The Microbiology of Skin, Soft Tissue, Bone and Joint Infections

By Academic Press

The Microbiology of Skin, Soft Tissue, Bone and Joint Infections: Volume 2 discusses modern approaches in diagnosis, treatment, and prophylaxis of skin, soft tissue, bone, and joint infections. The volume has been divided into three sections.

The first section includes chapters on diagnosis, treatment, and prophylaxis of skin and soft tissue infections. It discusses antimicrobial and surgical treatment of wounds, diabetic foot, and different soft tissue infections. Ten chapters are devoted to cutaneous and musculoskeletal infections in special groups of patients, which have their own specificity, i.e. in pediatric and HIV-infected patients. Together with chapters on commonly present diseases, there are chapters which discuss interesting but not well studied pathologies (natal cleft pilonidal sinus) and pathogens (Malassezia and Shewanella spp.).

The second section reviews etiology, pathogenesis, diagnosis and treatment of bone and joint infections, mainly osteomyelitis and prosthetic joint infections. Also, one chapter in this section discusses a newly emerging bacterial pathogen that causes skeletal infections, Kingella kingae. The third section incorporates alternative and new approaches—such as nanotechnology, ultrasound, novel delivery approaches and phyto-derived medicines—to the treatment and prophylaxis of skin, soft tissue, bone, and joint infections.

• Encompasses a broad range of skin, soft tissue, bone, and joint infections, including questions of etiology, pathogenesis, diagnosis, prognosis, treatment, and prophylaxis
• Written by highly professional and eminent surgeons, microbiologists, and infectious disease specialists
• Discusses topics using modern insight, providing all necessary scientific information on each aspect
• Includes scientific understanding and practical guidelines, which make it interesting for both research scientists and practitioners working with skin, soft tissue, bone, and joint infections

• Language: English
• Publisher: Academic Press
• Release date: Apr 25, 2017
• ISBN: 9780128110935

Book preview

Section I

Skin and Soft Tissue Infections: Diagnosis and Treatment

Chapter 1

Soft Tissue Infections

Consideration Regarding Different International Guidelines

M. Sartelli*; F. Coccolini†; F. Catena‡; L. Ansaloni†    * Macerata Hospital, Macerata, Italy

† Papa Giovanni XXIII Hospital, Bergamo, Italy

‡ Parma University Hospital, Parma, Italy

Abstract

Skin and soft tissue infections (SSTIs) encompass a variety of pathological conditions ranging from simple superficial infections to severe necrotizing soft tissue infections.

Necrotizing soft tissue infections (NSTIs) are a rapidly progressive form associated with widespread necrosis and systemic toxicity and represent potentially life-threatening infections.

Two different sets of guidelines outlining the clinical management of soft tissue infections (SSTIs) have been published in recent years, including recent Infectious Diseases Society of America (IDSA) guidelines and 2014 World Society of Emergency Surgery (WSES) guidelines.

The aim of the chapter is to compare these two different sets of guidelines for management of soft tissue infections.

Keywords

Soft tissue; Infections; Necrotizing; Cellulitis; Fasciitis; Abscess

1 Introduction

In 2014 the Infectious Diseases Society of America (IDSA) published new guidelines for the diagnosis and management of soft tissue infections.¹ These new IDSA guidelines replaced those previously published in 2005.²

The 2014 World Society of Emergency Surgery (WSES) guidelines represent an additional contribution to the debate and were written by consensus of a group of worldwide specialists, mainly surgeons with interest in surgical infections.³ The WSES guidelines, written by surgeons for surgeons, have a more practical approach than the IDSA guidelines.

Both sets of guidelines focus on the dramatic emergence of resistance to many of the antimicrobial agents commonly used to treat Skin and soft tissue infections (SSTIs) in the past. Particularly, infections due to S. aureus are an important health problem worldwide,⁴ and treatment of these infections has become more difficult in the last decade due to the emergence and rapid spread of methicillin-resistant S. aureus (MRSA).

