This document summarizes common skin conditions and infections of surgical importance. It discusses bacterial infections like folliculitis, furuncles, carbuncles and cellulitis. It also covers fungal infections like actinomycosis and viral infections like human papilloma virus. Benign and malignant skin tumors are outlined. Deeper skin infections such as necrotizing fasciitis, pyomyositis and hidradenitis suppurativa are also described. Diagnostic testing, treatment options and management approaches are provided for many of the conditions.

1. Skin conditions of surgical
Importance
Dr Janai A. M Ondieki
For Clinical Medicine Diploma Class
yr 2

2. Anatomy of the Skin

3. Outline
• Common skin infections of surgical importance
– bacterial
• Folliculitis, furuncles, Carbuncles
• Cellulitis
• Necrotizing Infections
• Cellulitis
• Hidranitis Suppurativa
– Fungal
• Actinomycis
– Viral
• Human papilloma virus

4. • Skin Tumours
– Benign
• Seborrhoiec keratosis
• Cysts- epidermal inclusion cysts, dermoid cysts
• Lipomas
• Haemangiomas
• Naevi
– Malignant
• Malignant Melanoma
• Squamous cell carcinoma
• Basal cell carcinoma

5. Skin Infections involving hair follicles
• Folliculitis
– Superficial bacterial infection
of the hair follicles
– Presents as small, raised,
erythematous pustules <
5mm in diameter
– ! Genital folliculitis maybe STI
– Pathogens:
• Staph aureus most common
• Pesudomonas esp. from hot
tubs and swimming pools
• Candida genital folliculitis

6. • Furuncle/Furunculosis/Boil
– Acute round tender
circumscribed perifolliclar
abscess that generally ends in
central suppuration
– More deep seated than
folliculitis
• Furunculosis – when they
are multiple

7. • Carbuncle
– Coalescences of several
inflammed follicles into a
single mass with
purulent drainage from
multiple follicles
– Staph aureus is most
common pathogen

8. Treatment
• Folliculitis
• Thorough cleaning with antibiotic
soap
• Oral/topical antibiotics
• Deep seated lesions should be
drained
• Furuncles/Carbuncles
• These are subtypes of abscesses
preferentially occurring on skin
areas containing hair follicles
exposed to friction and
perspiration
• Use of oral antibiotics
• Small ones can be done warm
compresses to encourage
spontaneous drainage
• Large ones require drainage as
abscess

9. Hidradenitis suppurativa
• Hidradenitis suppurativa is a disorder of the terminal follicular epithelium
in the apocrine gland–bearing skin.
• This condition is a chronic disabling disorder that relentlessly progresses,
frequently causing keloids, contractures, and immobility.
• usually occurs in otherwise healthy adolescents and adults. It rarely may
begin before puberty.
• characterized by comedolike follicular occlusion, chronic relapsing
inflammation, mucopurulent discharge, and progressive scarring.

10. • Treatment
• Local hygiene and ordinary hygiene
• Weight reduction in patients who are obese
• Use of ordinary soaps and antiseptic and
antiperspirant agents (eg, 6.25% aluminum chloride
hexahydrate in absolute ethanol)
• Application of warm compresses with sodium
chloride solution or Burow solution
• Wearing of loose-fitting clothing
• Laser hair removal
• Cessation of cigarette smoking
• Surgical excision may be used in advanced cases
• Radiotherapy may also be used in the early stages

11. Serious infections of deeper skin
structures

12. Cellulitis
• An acute, diffuse, spreading non necrotizing
infection of the skin, involving the deeper
layers of the skin and the subcutaneous tissue.
• Periorbital cellulitis is a special form of
cellulitis that usually occurs in children. In this
form of cellulitis, unilateral swelling and
redness of the eyelid and orbital area, as well
as fever and malaise are usually present.

