or erythematous macules and plaques in patients with impaired consciousness. Blisters vary in size, and may measure up to 45cm; their content is usually serous and rarely bloody. They usually appear 24 hours after initiation of drug treatment, and 48-72 hours after onset of coma. […] Coma blisters have traditionally been associated with overdose of CNS depressants, particularly barbiturates, tricyclic antidepressants, hypnotics, opiates, antipsychotics, and alcohol. Other less frequent scenarios include carbon monoxide poisoning; neurological conditions including cerebrovascular disease, head trauma, and viral encephalitis; and such metabolic alterations as hypoglycaemia, diabetic ketoacidosis, hypercalcaemia, and hepatic encephalopathy. Coma blisters have also been reported in non-comatose patients with severe neurological disease.

• #23 Coma blisters. A key to neurological diagnosis | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-articulo-coma-blisters-a-key-neurological-S2173580820301383

  In most cases, clinical findings are sufficient for diagnosis. In case of doubt, skin biopsy helps differentiate coma blisters from such other skin lesions as friction blisters and bullous drug eruptions. […] We initially suspected that our patient’s lesions were caused by drug toxicity secondary to a pathogenic mechanism similar to that associated with other drug-induced skin reactions. This hypothesis is supported by the fact that these lesions often appear in the context of sedative overdose; these drugs are normally excreted through the sweat glands, which are typically necrotic in biopsy studies. However, as we mentioned previously, not all cases of coma blisters are drug-induced. It seems clear that pressure, friction, and local hypoxia are also involved, since most lesions appear in pressure sites and show vascular damage without significant inflammatory infiltrate.

• #24 Coma Blister (Comma bullae, drug-induced coma blisters, barbiturate blisters, neurologic blisters) – Dermatology Advisor

  https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/coma-blister-comma-bullae-drug-induced-coma-blisters-barbiturate-blisters-neurologic-blisters/

  Be alert for an immoblized patient with bullae formation at pressure sites. […] Characteristic findings include blisters or bullae at sites of pressure. Normal skin develops erythematous patches or plaques about 24 hours after immobilization begins, which then progress into blisters within 48-72 hours. […] Histopathology reveals a subepidermal blister with eccrine gland necrosis. […] Coma blisters are caused by pressure leading to local hypoxia and necrosis. It was once believed to be associated with barbiturate overdose, by way of direct toxic affect on the eccrine glands leading to necrosis. […] Drug overdose remains a frequent predisposing factor for the formation of coma blisters, although coma blisters are no longer believed to be due to the toxic effect of the drug. […] This article discusses the history of coma blisters and presents seven cases to demonstrate that coma blisters are a result of pressure-induced ischemia and anoxia rather than direct toxic effect from a drug or other endogenous substance.

• #25 Coma blisters. A key to neurological diagnosis | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-articulo-coma-blisters-a-key-neurological-S2173580820301383

  Direct immunofluorescence usually yields negative results; however, some patients display immunoglobulin and complement deposition both in the walls of dermal vessels and in keratinocytes. However, these pathogenic mechanisms are not considered to be immune-mediated, but rather nonspecific. […] Therefore, our patient’s blisters can be attributed to coma secondary to a cerebrovascular event or to treatment (either CNS depressants or antiepileptics), in spite of the short treatment duration (2 days), or even to a combination of both factors. […] Coma blisters usually resolve spontaneously within 12 weeks, occasionally with residual scaling. In our patient, the lesions resolved within 2 weeks, with isolated blisters occasionally appearing until the patient regained consciousness. Frequent repositioning may help prevent and treat coma blisters. […] In conclusion, diagnosis of coma blisters is mainly clinical; the condition may be associated with underlying neurological disorders.

• #26 Herpes virus infection pathology

  https://dermnetnz.org/topics/herpes-virus-infection-pathology

  The histology of herpes infections is very distinctive. The low power pattern of a typical lesion is of an intraepidermal blister. The key feature is acantholysis with solitary keratinocytes within the blister cavity. Keratinocytes will show nuclear changes in viral infection. These included margination of the nuclear chromatin, multinucleation and nuclear inclusions. The viral inclusions are small pink deposits with a clear halo seen within the nucleus. When present in herpes virus infection and present with the other nuclear changes of this infection they are called Cowdry Type A inclusions. […] Early changes of vacuolation in the cytoplasm may be seen along the basal keratinocytes. As the cells swell and separate, the cytoplasm becomes eosinophilic, particularly notable in the multinucleated cells. The inflammatory infiltrate is mixed, predominantly lymphocytes and neutrophils with scattered eosinophils frequently seen. […] Blisters show intraepidermal vesiculation and acantholysis without nuclear inclusions or multinucleation.

