Presentando un caso intrigante di vesciche dolorose recalcitranti e porpora in un paziente con comorbilità multiple, questi autori discutono del lavoro del paziente, dei test diagnostici e dell’importante ruolo della valutazione multidisciplinare.
Il metotrexato è un farmaco anti-metabolita che agisce come analogo dell’acido folico per inibire la sintesi del DNA. Inizialmente, i medici utilizzavano il metotrexato esclusivamente per il trattamento della leucemia pediatrica, ma il farmaco è stato successivamente approvato per la psoriasi, l’artrite reumatoide, la dermatite atopica e la malattia vascolare del collagene. 1,2
Sebbene il metotrexato sia efficace, ci sono effetti collaterali comuni che includono anomalie epatiche, nausea, soppressione del midollo osseo e problemi gastrointestinali. 3 Secondo quanto riferito, gli effetti collaterali meno comuni includono eruzioni cutanee vescicole, necrosi cutanea ed erosione di placche psoriasiche preesistenti. 4,5 Quando si tratta di estremità inferiore, la vescica e la porpora non sbiancabile sono segni clinici di tossicità da metotrexato. 4-7
Questo caso clinico evidenzia un caso di un paziente, che inizialmente si è presentato a un centro traumatologico di Livello I per dolore bilaterale, gonfiore e formazione di vesciche ai suoi piedi. Questo caso sottolinea l’importanza di un’anamnesi approfondita e di un esame fisico per una diagnosi e un trattamento adeguati di una condizione rara.
Uno sguardo più attento all’allenamento per un paziente con dolore acuto, aggravante, gonfiore e vesciche di entrambi i piedi
Un maschio di 61 anni con diverse comorbidità, tra cui artrite reumatoide, ipertensione, malattia coronarica e cancro alla prostata, si è presentato in ospedale con una storia di due giorni di peggioramento del dolore, gonfiore e formazione di vesciche ai piedi bilaterali. Il paziente non aveva una storia precedente di questa vescica e non ha riportato una storia di traumi. Tentò di alleviare il dolore immergendo i piedi nell’acqua calda senza miglioramenti significativi.
Il paziente ha avuto un completo workup al momento del ricovero in un altro ospedale qualche mese prima per neutropenia e trombocitopenia. L’allenamento includeva una biopsia del midollo osseo, che era negativa per la malignità. A causa della soppressione del midollo osseo del paziente, i fornitori dell’altro ospedale hanno interrotto la sua malattia modificando i farmaci anti-reumatici (DMARD), ma il paziente ha riavviato i farmaci da solo dopo questo ricovero senza che il medico lo sapesse.
Quando il paziente si presentò al pronto soccorso alcuni mesi dopo, la sua diagnosi iniziale fu una vescica acuta bilaterale al piede secondaria a ustioni basata sulla storia dell’immersione in acqua calda. Il team di chirurgia plastica ha valutato il paziente nel pronto soccorso e il paziente è stato successivamente dimesso con sette giorni di doxiciclina orale. Tuttavia, il paziente è tornato due giorni dopo con un peggioramento dei sintomi e dati anormali di laboratorio rispetto alla visita iniziale al pronto soccorso.
Al momento del ricovero, la conta dei globuli bianchi del paziente era di 2,6 x10 3 cellule per mm 3 , la sua conta piastrinica era di 81 x 10 3 per mm 3 , l’emoglobina era di 9,4 g / dl e il volume corpuscolare medio (MCV) era di 98,4 fL. La nostra preoccupazione immediata e urgente per questo paziente era la fascite necrotizzante. Il team di chirurgia generale ha escluso questo processo di malattia sulla base dei risultati clinici e ha raccomandato che la chirurgia plastica rivalutasse il paziente.
Con una seconda occhiata, il team di chirurgia plastica non ha avuto ulteriori raccomandazioni oltre a raccomandare la cura della ferita locale e la valutazione podologica. Dopo aver valutato il paziente, il team podiatrico ha notato porpora non blanchable e formazione di vesciche con drenaggio sieroso, ma non ha apprezzato i segni di infezione acuta o malattia vascolare (vedere le prime due foto sopra). I team di podologia e dermatologia hanno entrambi concordato sulla necessità di una biopsia del punch e i risultati hanno dimostrato emorragia subdermica e infiammazione cronica. I risultati del test hanno anche escluso condizioni gravi come la sindrome di Stevens-Johnson, il pemfigo volgare e il pemfigoide bolloso.
Per quanto riguarda ulteriori test diagnostici, un angiogramma di tomografia computerizzata ha rivelato il deflusso di tre vasi al piede, che escludeva la malattia vascolare periferica. Gli ultrasuoni duplex venosi degli arti inferiori hanno escluso la trombosi venosa profonda. Dato che la diagnosi non era ancora chiara a questo punto, il paziente è stato sottoposto a malattia infettiva, ematologia e reumatologia per ulteriori valutazioni e input.
Dopo aver ottenuto e rivisto uno striscio di sangue periferico, l’ematologia ha notato l’anisocitosi con ovalociti, poikilocitosi, cellule lacrimali sparse e alcuni granulociti ipersegmentati (vedere le ultime due immagini sopra). Sulla base del processo megaloblastico, il team ha stabilito che ciò potrebbe essere secondario alla tossicità del metotrexato. La reumatologia ha suggerito l’uso dell’acido folinico (noto anche come leucovorina) come trattamento empirico per la vasculite poiché il farmaco può fornire un trattamento indiretto della tossicità del metotrexato se ciò si dimostra la causa.
Con il trattamento, la citopenia è migliorata insieme al sollievo immediato dal dolore dei piedi bilaterali del paziente. Sulla base del trattamento con leucovorin, i team hanno concluso che questa porpora non sbiancabile dei piedi era effettivamente secondaria alla tossicità del metotrexato. Il paziente ha quindi iniziato il prednisone orale 70 mg al giorno e ha interrotto il metotrexato. Fu dimesso dall’ospedale in condizioni stabili e con un appuntamento di follow-up programmato con reumatologia.