13. CAUSES
• Staphylococcus
• Streptococcus Group A β
• H. Influenzae (periorbital cellulitis)
• pasteurella multocida
• Facial cellulitis in children < 3 years old
Hemophilus influenzae or Streptococcus
pneumoniae

15. PREDISPOSING RISK FACTORS
– Local trauma (e.g., lacerations, insect bites,
wounds, shaving)
– Skin infections such as impetigo, scabies, furuncle,
tinea pedis
– Underlying skin ulcer
– Fragile skin
– Immunocompromised host
– Diabetes mellitus
– Inflammation (e.g., eczema)
– Edema secondary to venous insufficiency or
lymphedema

16. TYPICAL FINDINGS OF CELLULITIS
History
• Presence of predisposing
risk factor
• Area increasingly red, warm
to touch, painful
• Area around skin lesion also
tender but pain localized
• Edema
• Mild systemic symptoms –
low-grade fever, chills,
malaise, and headache may
be present

17. Physical Assessment
• Local symptoms:
– Erythema and edema of area
– Warm to touch,
– Possibly fluctuant (tense, firm
to palpation)
– May resemble peau d’orange
– Advancing edge of lesion
diffuse, not sharply
demarcated
– Small amount of purulent
discharge may be present
– Unilateral
• Systemic symptoms:
– Increased temperature
– Increased pulse
– Lymphadenopathy of regional
lymph nodes and / or
lymphangitis

18. • Erysipelas
– Superficial form of cellulitis with
marked dermal lymphatic
involvement( causing skin to be
oedematous or raised)
– Main pathogen- Group A
Streptococcus
– Usually affects face and lower
extremities
– Presents with pain, superficial
erythema & plaque like oedema
with sharply defined margins
– Associated with high WBC count
<20,000/mcl
– May be preceded by chills, fever,
headache vomiting and joint pain
– Treatment Oral antibiotics and
elevation of involved area

19. Diagnostic Tests
• Swab any wound discharge for culture and sensitivity
• Full blood count
• Blood cultures should also be done in the following circumstances
– Moderate to severe disease[ (eg, cellulitis complicating lymphedema)
– Cellulitis of specific anatomic sites (eg, facial and especially ocular areas)
– contact with potentially contaminated water[
– Patients with malignancy who are receiving chemotherapy
– Neutropenia or severe cell-mediated immunodeficiency
– Animal bites
• Radiographs of the affected limb
• Doppler ultrasound in suspected DVT

20. MANAGEMENT AND INTERVENTIONS
• Do not underestimate
cellulitis. It can spread
very quickly and may
progress rapidly to
necrotizing fasciitis. It
should be treated
aggressively and
monitored on an ongoing
basis

21. Goals of Treatment for Mild Cellulitis
• Resolve infection
• Identify formation of abscess
• Check tetanus prophylaxis

22. Non-pharmacologic Interventions
• Apply warm or, if more comfortable, cool
saline compresses to affected areas for 15
minutes.
• Mark border of erythema with pen to monitor
spread.
• Elevate, rest and gently splint the affected
limb.

23. • Pain management
• Oral antibiotics non-purulent cellulitis
• Patients with purulent/Severe cellulitis:
– Inpatient management
– incision and drainage of the abcess
– Parenteral antibiotic therapy initially braod
spectrum the culture bases

24. Necrotizing fasciitis
• A progressive life-threatening soft-tissue infection
(with liquifactive necrosis of subcutaneous fat and
fascia) ± skin . Rapidly progressive bacterial
infection
• Pain, erythema edema, fever->severe pain with
limb swelling->high fever, bluish discoloration &
blisters Gangrene and & muscle necrosis

25. 1. Oedema beyond area of erythema
2. Crepitus
3. Skin blistering
4. Fever (often absent)
5. Greyish drainage (‘dishwater pus’)
6. Pink/orange skin staining
7. Focal skin gangrene (late sign)
8. Final shock, coagulopathy and multiorgan failure
Sign of necrotising infections

28. • Polymicrobial, synergistic infection –
• Most commonly a streptococcal species (group
aβ haemolytic) in combination with
• Staphylococcus,
• Escherichia coli,
• Pseudomonas,
• Proteus,
• Bacteroides or
• Clostridium;
• 80% have a history of previous trauma/infection
• over 60% commence in the lower extremities.
Pathogens