MRSA has usually been acquired during exposure to hospitals and other healthcare facilities (healthcare-associated MRSA). However, by the late 1990s, MRSA infections acquired from the community were recognized as a distinct clinical entity affecting young and healthy individuals without healthcare risk factors and with relatively preserved antimicrobial susceptibility patterns.⁵

2 Classification

The practice guidelines of IDSA¹ classify SSTIs into four groups: purulent, nonpurulent, infections associated with bites and animal contact, and surgical site infections. In addition, because of an increasing number of immunocompromised hosts worldwide, this set of guidelines addresses the wide array of SSTIs that occur in this population.

The WSES expert panel classified soft tissue infections using the following classification system³:

Surgical Site Infections

Incisional

• Superficial

• Deep

Nonnecrotizing SSTIs

• Superficial infections (impetigo, erysipelas, cellulitis)

• Simple abscess, boils and carbuncles

• Complex abscesses

Necrotizing SSTIs (NSTIs)

• Necrotizing cellulitis

• Necrotizing fasciitis

• Fournier gangrene

• Necrotizing myositis

The first group includes surgical site infections (SSIs). These infections represent a separate chapter among the soft tissue infections.³ They are postoperative infections and because of their multifaceted aspects they are framed into a separate group.

Soft tissue nonsurgical site infections are divided into nonnecrotizing and necrotizing soft tissue infections.

Nonnecrotizing soft tissue infections typically involve one or both of the superficial layers of the skin (epidermis and dermis) and the subcutaneous tissue, such as complex abscesses, but may occasionally involve deeper structures. Generally, these infections are treated by antibiotics alone (nonpurulent superficial infections such as impetigo, erysipelas and cellulitis) or surgical drainage (purulent superficial infections such as simple abscesses, boils and carbuncles). In some cases, complex abscesses need both surgical drainage and antibiotics.

Conversely, necrotizing soft tissue infections (NSTIs) are life-threatening, invasive and aggressive soft tissue infections.

3 Necrotizing Soft Tissue Infections

NSTI is an inclusive term intended to describe all infections with a necrotizing component involving any or all of the layers of the soft tissue compartment, from the superficial dermis and subcutaneous tissue to the deeper fascia and muscle. NSTIs include necrotizing cellulitis, necrotizing fasciitis, Fournier gangrene and necrotizing myositis.

Microbiologically, NSTIs may be classified into three types: type 1 (polymicrobial), type 2 (monomicrobial), and type 3 (monomicrobial infections initiated by a variety of virulent Gram-positive or Gram-negative bacilli such as Clostridia, Vibrio, Aeromonas, Eikenella, and Bacillus species).³

NSTIs rank among the more difficult disease processes encountered by physicians and surgeons and should be clearly separated from nonnecrotizing infections. The WSES classification³ stresses the differentiation between nonnecrotizing infections and necrotizing infections. However, both guidelines focus on the necessity for a prompt diagnosis of these infections.¹,³

In practice, clinical judgment is the most important element to diagnose necrotizing fasciitis. Clinical findings that suggest involvement of necrotizing fasciitis include: severe pain disproportional to the clinical findings; failure to respond to initial antibiotic therapy; evolving systemic toxicity; edema or tenderness extending beyond the cutaneous erythema; crepitus, indicating gas in the tissues; and in a subsequent phase skin necrosis or ecchymoses.

NSTIs are typically caused by toxin-producing bacteria and manifest a very rapid progression of disease with significant local tissue destruction. Systemic toxicity depends on the strain of bacteria and toxins produced. In most cases the progression of disease is typically measured in hours and an early diagnosis and treatment are crucial to survival.⁶ The key to a successful outcome is a high index of suspicion and an aggressive and prompt management. Delay in diagnosing and inappropriate treating increases the risk of mortality.

Both computed tomography (CT) and magnetic resonance imaging (MRI) may be useful for diagnosing necrotizing soft tissue infections. MRI has been the imaging modality of choice for necrotizing fasciitis. However, MRI may be difficult to perform under emergency situations.

In these infections a multidisciplinary approach, including prompt aggressive source control, appropriate antimicrobial therapy and supportive management, are crucial for the patient's outcome.