Un paziente può presentare tossicità da metotrexato sotto forma di nausea, soppressione del midollo osseo e anomalie epatiche. Tuttavia, secondo quanto riferito, l’eruzione cutanea della vescica è meno comune in letteratura. 7In questo caso di un maschio di 61 anni con porpora inspiegabile a pedale bilaterale inspiegabile, i sintomi non erano diretti a una diagnosi ovvia. Durante il corso in ospedale del paziente, diversi team di consulenti lo hanno valutato per i bassi livelli di cellule del sangue e per le vesciche inspiegabili. I risultati della biopsia del punzone hanno guidato la diagnosi verso la tossicità del metotrexato. Il trattamento successivo con leucovorin per via endovenosa ha portato a un significativo miglioramento della sua neutropenia e trombocitopenia. I medici curanti hanno consigliato al paziente di interrompere l’assunzione indefinita di metotrexato e hanno programmato un attento follow-up con il paziente in regime ambulatoriale.
Questo caso dimostra l’importanza di una storia approfondita e di un esame fisico per una valutazione completa della patologia poco chiara. Mentre i podologi vedono comunemente ischemia periferica, congelamento e ustioni, questa presentazione clinica unica e il case work up forniscono l’intuizione e l’importanza di ampi differenziali per il trattamento ottimale e gli esiti dei pazienti.
Nessuno studio ha riportato stime del carico globale sulla disabilità per le complicanze individuali degli arti inferiori associate al diabete (DRLEC). Lo studio Global Burden of Disease (GBD) offre una solida opportunità per colmare questa lacuna.
PROGETTAZIONE E METODI DI RICERCA Sono stati utilizzati dati GBD 2016, tra cui prevalenza ed anni vissuti con disabilità (YLD), per i DRLEC di neuropatia diabetica, ulcera del piede e amputazione con e senza protesi. Il GBD ha stimato la prevalenza utilizzando i dati delle revisioni sistematiche e DisMod-MR 2.1, uno strumento di meta-regressione bayesiana. Gli YLD sono stati stimati come il prodotto delle stime di prevalenza e dei pesi di disabilità per ciascun DRLEC. Abbiamo riportato stime globali e per sesso, età, regione e nazione per ciascun DRLEC per il 1990 e il 2016.
RISULTATI Nel 2016, circa 131 milioni (1,8% della popolazione mondiale) avevano DRLEC. Si stima che 16,8 milioni di YLD (2,1% di YLD globali) siano stati causati da DRLEC, di cui 12,9 milioni (intervallo di incertezza del 95% 8,30-18,8) solo per neuropatia, 2,5 milioni (1,7-3,6) da ulcere del piede, 1,1 milioni (0,7-1,4) dall’amputazione senza protesi e 0,4 milioni (0,3-0,5) dall’amputazione con protesi. I tassi YLD standardizzati per età di tutti i DRLEC sono aumentati tra il 14,6% e il 31,0% dalle stime del 1990. I rapporti YLD maschio-femmina variavano da 0,96 per la neuropatia solo a 1,93 per le ulcere del piede. La fascia d’età di 50-69 anni rappresentava il 47,8% di tutti gli YLD dei DRLEC.
CONCLUSIONI Queste prime stime globali suggeriscono che i DRLEC contribuiscono in modo ampio e crescente all’onere della disabilità in tutto il mondo e colpiscono in modo sproporzionato i maschi e le popolazioni di mezza età. Questi risultati dovrebbero consentire ai responsabili politici di tutto il mondo di indirizzare le strategie alle popolazioni colpite in modo sproporzionato dai DRLEC.
Recently, the function of nanofiber membranes prepared from electrospinning in accelerating wound healing has attracted wide attention. In this study, novel nanofiber membranes consisted of cellulose acetate (CA) and zein were fabricated to provide efficient delivery vehicles for sesamol, then the effect of sesamol-loaded composite nanofiber membrane on the wound healing process for diabetic mice was studied. It was found the critical concentration of CA was between 15% and 25% (w/v), and the most suitable concentration of stabilizing fibers was 22.5%. When the CA/zein ratio was 12:8, the fiber obtained the small diameter and uniform distribution, the stable intermolecular structure, the low infiltration speed and high stability in water. The composite nanofiber membrane with high-dose sesamol (5% of total polymer concentration, w/w) promoted formation of myofibroblasts by enhancing TGF-β signaling pathway transduction, and promoted keratinocyte growth by inhibiting chronic inflammation in wounds, thus enhancing wound healing in diabetic mice. This study could further broaden the application range of sesamol, CA and zein, and provide reference for the design and development of new wound dressings in the future.
Materiali medicazione sono ampiamente utilizzati per proteggere le ferite dall’esterno dell’ambiente e per promuovere la ferita guarigione. Tuttavia, le medicazioni per ferite convenzionali mancano di proprietà adesive dei tessuti e di funzioni antinfiammatorie, che portano a fibrosi e stenosi, in casi come ferite gastrointestinali dopo chirurgia endoscopica. Nel presente studio, riportiamo le proprietà adesive e antinfiammatorie dei tessuti di una medicazione composta da particelle di gelatina modificate con corticosteroidi. L’idrocortisone (HC), che è una classe di corticosteroidi antinfiammatori, è stato usato per modificare la gelatina di pollock dell’Alaska (ApGltn) per sintetizzare l’ApGltn modificato con HC (HC-ApGltn). Le microparticelle (MP) di HC-ApGltn sono state fabbricate aggiungendo etanolo in soluzione acquosa HC-ApGltn ed eseguendo la reticolazione termica (TC) senza l’uso di tensioattivi tossici e reagenti di reticolazione. La modifica di ApGltn con HC idrofobo contenente la struttura della spina dorsale del colesterolo ha migliorato la sua forza di adesione ai tessuti sottomucosi gastrici in condizioni umide a causa di interazioni idrofobiche. Questa ritenzione della proprietà adesiva in condizioni di bagnato consente una protezione stabile delle ferite dall’ambiente esterno. Abbiamo scoperto che gli MP di HC-ApGltn sono stati ripresi dai macrofagi e hanno efficacemente soppresso i cambiamenti morfologici dei macrofagi attivati da LPS e il livello di espressione della citochina infiammatoria. Adesivi per tessuti robusti e MP anti-infiammatori possono servire da medicazione avanzata in grado di proteggere le ferite e sopprimere le risposte infiammatorie per promuovere la guarigione delle ferite. Questa ritenzione della proprietà adesiva in condizioni di bagnato consente una protezione stabile delle ferite dall’ambiente esterno. Abbiamo scoperto che gli MP di HC-ApGltn sono stati ripresi dai macrofagi e hanno efficacemente soppresso i cambiamenti morfologici dei macrofagi attivati da LPS e il livello di espressione della citochina infiammatoria. Adesivi per tessuti robusti e MP anti-infiammatori possono servire da medicazione avanzata in grado di proteggere le ferite e sopprimere le risposte infiammatorie per promuovere la guarigione delle ferite. Questa ritenzione della proprietà adesiva in condizioni di bagnato consente una protezione stabile delle ferite dall’ambiente esterno. Abbiamo scoperto che gli MP di HC-ApGltn sono stati ripresi dai macrofagi e hanno efficacemente soppresso i cambiamenti morfologici dei macrofagi attivati da LPS e il livello di espressione della citochina infiammatoria. Adesivi per tessuti robusti e MP anti-infiammatori possono servire da medicazione avanzata in grado di proteggere le ferite e sopprimere le risposte infiammatorie per promuovere la guarigione delle ferite.