• #27 Pre-operative management of fracture blisters: a systematic review in: EFORT Open Reviews Volume 10 Issue 3 (2025)

  https://eor.bioscientifica.com/view/journals/eor/10/3/EOR-2024-0074.xml

  Fracture blisters pose a significant challenge in clinical practice, leading to delays in surgery, suboptimal surgical approaches and complications in wound healing post-operatively. […] Currently, there is no consensus describing the optimal management of these blisters. […] This review challenges the conventional belief that fracture blisters are sterile, highlighting that the application of topical agents to the deroofed blister bed may expedite surgical readiness. […] Despite the pathogenesis of these blisters being well described, review of the literature reveals no consensus on pre-operative fracture blister management. […] The current literature indicates that these blisters are associated with an increased risk of wound breakdown and surgical site infection when incisions are made through the blister bed, especially in blood-filled blisters.

• #28 Pre-operative management of fracture blisters: a systematic review in: EFORT Open Reviews Volume 10 Issue 3 (2025)

  https://eor.bioscientifica.com/view/journals/eor/10/3/EOR-2024-0074.xml

  The findings from this review challenge the previously held dogma that these blisters are sterile, re-emphasizing that if present within the zone of injury, they should not be deroofed intra-operatively and skin incisions should not be made through them. Following deroofing, re-epithelialization occurs sooner in serous blisters compared to haemorrhagic ones and the time to surgical readiness can be improved if the blister bed is treated with a topical agent. Recent studies have reported favourable outcomes utilizing silver sulfadiazine antibiotic formulations for blister bed treatment, while one randomized controlled trial reported superior rates of time to surgical readiness with silver-impregnated fibrous hydrocolloid dressings. Further research with high-quality prospective randomized trials is advisable in order to confirm the best clinical management of fracture blisters while accounting for stratification and selection bias.

• #29

  https://link.springer.com/article/10.2165/00007256-199520030-00002

  Clinical experience suggests draining intact blisters and maintaining the blister roof results in the least patient discomfort and may reduce the possibility of secondary infection. […] There is no evidence that antibiotics influence blister healing. […] Considering the pervasive nature of friction blisters, there is a substantial amount of basic and applied research that remains to be performed, especially in the areas of prevention and treatment.

• #30 Foot Blisters and Toe Blisters (And What To Do About Them) | PediFix®

  https://www.pedifix.com/t-blisters.aspx?srsltid=AfmBOorntwnXmlIb_wa-6KXoR5uYG7egDTZjLjOxz9loFmgtUAfnMXUx

  A blister on your toe or foot is a collection of fluid underneath the top layer of the skin (the epidermis). […] It is a defense mechanism, or „natural bandage”, created by the body to help repair damaged skin. […] Friction is the most common cause of a blister on the foot or toes. When skin constantly rubs against another surface, tearing the upper layers of the skin and filling the injured area with fluid. […] Common causes of blisters on feet from shoes or hosiery occur because they do not fit properly. Other causes of blisters include burns, allergic reactions, infections or autoimmune disorders. […] Ideally, you should not pop a toe or foot blister. […] When the wound is left intact, the fluid sealed inside the foot blister will soothe the bottom layer of the damaged skin. This will keep it moist while the area heals naturally. In addition, a closed wound is less likely to get infected. […] If the wound becomes additionally painful, reddened, secretes colored pus, develops yellow crusting or does not show signs of healing after a few days, consult a medical professional for additional advice.

• #31

  https://journals.lww.com/acsm-csmr/fulltext/2020/11000/exploring_the_mechanism_for_blister_prevention.5.aspx

  Moleskin is a commonly used material in podiatry and sports medicine for blister prevention and treatment. Common understanding regarding its protective mechanism is reduction of friction at the interface between the foot and the sock/shoe. We argue that moleskin may actually increase friction at this interface, but nonetheless prevents blisters by dispersing shear load within the skin across a wider surface area, reducing potential for skin damage. […] However, it is our opinion that moleskin is often incorrectly used. This is because of a fundamental misunderstanding of moleskin’s protective mechanism. Most users and prescribers of moleskin assume that it reduces friction. However, it is our professional opinion that moleskin may actually increase friction levels. […] In considering friction in the context of moleskin, it can be defined as the resistance to the movement of one surface across another. High friction levels yield more resistance, whereas low friction levels yield less resistance. High friction levels cause higher shear distortions within the skin, which is the ultimate cause of blisters. Low friction levels cause low shear distortions and, therefore, reduced chance of blisters.

• #32

  https://journals.lww.com/acsm-csmr/fulltext/2020/11000/exploring_the_mechanism_for_blister_prevention.5.aspx

  Despite the clear evidence against moleskin as a significant friction reducer, there is no doubt moleskin provides relief for some people’s hot spots and blisters. If not from friction reduction, from where does this relief derive? […] It is our professional opinion that moleskin works by spreading shear load across a larger area of skin, similar to the mechanism of athletic tape. […] We hope this has been a sufficient illustration to suggest that the mechanism by which moleskin prevents blisters is not by reducing friction, but by spreading shear load across a larger surface area of skin.

Zobacz więcej