Most patients require multiple surgical debridements and often have large and complex wounds requiring soft tissue coverage and prolonged hospitalizations. Early appropriate empiric antibiotic therapy against suspected pathogens should be started as soon as possible. Both guidelines suggest antibiotics suppressing streptococcal toxin and cytokine production (such as clindamycin). Since it is impossible to exclude with certainty a polymicrobial infection, an aggressive broad-spectrum empiric antimicrobial therapy should initially be started covering Gram-positive, Gram-negative, and anaerobic organisms, until culture-specific results and sensitivities are available.

IDSA guidelines suggest¹ vancomycin, linezolid, or daptomycin combined with one of the following options: piperacillin-tazobactam, a carbapenem (imipenem-cilastatin, meropenem, and ertapenem), ceftriaxone plus metronidazole, or a fluoroquinolone plus metronidazole.

WSES suggestions for antimicrobial therapy of necrotizing fasciitis are very similar³: linezolid and piperacillin/tazobactam or daptomycin+piperacillin/tazobactam+clindamycin.

In Fournier gangrene, WSES guidelines³ suggest piperacillin/tazobactam+clindamycin if signs and symptoms of severe sepsis are not present or meropenem+linezolid if signs and symptoms of severe sepsis are present.

An appropriate deescalation of antimicrobial therapy is suggested by both guidelines once culture results return.

The efficacy of intravenous immunoglobulin (IVIG) in treating streptococcal toxic shock syndrome has not been defined. However, as extracellular streptococcal toxins have a role in organ failure, shock, and tissue destruction, neutralization of these toxins theoretically could be beneficial. WSES guidelines suggest³ (with low quality of evidence and weak recommendation) IVIG in all patients with NSTI and evidence of organ dysfunction. On the other hand, IDSA guidelines¹ state that additional studies of the efficacy of IVIG are necessary before a recommendation can be made supporting its use in this setting.

4 Conclusion

SSTIs encompass a variety of pathological conditions ranging from simple superficial infections to severe necrotizing soft tissue infections.

Among skin and soft tissue infections, NSTIs are a rapidly progressive form representing potentially life-threatening infections.

Both WSES and IDSA guidelines stress the high suspicion that clinicians should always have when confronted with a case or suspected case of necrotizing infections, where the key for a successful outcome is an aggressive and prompt management.

References

1 Stevens D.L., Bisno A.L., Chambers H.F., Dellinger E.P., Goldstein E.J., Gorbach S.L., et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10–e52.

2 Stevens D.L., Bisno A.L., Chambers H.F., Everett E.D., Dellinger P., Goldstein E.J., et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373–1406 Epub 2005 Oct 14. Erratum in: Clin Infect Dis 2006;42(8):1219.

3 Sartelli M., Malangoni M.A., May A.K., Viale P., Kao L.S., Catena F., et al. World Society of Emergency Surgery (WSES) guidelines for management of skin and soft tissue infections. World J Emerg Surg. 2014;9(1):57.

4 Klein E., Smith D.L., Laxminarayan R. Hospitalizations and deaths caused by methicillin-resistant Staphylococcus aureus, United States, 1999–2005. Emerg Infect Dis. 2007;13:1840–1846.

5 Sowash M.G., Uhlemann A.C. Community-associated methicillin-resistant Staphylococcus aureus case studies. Methods Mol Biol. 2014;1085:25–69.

6 Hakkarainen T.W., Kopari N.M., Pham T.N., Evans H.L. Necrotizing soft tissue infections: Review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg. 2014;51(8):344–362.

Chapter 2

Evidence-Informed Approach to Pilonidal Sinus Disease and Related Disorders

C.L. Harris*; K. Laforet*; R.G. Sibbald†; R. Somayaji‡    * Western University, London, ON, Canada

† University of Toronto, Toronto, ON, Canada

‡ University of Calgary, Calgary, AB, Canada

Abstract

Sacrococcygeal pilonidal sinus disease (PSD) is a chronic, painful soft tissue infectious disorder that affects mostly young people. It is socially disabling, interrupts work and school, and causes physical and emotional suffering. PSD places significant financial burden on the patient, family, and community in terms of days lost, as well as overall costs to the health care system. This chapter discusses the evidence published in the past 10 years focusing on pathophysiology, known risk factors, differential diagnosis, and components of care required for this condition. While management of localized and deep/surrounding tissue infection is a vital component of the care for PSD, the challenges to success are complex. Effective treatment of pilonidal sinus disease requires a comprehensive assessment and management plan that incorporates local, systemic, and patient factors. Successful PSD management requires a systematic interprofessional approach.