Using maggots to treat wounds dates back to 1931 in this country. Until the advent of antibiotics in the 1940s, maggots were used routinely. In the 1980s, interest in them revived due to the increasing emergence of antibiotic-resistant bacteria.
At Select Specialty Hospital Houston in Texas, we recently decided to try maggot therapy for a patient with a particularly difficult wound. In this case study, we share our experience.
About the patient
Mr. Green, age 52, had a history of diabetes, which led to bilateral below-the knee amputations. His medical history also included coronary artery disease, peripheral arterial disease, and anemia.
Alert and oriented, he was able to give a detailed account of his recent wound. On August 12, 2015, Mr. Green cut the distal tip of his right third finger while preparing food. Having already lost his legs, he was concerned about the possible need for another amputation, so he made an appointment to see his primary care physician. The physician instructed him to keep his finger clean and dry and to observe it. Nonetheless, it became infected and his finger had to be amputated at the base on September 11. A week later, he was admitted to an acute-care hospital for pain, swelling, and erythema. He received I.V. antibiotics along with pulsed lavage, treatment with Arobella Medical’s Qoustic Wound Therapy System™, ultrasound, and finally, negative-pressure wound therapy (NPWT).
When Mr. Green was admitted to our long-term acute care hospital, the wound bed was pale pink with the hazy, gelatinous look associated with high bioburden tissue, although no bacteriologic testing was done. (See About biofilm.) The wound measured 5 cm x 3.2 cm x 0.9 cm, and lacked the cobblestone appearance usually seen with recently discontinued NPWT.
Based on the difficulty of healing this wound, we decided Mr. Green was a good candidate for maggot therapy, which we’d been wanting to introduce into our facility. Mr. Green and his family were concerned about his lack of healing and eager to try maggot therapy. We selected maggots contained within mesh bags because nurses were reluctant to handle free-range ones. (See Maggot application options.)
Applying the maggots
With Mr. Green’s consent, 10 clinical staff members attended the first day of maggot therapy, when the maggot-therapy containment dressing was applied to the wound. Most were surprised to learn that larvae don’t have teeth in their mouths and don’t bite. Instead, they score the wound surface with their mandibles and secrete an enzyme that liquefies the microbes, which they then ingest. The excess fluid is absorbed by the upper dressing.
Applying the containment dressing took 5 minutes. Then zinc oxide cream was rubbed into the periwound skin to protect it from moisture damage and the bag containing the maggots was placed where it contacted the wound bed. Wound location made this a bit difficult, but we managed it by placing multiple pieces of fluffed saline moist gauze on top of the bag and wrapping it firmly with a sterile gauze bandage.
Changes in the wound bed
After 24 hours, the wound bed was predominately a beefy red color and the dressing was saturated. What we’d assumed was slough in the bed actually was a tendon; striae were clearly visible and the surface had a shiny cream color. After 3 days of maggot therapy, the wound bed consisted entirely of moist red granulation tissue. Mr. Green experienced some pain, as would be expected with a wound proximal to nerves in the hand. We also suspected the biofilm had been coating and protecting the nerves until this time, so we chose to remove the maggots with the understanding that the biofilm should have been eradicated.
Additional therapy Mr. Green then underwent NPWT for 1 week, after which antibiotic ointment, petrolatum gauze, and sterile gauze were applied daily until discharge. He was discharged November 25, 2015 with an appointment to see a plastic surgeon to evaluate him for a planned skin graft; at discharge, the wound measured 1.6 cm x 2.5 cm x < 0.1 cm. The plastic surgeon told Mr. Green he’d need no further treatment.
Broadening the treatment options
Engaging other staff members and encouraging them to attend dressing changes contributed to the success of this first use of maggot therapy in our facility. After the first dressing change, Mr. Green’s wound improvement was so dramatic that it made a vivid impact on staff. This motivated them to discuss the results with their coworkers. Soon, staff from other disciplines began to approach me with questions and ask if they could attend the next scheduled dressing change.
Thanks to the success of our experience, we introduced maggot therapy throughout the Select Specialty Hospitals’ network of facilities in January 2016. Since then, we’ve treated at least a dozen patients.
Sally Anne Jewell is manager of wound care at Select Specialty Hospital Houston in Texas. (Mr. Green’s name in the case study was fictitious.)
Silver Antimicrobial Wound Dressings are a relatively new family of advanced wound care dressings for the treatment of infected wounds. A silver dressing is a wound dressing impregnated with ionic silver. The ionic silver is responsible for the antimicrobial activity against infection caused by bacteria.
The report forecast global Silver Antimicrobial Wound Dressing market to grow to reach xxx Million USD in 2019 with a CAGR of xx% during the period 20202025.
The report offers detailed coverage of Silver Antimicrobial Wound Dressing industry and main market trends. The market research includes historical and forecast market data, demand, application details, price trends, and company shares of the leading Silver Antimicrobial Wound Dressing by geography. The report splits the market size, by volume and value, on the basis of application type and geography.