29. 1. Diabetes
2. Smoking
3. Penetrating trauma
4. Pressure sores
5. Immunocompromised states
6. Intravenous drug abuse
7. Skin damage/infection (abrasions, bites & boils)
Predisposing conditions

30. Classical clinical signs
• Febrile and tachycardic (early
stages)
• Very rapid progression to
septic shock.
• Oedema stretching beyond
visible skin erythema,
• Disproportionate pain in
relation to the affected area
• Skin vesicles
• Palpation
– A woody hard texture to the
subcutaneous tissues,
– An inability to distinguish
fascial planes & muscle groups
– Soft-tissue crepitus.
• Lymphangitis tends to be
absent.

31. • Radiographs : air in the
tissues
• Diagnosis: on the basis
of symptoms and signs
without recourse to
‘screening radiography’
• unnecessary delay may
be lethal.

32. Management
1. Urgent fluid
resuscitation,
2. Monitoring of
haemodynamic status
3. High-dose broad-
spectrum IV antibiotics.
4. Surgical debridement-
diseased area should be
debrided ASAP until
viable, healthy, bleeding
tissue is reached.
5. Secondary closure later
with flaps or skin grafts

33. Pyomyositis
• Pyomyositis is a purulent infection of skeletal muscle that
arises from hematogenous spread, usually with abscess
formation.
• Predisposing factors for pyomyositis include
immunodeficiency
– Trauma
– injection drug use
1. concurrent infection
– Malnutrition
• Local injection site infection and abscess extension into
muscle tissue should not be confused with true
pyomyositis caused by hematogenous seeding of muscle
groups distant from injection sites.

34. • Aeriology
• Staphylococcus aureus
• Group A streptococci Less
common causes include
non-group A streptococci,
pneumococci and gram-
negative enteric bacilli.
• E. coli pyomyositis among
patients with hematologic
malignancy.

35. Clinical presentation
• Stage 1 Pyomyositis presents with fever and pain with cramping localized
to a single muscle group.
• The disease occurs most often in the lower extremity (sites include the
thigh, calf and gluteal muscles), but any muscle group can be involved,
including the iliopsoas, pelvic, trunk, paraspinal and upper extremity
muscles
• Stage 2 A frank abscess may be clinically apparent, and aspiration of the
affected muscle typically yields pus.
• Stage 3 Characterized by systemic toxicity.
• The affected muscle is fluctuant.
• Complications of S. aureus bacteremia such as septic shock, endocarditis,
septic emboli, pneumonia, pericarditis, septic arthritis, brain abscess, and
acute renal failure can occur

37. Diagnosis
• Radiography
– Ultrasound
– CT Scan
– MRI
• cultures,
– Blood cultures
– Pus cultures
• laboratory data.
– Full bllod count – raised
wbc count
– Raised ESR, CRP

38. • Treatment
– Incision and drainage
– Broad spectrum
intravenous antibiotics
– Wound care
– Treat underlying
pathology

39. Warts
• Warts are benign proliferations of skin and mucosa
caused by the human papillomavirus (HPV)
• Currently, more than 100 types of HPV have been
identified. Certain HPV types tend to infect skin at
particular anatomic sites; however, warts of any HPV
type may occur at any site.
• The primary clinical manifestations of HPV infection
include
– common warts,
– genital warts,
– flat warts, and
– deep palmoplantar warts (myrmecia).

40. • Warts are transmitted by direct or indirect
contact, and predisposing factors include
disruption to the normal epithelial barrier.
• A small number of high-risk HPV subtypes are
associated with the development of
malignancies, including types 6, 11, 16, 18, 31,
and 35.
• Malignant transformation most commonly is seen
in patients with genital warts and in
immunocompromised patients.

42. Treatment of warts
• Medical
– Benign neglect
– Topical agents
• Salicylic acid
• Podophyllotoxin
• Antiviral agents- Cidofovir
• 5-fluorouracil
• Tretinoin
– Intralesional Injection
• Bleomycin
• Surgical
– Crysurgery
– Laser surgery
– ElectroDessication/ cautery
– Curretage
– Excision