Keywords

Pilonidal sinus disease; PSD; Treatment; Harris protocol

1 Introduction

Sacrococcygeal pilonidal sinus disease (PSD) is a chronic, painful soft tissue infectious disorder that affects mostly young people. The disease was first described by Mayo in 1833,¹ and Anderson² in 1847, with Hodges³ assigning the name in 1880, using the Latin words pilus (hair) and nidus (nest). PSD occurs in the intertriginous natal cleft or buttock crease where moisture, friction, and bacteria abound. Similar abscesses can occur elsewhere on the body (axilla, umbilicus, interdigital, breast, etc.) although these are relatively rare.⁴–⁶ For the purposes of this chapter, the focus will be on care of sacrococcygeal/natal cleft pilonidal sinus disease and the resultant wounds.

Often presenting as acute abscesses, the all-too-frequent resultant chronic wounds cause significant upset, being socially disabling, interrupting work and school, and causing physical and emotional suffering. PSD places significant financial burden on the patient, family, and community in terms of days lost, as well as overall costs to the health care system. It can be frustrating for the physicians and clinicians who are involved in the care, and often requires repeated surgeries to achieve healing. Despite more than 100 years of refining surgical and wound care approaches for this etiology, there is still no consensus as to the most effective method of surgery, or wound care, or lifestyle changes, reflected in the large number of articles that exist in the literature; more than 1000 since 2005 were identified.

This chapter reflects on the evidence published in the past 10 years focusing on pathophysiology, known risk factors, differential diagnosis, and the multiple components of care required for this condition: type of surgery, management of bacterial balance, positioning, periwound skin care, type of dressing, level of physical activity, pain management, nutrition, self-care and psychosocial considerations. Successful PSD management requires a systematic interprofessional approach that addresses these principles.

2 Pathophysiology

PSD has been considered as one of a tetrad of follicle occlusion disorders described in 1975⁷ that also includes hidradenitis suppurativa (HS, formerly termed acne inversa), dissecting cellulitis of the scalp, and severe acne congoblata.⁸ In fact, HS is present in 20% of patients with PSD.⁹ Earlier literature considered PSD as a congenital disorder. More recent theories suggest the disorder is an acquired acute or chronic exacerbating, inflammatory reaction,¹⁰,¹¹ caused by the anatomical location, friction, shearing and pressure forces. Natal cleft PSD can present as acute, chronic or silent. The abscesses or tracks often contain a bundle or nest of hairs, as well as keratin scales from dead keratinocytes, fibrosis, and granulation tissue. Surrounding tissue may contain chronic inflammatory changes.

3 Theories of Formation

Bascom¹⁰ first identified that hair follicles become irritated and associated with bacterial damage due to a build-up of keratin and inverted hairs that create an inflammatory response.¹⁰ After studying 6545 cases over 35 years, Karydakis¹² formulated a pathogenic formula citing that three primary variables—loose hair (H), applied with force (F) to vulnerable local skin and tissues (V)—results in insertion of the hair at the depth of the natal cleft (G), leading to local infection and deep and surrounding abscess formation. He noted that the insertion never occurred in the sides of the cleft. A deep natal cleft retains moisture from sweating or bathing that subsequently softens the epidermal layer, making it vulnerable to anaerobic bacterial invasion and accumulation of trapped hair with associated debris.¹³ Folliculitis may also occur in this environment, with similar consequences. Hair is trapped due to the friction forces caused by movement of the buttocks, referred to as a cigarette-rolling effect of the skin surfaces.¹⁴ Sharp hair ends (from split and broken hair shafts originating from the natal cleft, back, head, or neck) or chisel-like root ends facilitate traumatic insertion¹²,¹³ into an enlarged, inflamed hair follicle or into a preexisting sinus track.⁸,⁹,¹⁵,¹⁶ Barbs on the shaft of the hair prevent expulsion.¹⁶ Once one hair has entered, others can easily follow.¹² Early PSD is associated with high midline or lateral pits 2–5 cm from the midline due to hyperkeratosis of the enlarged hair follicle ostium.¹⁶ These pits are the secondary exit point of the hairs. Although they are not the cause of the process, they can be an entry point for subsequent hair insertions.⁹,¹²,¹⁵,¹⁶ Pits are different from sacrococcygeal dimpling in the natal cleft, seen at birth in 0.5% of individuals as a benign variant.¹⁷Another theory proposes an influence of increased sex hormones during puberty, which coincides with the peak incidence of PSD between the ages of 15 and 20. The hormonal sequelae are enlarged hair follicles that have potential for hair penetration, follicular inflammation, infection, and abscess formation. The process is illustrated in Fig. 1.