First, this report covers the present status and the future prospects of the global Silver Antimicrobial Wound Dressing market for 20152025.
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Market Overview, Development, and Segment by Type, Application Region
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AsiaPacific Market by Type, Application Geography
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Company information, Sales, Cost, Margin etc.
Market Segment as follows:
AsiaPacific[China, Southeast Asia, India, Japan, Korea, Oceania]
Europe[Germany, UK, France, Italy, Russia, Spain, Netherlands, Turkey, Switzerland]
North America[United States, Canada, Mexico]
Middle East Africa[GCC, North Africa, South Africa]
South America[Brazil, Argentina, Columbia, Chile, Peru]
With the ongoing increase in available wound care products and services, this author discusses how to approach coding for these complex cases.
Wound care is a large part of many podiatry practices today. There has been an explosion of wound care products and techniques that we may utilize in trying to treat the stubborn wounds we deal with on a day-to-day basis. Unfortunately, with the increased volume and cost of these items comes increased scrutiny of how and when we use these products and services. It is important to understand the most common aspects of billing and coding for wound care in order to succeed for both your practice and your patients.
Wounds can be very complicated with frequent and ongoing reevaluation of treatment outcomes. Some wounds go on to heal with simple measures and we are primarily monitoring progress until healing is eventually complete. These two scenarios differ from one another when considering proper coding. When billing an evaluation and management service (E&M) at the same encounter for which you are billing a procedure (such as debridement), there must be a significant and separately identifiable E&M service from the procedure in order to be paid for both services. This would require taking a history, performing an examination and then eventual decision-making. These three key components are the basis for an E&M service.
Remember that for a follow-up E&M service to be eligible for payment, you must document two of the three E&M components as being significant and separately identifiable. Also, for every procedure, there is an “E&M” portion built into the allowed fee. In this instance, one must document and show that there is more history, examination and decision making than would be included in the fee allowance for the procedure.
For example, a patient presents to your office with a new wound. You obtain a history of the wound, examine the wound and then decide what treatment to pursue. You also perform an in-office debridement. As a result, at this initial presentation of the wound an E&M service would be appropriate in addition to the procedure. The level of E&M service billed would NOT necessarily be based solely upon the complexity of the wound (e.g. exposed bone) but rather the level of each key component performed and the resulting level of documentation in your chart. As always, charting is key.
The patient then returns the next week for a follow-up visit. If there are no significant history or examination changes from the previous visit and the wound is progressing as expected, then there may not be an eligible E&M service separate from any procedure that one may also perform on that day. However, if at a subsequent visit, the physician needs to alter the wound care protocol (if the wound is deteriorating and additional imaging is necessary, or one needs to initiate or change antibiotic therapy), then an E&M service would be appropriate to bill based upon your level of documentation. The chart notes would need to document the changes that occurred since the last encounter and the associated decision-making.
Benefits And Pitfalls Of EHRs In E&M Documentation
With many office EHRs, there is the ability to bring information forward from previous patient encounters. This can be deemed templating or cloning of charts, but this is a double-edged sword. EHR-associated templating can make our lives easier when it comes to documentation and completeness of a chart note. However, you cannot use patient data or information brought forward from a previous chart note to augment your current chart note just to bill an E&M service, or a higher level of service.
Simply cutting and pasting the history from week to week does not meet proper documentation requirements. You would only get “credit” for any history that has changed since the last encounter. Similarly, if the examination is unchanged except for the fact the wound is getting smaller and progressing as expected, then there is no real “credit” there either. Lastly if your decision making is essentially to “continue with current treatment course,” there is no added consideration there as well. Without documentation of changes in history, additional examination or decision making (at least two of three components), there is no additional E&M service to bill. Lastly, be very careful with templates as one may inadvertently bring charting errors forward as well that can make your chart look poor and clearly templated.
Key Concepts In Coding For Wound Debridement
Debridement is a common part of the treatment algorithm for wounds. There are two debridement code series, Current Procedural Terminology (CPT) 9759X and 1104X, that clinicians can utilize. CPT series 9759X involves selective debridement of epidermal and dermal tissue, and superficial biofilm. CPT series 1104X involves the excisional debridement of deeper tissue including subcutaneous tissue, muscle, tendon or bone. One also needs to clearly identify the type of tissue he or she has debrided in the chart notes.
In addition, proper documentation should include the location of the wound, the size of the wound, the instruments one uses for debridement, if anesthesia is required and the type and anatomic depth of debridement. Additionally, examination documentation should include the condition and characteristics of the wound bed as well as notation on any drainage, odor or cellulitis.
We often see multiple wounds on the feet and selection of the appropriate code is based upon the aggregate size of similar wounds, not on a right foot or left foot basis. Remember that wound codes are not foot specific. They apply to the entire body. Accordingly, one determines the codes based on the tissue type debrided and these codes are applicable to any body part. Therefore, add up all similar wounds of similar debridement depths and combine them into one code per the appropriate aggregate sizing.
If there are three wounds on a foot, two of which require debridement to subcutaneous tissue and a third wound requires only dermal debridement, the proper coding would be CPT 11042 (debridement of subcutaneous tissue) for the composite two wounds requiring subcutaneous tissue debridement and CPT 97597 (debridement of non-viable tissue) for the third wound, which requires only more superficial selective debridement. Do not use right or left foot modifiers as those are incorrect and will result in your claim being denied. A -59 modifier is necessary to be paid for both debridement codes when you bill them on the same day.
These wound care codes are listed per 20 sq cm. If the aggregate size of similar wounds exceeds that amount, there are add-on codes that clinicians can bill. Accordingly, for the debridement of an aggregate 60 sq cm wound through subcutaneous tissue, CPT 11042 applies for the first 20 sq cm and CPT 11045 (two units in this case) applies for each additional 20 sq cm.