Fig. 1 Formation of pilonidal sinus disease.

4 Epidemiology and Risk Factors

The prevalence of PSD is estimated at 0.5% to 1% of the general population, affecting predominantly young hairy males of Mediterranean descent. Thompson et al.¹⁸ identified that PSD is rare in East Asia, Oceania and sub-Saharan Africa. The sex ratio is estimated to be 2.2 to 3 males to one female.⁹,¹⁹ The symptom onset is in the late teens: the average age is 21 years for men and 19 for women; then new lesions decrease after age 25.²⁰ Doll et al.¹³ confirmed this in their research on the military population, where older soldiers presenting with the same risk factors as their younger counterparts had significantly lower incidence. In the United States, symptomatic PSD incidence is 26 per 100,000 population,²¹ or 70,000 cases per year.²² This is a consistent finding with other countries, including Norway²¹ and France²³ where the average PSD incidence is 0.7%.

There are several risk factors commonly associated with PSD. People with a triad of extensive body hair, sedentary occupations (i.e., sitting >6 hours), and low frequency of bathing (≤2 times per week) are at a 219-fold increased risk for sacrococcygeal PSD than those without these risk factors.²⁴

Occupation or lifestyle has been demonstrated as a causal factor in PSD. During the Second World War, PSD was nicknamed jeep driver disease.²⁵ Akinci et al.¹⁹ in their study of Turkish soldiers detected 58/88 (65.9%) persons with PSD were vehicle drivers, where rigid suspensions and hard seats may cause minor but repetitive trauma.²¹ Benign dimpling of the natal cleft does not pose a risk unless it becomes a source of recurrent infection. A correlation between obesity and pilonidal sinus incidence and risk of recurrence has been studied several times, with varying results. While not all studies have demonstrated causality, there is sufficient evidence to support the need to modify risk factors where possible to improve outcomes (Table 1). Often a combination of risk factors contributes to PSD.

Table 1

Risk factor analysis and statistics

5 Types of PSD

5.1 Acute, Infected Abscesses

Fifty-four percent of cases present with an acute abscess,²¹ that may rupture spontaneously or require intervention. Abscess formation may occur due to involvement of multiple hair follicles (inflammation→infection→abscess formation) and require drainage and possible systemic antimicrobial therapies. Acute PSD has fewer sinuses, although edema and inflammation may prevent identification of these sinuses.¹³

5.2 Chronic Fistula Cavity

A consecutive foreign body giant cell reaction to the hair, partial epithelization of tracts (due to epithelial cells from the original hair follicle) and chronic infection were thought to be the key tissue responses which lead to chronic fistulas or abscess-forming disease.³² However, it is now believed that multiple sinus formation originates before or at the beginning of symptomatic PSD and a younger age of onset is related to more sinuses present at the time of surgery.¹³ The findings demonstrate that chronic sinus formation appears only when the onset is between the ages of 21.5 and 22.5 years. While all pilonidal sinus wounds (PSWs) contain chronic bacterial infection, additional sinuses or tracks are most likely unrelated to chronic infection. As with most chronic wounds, individuals who have chronic PSD are at risk for developing squamous cell carcinoma (approximately 0.1% of chronic PSD patients) and need to be monitored closely.³³

5.3 Asymptomatic PSD

In autopsies on 100 children, aged 1 day to 10 years, Chamberlain and Vowter³⁴ detected that seven had asymptomatic PSD, with no clinical symptoms, and summarized that the incidence of asymptomatic PSD was double that of clinical acute or chronic PSD. Doll et al.³⁵ described incidental PSD sinus(es) revealed during investigation on persons without history of exudate or symptoms. By performing three biopsies in the natal cleft on each of 432 adult bodies during autopsy, Aysan et al.³⁶ discovered that 20 (4.6%) had at least one visualized sinus tract external tip, and considered that to be a positive clinical sign of silent or incidental PSD. By checking for five additional histopathological features, they determined that an additional 16 (3.7%) cases had >3 features, with no clinical signs of natal cleft PSD. The histological markers included:

• enlarged hair follicle bulb, with or without inflammation

• intrafollicular keratinous debris, inflammatory cell infiltration of natal cleft tissue

• one or more hair shafts at any depth of the subepidermal area and/or in the sinuses

• diffuse spreading of collagen fibers causing fibrosis.

The authors considered these histological features characteristic of silent or asymptomatic PSD.

Table 2 outlines the possible variations that Doll et al.¹³,³⁵ have identified in their review of 1731 patients presenting for PSD surgery.

Table 2

Type of PSD and percentage of cases

6 Differential Diagnosis

A differential diagnosis is critical to ensure a correct diagnosis. People with PSD experience an average of 3–5 years of pain and suffering before being appropriately diagnosed.²,¹⁵,²¹,³⁷

i. Abscesses or sinuses: These lesions extend beyond the natal cleft, or elsewhere on the body, such as anterior groin, axillae or under the breasts. A history or presence of additional abscesses or sinus may indicate coexisting follicular occlusion disorders (e.g., HS). In this situation, PSD is associated with HS requiring systemic treatment that may include antibiotics and prednisone. Destructive therapies for HS include surgical excision with skin grafting or occasionally radiation with laser epilation of hair follicles for dissecting cellulitis.⁸

ii. Furuncles/boils involving the deep hair follicle system may be associated with PSD but usually appear elsewhere on the body and Staphylococcus aureus (including methicillin-resistant strains) is the most common organism associated with this skin lesion.

iii. Anal fistula: This is a tract traveling from the skin to the anal canal. Identify the tract connection with the anus or the opening using rectal digital exam. Treatment options are dependent on whether the anal sphincter is involved. These modalities include a fistulotomy where there is no risk of fecal incontinence, a Seton Suture, Advancement flap procedure, bioprosthetic plug or ligation of the intersphincteric fistula tract (LIFT) procedures.³⁸Although an anal fissure is not a pilonidal sinus, some of the self-care and hygiene aspects of the Harris Pilonidal Sinus Disease Protocol³⁹ can be applied.

iv. Perianal ulcers: These ulcers are often associated with herpes simplex with herpetiform (weeping vesicles in clusters) present on an erythematous base or perianal syphilis, which may appear as a solitary ulcer or two ulcers that may be opposite each other in a kissing configuration. The Centers for Disease Control⁴⁰ advise that evaluation of unusual genital, anal, or perianal ulcers include:

• syphilis serology, darkfield examination, or PCR testing if available

• culture or PCR testing for genital herpes

• serologic testing for type-specific HSV antibody.⁴⁰

Genital herpes, syphilis, and chancroid have been associated with an increased risk for HIV acquisition and transmission. Perianal tuberculosis may mimic pilonidal sinus disease but would also have inguinal lymphadenopathy (higher incidence with HIV infection).

v. Unusual thickened or persistent lesions: There is a need to rule out verrucous (condylomata or genital warts) caused by sexually transmitted viruses, the human papilloma virus (HPV), types 6 and 11. As mentioned, an area of persistent inflammation may develop a squamous cell carcinoma (keratotic papule or nodule).

vi. Perianal Crohn's disease (PCD): is defined as inflammation at or near the anus, including tags, fissures, fistulae, abscesses, or stenosis that is often present in up to 80% of individuals with Crohn's disease.⁴¹

7 Surgical Treatment

Although, this chapter does not focus on surgical techniques, Lee et al.⁴² summarized the different surgical techniques for the treatment of PSD: Open wound (healing by planned secondary intention), fistulotomy and curettage, marsupialization, excision and closure: either midline or asymmetric/oblique (e.g., Karydakis, Bascom procedure, cleft closure) or flaps (e.g., rhomboid, V-Y advancement, Z-plasty, or gluteal-myocutaneous). Tezel⁴³ describes a five-level classification for PSD to inform treatment decision making, based on severity of disease, and defined by the lateral edges and posterior extent of the natal cleft (Table 3).