Correct measurement of wounds is important not only to document the presence or absence of improvement, but also to properly select the appropriate CPT debridement code. A wound may be 4 cm in overall diameter but the base of the wound, which has the subcutaneous tissue you are debriding, is only 2 cm in diameter. Billing is based upon the deepest tissue debrided and the amount of that specific tissue in square centimeters. In this scenario, one is debriding two sq cm. Keep in mind that if the wound extends deep to bone but you only debride subcutaneous tissue, the proper billing level would be CPT 11042 (debridement subcutaneous tissue), not CPT 11044 (debridement of bone).
When applying skin substitutes, one needs to perform some basic wound preparation/care prior to the application of the product. This wound preparation may include some tissue debridement. CPT 15271 is used for application of the product on the leg and CPT 15275 for the foot. You cannot bill both CPT series 1527X in combination with either CPT 9759X/1104X series codes as this would be essentially duplicate billing. You can only bill for the wound preparation codes when applying a wound care product. CPT 15271 for application of the product on the leg and CPT 15275 for the foot are designated in 25 sq cm increments. The add-on codes are CPT 15272 (for the leg) and CPT 15276 (for the foot) are used for aggregate wounds greater than 25 sq cm and billed per each 25 sq cm increment. If the wounds were to exceed aggregate 100 sq cm in size, CPT 15273/15274 and CPT 15277/15278 codes are to be used as a single code (i.e you cannot bill CPT 15277 in addition to 15275 and 15276, but these should be rare in the foot and ankle).
Choosing Proper Coding For Skin Substitute Products
The next issue is selection of a skin substitute product. Many products have specific FDA indications. Some are only indicated for diabetic foot wounds or venous leg ulcers. Reimbursement for the use of these products is limited to those indications. If the patient has an ulcer but is not diabetic, some wound care products may not be approved if the indication is only for a diabetic foot wound. Not all products are indicated for exposed bone or tendon, either. Some insurance companies have additional requirements. One example may be in regard to the coverage or lack thereof for small wounds. There may be a minimum one cm diameter wound size requirement, which clinicians need to be aware of. Additionally, some insurances have limitations on the number of times a clinician can use a product without additional authorization.
Each skin substitute product has a specific Q code, which identifies the product. Make sure the product you use is properly identified. Exercise caution if a manufacturer representative tells you to bill his or her company’s product using a certain Q code just because it is “similar” to some other product.
Therefore, when dealing with private insurance carriers, it is important to pre-authorize every wound care product. This applies to both primary as well as any secondary insurance carriers. These products are very expensive and if the product is not allowed for any reason then the facility, provider or patient will be billed in full for the product.
Many patients today have insurance plans with very high deductibles so even though the use of skin substitute and other advance wound care products maybe a covered benefit they may or may not be affordable. Even a 20 percent co-insurance may be out of reach for some patients. Keep this in mind when selecting products for your patient. One may need to make compromises when selecting products based, unfortunately, on financial concerns. In addition to any medical indications, the place of service may also be an issue. Some products are only reimbursable when the application is in an operating room setting versus a private office or wound care center.
The next question is when to start using skin substitutes. That obviously depends on the quality of the base of wound. This documentation is also necessary from a medicolegal aspect as well. If the wound bed is poor, one first needs to perform proper debridement and wound preparation. If there is significant venous insufficiency and edema, physicians need to address that promptly. Other things to consider are addressing out of control hemoglobin A1c levels and overall vascular status. Superficial or systemic infections warrant primary treatment as well. There also needs to be proper offloading. If one does not address these factors, these products, although very effective, can be significantly hindered in their ability to heal wounds. If the insurance carrier only allows five product applications, then using the product on an improperly prepared wound bed would be wasteful and detrimental to the patient.
Many insurance carriers require some level of more conservative care before initiating the start of skin substitutes or other advanced wound care products. This is obviously controversial. The current standard in wound healing is 50 percent closure of the wound in four weeks. One could make the argument of starting wound care products, such as skin substitutes, as quickly as possible for patients who have high morbidity issues. However, many carriers may want at least four to six weeks of conservative treatment that could include documentation of offloading, local debridement, compression and addressing infectious or metabolic issues. Documentation of wound size and quality is very important in these cases.
If one institutes conservative wound care measures and the wound is showing steady progress with these measures alone, then the question becomes “Should a skin substitute be used at all?” This is an area of discussion right now with various Medicare carriers. If the wound is going to heal on its own based upon addressing factors such as glucose levels, infection, offloading, and compression, then it may very well heal without applying skin substitutes. There needs to be documentation of why, if a wound is healing on its own in a reasonably steady fashion, skin substitutes are required. This is a current area of audit and Medicare scrutiny. If the wound healing has stalled or is progressing very slowly, then proper documentation of this may result in authorization from the insurance carrier and also protect you in the case of an audit.
I personally recommend making patients aware of insurance company regulations and restrictions so they can also help advocate for themselves. This can be helpful when dealing with the insurance company to get authorization for wound care services and products.
Navigating Off-Label Uses For Wound Care Products
There have been many recent audits surrounding wound care products. Many of these audits are related to not using the proper product for the proper type of wound. Newer audits are for non-wound-related uses of skin substitutes. Many products, imaging systems that are commonplace now were at one point off-label. If you are using a skin substitute for an off-label use, make sure you and/or your staff are very clear about the product you are using, and how you will use it when obtaining a pre-authorization.
Physicians are using wound care products in non-wound-related foot surgery to augment tendon repairs and act as an interface between tissue layers to limit adhesions and/or scarring. Unfortunately, I have seen requests for the use of these products in simple hammertoe repairs and even matrixectomies! Be able to prove some level of medical basis for the off-label use of these products in an appeal situation. A surgeon’s personal preference/past experience is not enough.
Also be careful when interacting with manufacturer representatives who may imply proper use of these products in situations that may indeed be inappropriate. This may get you flagged for an audit. Make sure you document the off-label use of the product and that you informed the patient you were using the product off-label. You should have the patient sign a form similar to an ABN stating that he or she acknowledges the off-label use of the product, agrees to pay for the product and that the insurance company will not be billed for it
Wound care has been an integral part of the podiatric profession for quite some time. This field and its available treatment options has exploded over the past few years. It can be a very professionally rewarding part of your practice. In order to best succeed in the treatment of wounds, make sure you and your staff are well versed in treatment options, product availability, indications and proper billing protocols.
Dr. Poggio is a California Podiatric Medicine Association Liaison to Noridian JE MAC and a medical consultant to several national health insurance and review organizations. He is a member of the American College of Podiatric Medical Reviewers and is board-certified by the American Board of Podiatric Medicine and the American Board of Podiatric Orthopedics and Primary Podiatric Medicine.
Summary of “Microtubule plus-end dynamics link wound repair to the innate immune response.”
The skin protects animals from infection and physical damage. In C. elegans, wounding the epidermis triggers an immune reaction and a repair response, but it is not clear how these are coordinated. Previous work implicated the microtubule cytoskeleton in the maintenance of epidermal integrity (Chuang et al, 2016). Here, by establishing a simple wounding system, we show that wounding provokes a reorganisation of plasma membrane subdomains. This is followed by recruitment of the microtubule plus end-binding protein EB1/EBP-2 around the wound and actin ring formation, dependant on ARP2/3 branched actin polymerisation. We show that microtubule dynamics are required for the recruitment and closure of the actin ring, and for the trafficking of the key signalling protein SLC6/SNF-12 towards the injury site. Without SNF-12 recruitment, there is an abrogation of the immune response. Our results suggest that microtubule dynamics coordinate the cytoskeletal changes required for wound repair and the concomitant activation of innate immunity.
Skin failure (SF) is a term that first appeared in the literature in 1991. La Puma1 theorized that the skin, like all other organs, can fail. As a result of this physical decline and organ failure, pressure injuries (PIs) can occur.1 Since then, there have been multiple published definitions and variations on the term.2–8 However, ongoing debate surrounds the definition of SF and associated terms such as acute SF (ASF), chronic SF, and end-stage SF, as well as the clinical presentation of and diagnostic criteria for the condition.8
The failure of human organs, such as the heart, lungs, liver, and kidneys, is well defined; associated biomarkers guide treatment and prognosis.9–12 For patients in the ICU, evidence-based categorization instruments provide a numerical score to assess morbidity and illness severity and predict mortality. Such calculations are only achievable because objective measures of organ dysfunction are available. However, objective diagnostic markers and clinical parameters related to the integumentary system and SF are lacking;13 this limits the formulation of a globally agreed-upon diagnosis, classification, and definition for this phenomenon.
Varying definitions for SF have been presented in both the dermatology and skin integrity/wound care literature (Table 1). Although these definitions refer to a pathophysiologic process that affects the skin, the definitions are very different. The SF definitions from the dermatology literature have been used to describe SF that is attributable to trauma, such as thermal burns, autoimmune disorders, and severe infection.14 These definitions describe the etiology of SF as the result of a primary dermatologic condition with pathophysiologic changes resulting from integumentary inflammation and generalized loss of skin integrity.
In contrast, the skin integrity and wound care literature describes the etiology of SF as the result of a secondary pathophysiologic process that originates from failure of one or more organs other than the skin. As a result of organ failure elsewhere in the body, skin can be compromised and subsequently fail. Langemo and Brown’s5 2006 definition suggested SF is an “event in which the skin and underlying tissue die due to the hypoperfusion that occurs concurrent with severe dysfunction or failure of other organ systems.” In 2017, Levine8 built on this definition and proposed SF be defined as a “result of compromised tissue where the cells can no longer survive in zones of physiological impairment that includes hypoxia, local mechanical stresses, impaired delivery of nutrients, and build-up of toxic metabolic by-products.” Levine15 describes this definition as a way to consolidate and simplify differing nomenclatures into a universal diagnosis, proposing that SF is the underlying pathophysiology in wounds occurring in “patients close to death, unavoidable pressure injuries, and skin impairment related to tissue ischemia.” However, the association between SF and unavoidable skin changes remains unclear.
Pressure injuries are defined as “localized damage to the skin and underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities and conditions of the soft tissue.”16 More than 100 intrinsic and extrinsic risk factors for PI have been identified, including impaired mobility, diabetes, and skin status.17,18 It is plausible that a PI may develop in the presence of SF; however, skin damage occurring solely as a result of SF is not limited to areas of tissue loading alone. Therefore, PI development in the presence of SF is not certain, and SF may manifest in other ways; for example, gangrenous fingers or toes, blisters, or skin mottling.19,20
The multitude of interrelated terms and concepts used throughout the literature regarding SF, PI, unavoidable PI, terminal ulceration, and skin changes at the end of life has resulted in linguistic and conceptual confusion.19 Currently, three types of SF are described within the literature: acute, chronic, and end stage.5 Acute SF occurs concurrently with a critical illness such as septic shock.7 Chronic SF occurs in the presence of an ongoing chronic disease state such as dementia.21 End-stage SF occurs at the end of life. A Kennedy terminal ulcer (an event deeply embedded within the PI schema) is a manifestation of SF in patients at end of life.22 These definitions are subjective, based on clinical judgment, and lack objective criteria to determine categorization or the potential transition between categories (eg, moving from ASF to chronic SF or from chronic to end-stage SF).5 This has resulted in multiple terms being used interchangeably throughout contemporary literature. It is uncertain whether SF categories overlap or represent a continuum of acuity, although that issue is beyond the scope of this review. This problem does, however, highlight the need to clarify terminology through rigorous analysis of each concept, including similarities, differences, and interrelationships to improve clarity and ensure that concepts and terms have a solid theoretical and biologic basis.19
The primary aims of this systematic review were to assess and appraise the quality of studies conducted on ASF in adult patients in the ICU and identify evidence and gaps within the literature. The research questions were as follows:
What is the definition of ASF in the adult intensive care population?
What are the risk factors, causes, and antecedent conditions of ASF in the adult intensive care patient population?
Is there an association between ASF and PI in the adult intensive care patient population?
This systematic review protocol has been registered in the International Prospective Register of Systematic reviews (PROSPERO): CRD42019126159.