Table 3

Classification of PSD and recommended interventions adapted from Tezel⁴³

© Harris et al.⁶⁶

The 2011 Cochrane review of the published literature determined that patients who had primary closure healed faster and returned to work earlier than patients whose wounds were left open to heal by secondary intention.⁴⁵ The review also found that primary closure was associated with a higher degree of recurrence than those healed by secondary intention. Each approach has its advantages and disadvantages, and the decision regarding which approach to select needs to be guided by the patient's own desired goals for treatment. Illustrating the ongoing search for an ideal surgical technique, three separate 2016 papers describe minimally invasive procedures. First, a prospective randomized controlled trial (RCT)⁴⁹ with 145 patients compared video-assisted ablation of pilonidal sinus, in which the entire sinus was removed with a minimal surgical wound, to Bascom's cleft lift procedure. There was little difference in complication rates, but patients having the endoscopic treatment had statistically significant less pain at 1 hour, 1 day, 1 week and 1 month postsurgery (P=.001 for all), and greater satisfaction at 1 and 6 months (P=.001 for both). A second prospective study⁵⁰ on endoscopic treatment with 250 patients tracked them for 12 months postop, and found that the failure to close and recurrence rates were both 5%. Third, in a study of 31 patients,⁵¹ a rotating Farrell applicator was used to ablate the sinus tracts, removing hair and debris trapped along the spiral thread each time it is removed. The procedure finished with scraping of the cutaneous orifices. If not healed at 15 days, the procedure was repeated, with an 87% heal rate overall. All three groups need longer follow-up to determine the long-term effects, but are promising. Table 4 provides an overview of information regarding the types of surgical interventions.

Table 4

Surgical techniques for pilonidal sinus disease

© Harris et al.⁶⁶

Lifestyle changes, which will be further discussed in the treatment section, and attention to patient-centered concerns may also improve wound closure rates and reduce recurrence, especially with discussion and counseling during the preoperative period. Al-Khayat et al.⁶³ found that, while excision and primary closure is an acceptable treatment in nonobese and nonsmoking patients with PSD, the infection rate in obese patients and smokers is unacceptably high. They recommended a program of preoperative weight loss and smoking cessation. If this could not be achieved, the planned approach would be excision and secondary closure.

8 Other Treatment Considerations

The modified Delphi technique used to create the Harris Pilonidal Sinus Wound protocol³⁹,⁶⁴ for open and infected pilonidal sinus wounds demonstrated the complexity of caring for and healing these wounds, further supported in 2012 and 2016.⁶⁵,⁶⁶ Delays in healing for this patient population are multifactorial and include:

• Inadequate positioning for wound assessment

• Hair entrapment in the wound cavity leading to inflammation with potential for infection with a need for source control (i.e., hair removal)

• Wound-related exudate with resultant moisture associated skin damage (i.e., maceration)

• Use of dressings that donate moisture to the wound surface aggravating the problem

• Suboptimal wound and periwound skin hygiene

• Hypergranulation or fragile epidermal/dermal components caused by excessive inflammation and/or bacterial damage in the wound or periwound skin (may be associated with pocketing and undermining)

• Unrecognized critical colonization or deep/surrounding infection (slough may facilitate biofilm formation)

• Inadequate nutrition (i.e., protein)

• Physical activities leading to friction or shear with subsequent tissue trauma

• Lack of adherence to meticulous treatment protocols (may be multifactorial).

The following section reviews and updates the 2010 Harris pilonidal sinus work.³⁹,⁶⁴ The protocol is principle-focused rather than prescriptive. It does not differentiate between PSD wounds healing by secondary intention, those treated with a local incision and drainage (I&D), or those where primary surgical intervention has failed, resulting in an open wound, because similar issues exist in all three