A preliminary literature search was undertaken using PubMed, MEDLINE (Medical Literature Analysis and Retrieval System), and CINAHL (Cumulative Index of Nursing and Allied Health Literature) to identify key terms and subject headings, with guidance from a specialized health sciences librarian. A systematic search for primary research was then undertaken in September 2018 using six databases: the Cochrane Library, Joanna Briggs Institute Evidence-Based Practice Database, CINAHL, Google Scholar, PubMed, and MEDLINE. The completed search strategy used for PubMed is detailed in Figure 1. The same keywords were used for all searches, and similar subject headings were used in the other five databases. Subject headings were explored where applicable. Limiters applied to the search were English language and dated from database inception to September 2018.
Inclusion and Exclusion Criteria
Qualitative or quantitative research studies that reported on ASF in critically ill adult human patients in the ICU setting were included.
Records were excluded if their study sample was animal or pediatric, if the study setting was not adult intensive care, and unrelated to SF. Studies were also excluded if they were written in a language other than English. Nonresearch publications, including conference papers, protocols, educational, opinion or commentary articles, other literature reviews, and guidelines, were excluded.
Abstracts were screened for eligibility and studies meeting the inclusion criteria were retrieved in full. The full-text publications were evaluated against the inclusion and exclusion criteria by two reviewers who worked independently and were blinded to each other’s assessments until selection was complete. Disagreements were resolved through discussion and consultations with third reviewers who acted as arbitrators where necessary.
Data Extraction and Synthesis
Data from the included records were extracted by one reviewer and summarized in data collection tables, which were checked and verified by the second reviewer.
Quantitative data synthesis was not attempted because of extensive heterogeneity attributable to the descriptive design of each study, lack of similar comparators, and lack of comparable data presented within the studies. Further, only one study23 used SF as a primary outcome; the other studies used PI development.7,24 A narrative synthesis approach was chosen to summarize the selected studies using the PICO (Population, Intervention, Comparator, and Outcome) framework.25 For each included record, study design, quality, population, intervention, comparator, outcome, and limitations were extracted. Each study also was assessed according to the National Health and Medical Research Council (NHMRC) evidence hierarchy.26 The results of the selected studies were tabulated to highlight important similarities and differences among studies (Table 2). The NHMRC evidence hierarchy was then used to define the recommendation grades: grade A is a body of evidence that can be trusted to guide practice; grade D is a body of evidence that is weak, from which recommendations should therefore be applied with caution.27
The quality of the studies was assessed by two independent reviewers using the Mixed Methods Appraisal Tool (MMAT), version 2018 (Table 3).28 The MMAT is based on constructionist theory and has been used in more than 100 systematic mixed study reviews.29 It is designed for systematic reviews that include qualitative, quantitative, and mixed-methods studies. It was chosen for this review to ensure the different design methods could be reviewed using the same tool. The MMAT categorizes research using an algorithm of study selection criteria; each category is then appraised using two screening questions and five method quality questions based on the study design category.28 This enabled the authors to appraise the most common types of empirical studies concomitantly and effectively.29
The MMAT has separate categories for researchers to use depending on the type of research design to be assessed. Each category can be answered with yes, no, or cannot tell. The 2018 MMAT version discourages the calculation of an overall score. Using this method, each criterion can provide a more detailed presentation to better inform the quality of the included studies.28 There was only one MMAT question for one study for which assessors disagreed (Nowicki and colleagues’24 study had a clear research question), resulting in an overall interrater agreement of 95.24%. However, this disagreement was resolved through discussion.
The search returned 991 records. After duplicates were removed, 801 records remained. After titles and abstracts were screened against the inclusion and exclusion criteria, 779 records were excluded. Following the review of 22 articles retrieved for full-text evaluation, an additional 19 studies failed to meet the inclusion criteria; therefore, 3 articles were included in this review.7,26,24
These were categorized as quantitative nonrandomized7 and quantitative descriptive.23,24 The purpose of all three studies was to identify and describe factors that contributed to ASF and determine predictors of ASF in intensive care. Two of the studies were set in a single site (tertiary hospital centers).23,24 The third was a multicenter study involving a 55-bed ICU in a tertiary urban medical center and an 18-bed ICU in a suburban teaching hospital.7 Two studies employed a retrospective design,7,24 and the other used a prospective method.23 The NHMRC level of evidence for the three studies ranged between III-27 and IV,23,24 resulting in an overall D grade.27
No studies included in this review described a specific research question; rather, all presented an aim or research purpose. The data collected in two studies addressed the stated aims and purpose.7,24 However, it was unclear whether the data collected in the other study addressed the stated aim: to identify and describe the characteristics of ICU patients with SF.23 None of the studies were a “yes” for all MMAT criteria questions because of their potential risk of bias7,23,24 and a lack of clarity regarding the completeness of the data sets analyzed.7,24
Retrospective analysis using databases and patient notes increases the risk of bias attributable to systematic errors, inaccuracies, and the potential for missing data.30 This is evident in Nowiki et al,24 in which recorded data for more than 3 years (June 2006 to October 2009) were only partially available because of limited data recording (ie, incomplete outcome data were reported). Further, Delmore and colleagues’7 use of purposive sampling in the selection of patients with PI is prone to selection bias31 because the research intentionally selected certain patients with the outcome measure of interest (PI) and randomly selected patients without PIs. Further, little information regarding the amount or nature of missing data was described within these two studies.7,24 Curry and colleagues’23 study is at risk of bias because the authors did not state the criteria used by the certified wound care nurses to diagnose ASF prospectively. This places the study at risk of research bias. It also may impact the validity of data collected in answering the research question.23
The studies included 1,307 intensive care participants, with 29 participants in the prospective study23 and the remaining 1,278 participants in the retrospective studies.7,24 Two studies were based in the US7,23 and one study in Australia.24 One study did not report the participants’ sex, age, or race.24 The other two included 328 males and 253 females, resulting in a 1.3:1 male-to-female ratio; this is representative of the ICU patient population, 60% of whom are male.7,23,32 The age of participants in these two studies ranged from 19 to 99 years (mean, 71 [SD, 15.7] years7 and 58.82 [SD, 15.29] years,23 respectively). The majority of study participants were white (n = 457, 78%).7,23 Other ethnic backgrounds represented were as follows: black/African American (n = 45, 8%), Hispanic (n = 47, 8%), Asian/Pacific Islander (n = 31, 5%), and other (n = 1, 0.2%), resulting in a rounded ratio of 4:1 white to cumulative minority groups.7,23
Study authors defined ASF using the Langemo and Brown5 definition in two of the three studies.7,23 The third study provided no ASF definition; rather, the authors describe SF occurring as a result of hypoperfusion and secondary to the underlying patient condition and use of vasoactive drugs, causing poor tissue tolerance and leading to PI formation.24 This study was included in the analysis because it met the inclusion criteria. Further, this distinction in terms demonstrates the linguistic and conceptual confusion currently surrounding this phenomenon.
In two retrospective studies, PI development was the primary outcome measure.7,24 The third study used a certified wound and ostomy care nurse to assess ASF prospectively,23 although again the diagnostic criteria were not described. As a result, the lack of diagnostic criteria may contribute to researcher bias and potentially influence reliability and consistency.
Comparator groups were used in both retrospective studies.7,24 One study compared PI rates in ICU patients with non-ICU patients and confirmed an increase in PI development over time in the ICU group (from 4.6% [71/1,532] PI incidence in 2006 to 7.5% [128/1,699] in 2015).24 The other study compared the physiologic characteristics of ICU patients who developed PIs with a control group of ICU patients who did not develop PIs.7 This comparison enabled a logistic regression analysis that showed independent predictors of ASF.7
Risk factors for ASF were determined by one study’s use of logistic regression analysis and reported statistically significant and independent predictors of ASF.7 This study found the predictive variables for ASF were: peripheral arterial disease (odds ratio [OR], 3.8; 95% confidence interval [CI], 1.64–8.66), mechanical ventilation longer than 72 hours (OR, 3; 95% CI, 1.78–5.05), respiratory failure (OR, 3.2; 95% CI, 1.82–5.40), liver failure (OR, 2.9; 95% CI, 1.05–8.08), and severe sepsis/septic shock (OR, 1.9; 95% CI, 1.14–3.20). Another study found more than 90% of their cohort diagnosed with ASF had the following antecedent conditions: renal failure, respiratory failure, more than one organ system (other than skin) failing, and albumin levels less than 3.5 mg/dL.23
The final study found an increase in ICU PI incidence from 4.6% (71/1,532) of ICU episodes of care to 7.5% (128/1,699) of ICU episodes of care over a 9-year period (2006–2015).24 This study also reviewed the clinical characteristics of a subset of 13 ICU patients with severe PIs (Stages 3 and 4)24 and found 30% (4/13) of this cohort had an admission diagnosis of septic shock; 38% (5/13) required extracorporeal membrane oxygenation therapy; 69% (9/13) required renal replacement therapy; and 100% (13/13) were treated with more than two vasopressors or inotropic pharmacologic agents. The authors hypothesized that the clinical characteristics of this subset of ICU patients may be more appropriately attributed to antecedents of SF rather than the predictors of PIs.24
Each study had several limitations. Single-site studies, although important, have limited generalizability.23,24 One study’s small sample size,23 as well as the lack of documented ASF diagnostic criteria identified in any of the studies, impacted the generalizability of these findings.7,23,24 A confounding bias for two studies was the use of PI development as a surrogate marker for ASF.7,24 Given the lack of evidence substantiating a pathophysiologic link between ASF and PI, it cannot be confirmed that the findings from these studies are specific to ASF alone.
Two studies lack generalizability because of the use of unique subspecialties such as elective cardiothoracic surgical patients.7,24 These patients are often stable prior to surgery and critically ill for only a short period.7 The lack of generalizability was also evident in the cohort mix, with a disproportionate ratio of whites to other ethnicities (4:1) represented within the collective studies.7,23
The two retrospective studies, despite having the largest cohorts,7,24 have limited generalizability because of their retrospective design. Further, one study had a 9-year timeline (2006–2015), resulting in data collection over a period in which differing classification systems were used to categorize PI stages.24 These limitations may have also been compounded with the use of multiple reporting systems to collect these data.24
The few studies eligible for inclusion in this review illustrate that research is limited regarding ASF in the adult intensive care patient population. This includes the apparent lack of consensus and evidence to define ASF in this cohort; limited understanding of risk factors, causes, and antecedent conditions for ASF; and scant evidence supporting PI etiology and development because of ASF.
Globally, ASF has no agreed-upon definition, and related research remains inconsistent as a result. The definition of ASF, although previously described within dermatologic literature, was redefined by Langemo and Brown within the wound care literature, citing an alternative etiology for the condition (hypoperfusion in the context of patient acuity).5 As a result, the definition of ASF not only lacks consensus within the wound care community, but it also has different meanings depending on whether it is used in the wound care or dermatology context.
Significant conceptual confusion surrounding ASF remains. This is most evident in the retrospective studies included in this review,7,24 in which ASF may have been erroneously labeled as PI. However, ASF does not require factors necessary for PI development such as mechanical stress. Acute SF can occur on the body in areas of no mechanical stress, manifesting, for example, as necrotic digits.14 Further, when the label ASF is applied retrospectively to only those patients who developed PIs, patients who may have developed ASF without PI development are missed. Whether this is right or wrong, this is the current point at which researchers and clinicians find themselves.
This systematic review illustrates a paucity of research available on ASF in the intensive care patient population and the need for rigorous analysis regarding the etiology and pathophysiology of ASF including similarities, differences, and interrelationships to other skin changes. This will ensure a solid theoretical and biologic foundation for defining the term and lead to practice improvement and global patient benefit.
This review has some limitations. First, the search strategy was limited to original research written in English; gray literature was excluded. Gray literature consists of a wide range of formats and scopes that can often be a rich source of evidence, although it is usually not subject to peer review.33 Second, the small number and heterogeneity of studies found on this topic prevented a true meta-analysis.
This systematic review aimed to present the current evidence regarding ASF by reviewing the risk factors, causes, and antecedent conditions; identifying associations between ASF and PI development; and understanding the definition of ASF in the adult ICU population.
The results of this systematic review highlight a substantial evidence gap in this area. Further research regarding etiology, diagnostic biomarkers, and predictors of SF is warranted to assist in formulating an accurate and agreed-upon definition, as well as improving skin integrity outcomes in patients who are critically ill.