By :-

Habieba
Usarani
Priyashini
Vincent
Farhana
vinoota
• Infection of soft tissue can be localised/spreading (generalised) and necrotizing/non-
necrotizing
• Mostly due to Gram +ve cocci (Staphylococcus aureus, Streptococcus pyogens)
• But also can due to animal bite, penetrating foreign body whereby more unusual
organism found
• Cellulitis is a non contagious bacterial infection involving deep layer of skin
(subcutaneous tissue)
• Usually generalised and associated with broken skin or pre-existing ulceration
• Preferentially involves the lower extremities, but generally may occur anywhere on the
body (arm, neck areas, head)
• Characterised by redness, swelling and heat, accompanied by pain and tenderness
• Most common causative organism: beta-haemolytic streptococci
• Can also due to Staphylococcus sp including community acquired MRSA (Methicillin-
resistant Staphylococcus aureus)
• Chronic leg swelling (oedema)
• Diabetes or other immune compromising disease/condition: HIV, chemotherapy
• Site of entry: leg ulcer, trauma, surgical wound, insect bite
• Underlying skin disorders: eczema, impetigo, tinea pedis (athlete’s foot)
• Conditions/disease that reduce blood circulation or lymphatic fluid circulation: venous
insufficiency, obesity, pregnancy
• Previous history of cellulitis
 SIGNS
• Erythema in involved area with poorly
demarcated margins, oedema and
warmth
• Tense and glossy appearance of skin
• Yellowish fluid discharge at centre of
swollen area
• Swollen lymph nodes near the area of
infected skin
SYMPTOMS
• Low grade fever
• Or high grade fever with chills and rigor
(in serious cellulitis)
• Pain at affected area
Cellulitis VS erysipelas: affected area is
raised and erythematous, also sharply
demarcated from normal skin
appearance
• Spread of infection into bloodstream or to other body tissues such as into heart
(endocarditis) and bones (osteomyelitis)
• Septic shock due to prolonged sepsis
• Tissue death (gangrene)
• Death
 INVESTIGATION DIAGNOSIS

• Full blood count • Usually based on a medical history

- Leukocytosis and physical examination
• ESR (erythrocyte sedimentation rate) & • Blood and skin samples may be taken
CRP to confirm the diagnosis and the type
- Elevated of bacteria that is present.
• Blood culture and sensitivity • A bacterial culture can identify the
- Positive organism causing the condition and
• Skin swab / fluid culture indicate the most effective antibiotic.
- Present of bacteria
• Treat underlying cause
• Clean, elevate and immobilize affected limb to reduce swelling
• Sterile setting to remove purulent exudate
• Proper dressing on infected site
• Antibiotics: cloxacillin and c-penicillin (non-diabetic), unasyn;ampicillin-sulbactam
(diabetic), vancomycin (MRSA cellulitis)
• Mild cellulitis: treat as outpatient, with oral antibiotic
• Moderate or severe cellulitis: admitted in ward to give IV antibitic
• Analgesic (if indicated)
 Cellulitis Erysipelas

Definition Bacterial skin infection involving Bacterial skin infection involving

deeper dermis and subcutaneous fat upper dermis and cutaneous
lymphatics

Epidemiology Middle age and older adults Young children and older adults

Etiology Most commonly streptococcus species

Pathophysiology Pre-existing injury in the skin

Common site Lower extremities/ leg Face

 Cellulitis Erysipelas
Clinical • Erythema, edema, warm
manifestation • Fever
• Petechiae or haemorrhage can be seen in erythematous skin
• Superficial bullae can occur
• Lymph node enlargement
• with/without purulence • Non-prurulent
• Localized symptoms • Acute onset of symptoms with systemic
manifestations (fever, chills, severe
malaise, and headache, muscle and
joint pain)
• Poorly demarcated margin • Well demarcated margin
• Not raised • clear line between involved and
uninvolved tissue
• raised above level of surrounding
normal tissue
 Cellulitis Erysipelas
Investigations Raised ESR and CRP
Bacterial culture
* Most of the time diagnosed clinically
Prognosis Recurrence Rarely recur if prompt treatment
given (Antibiotic)

Treatment:
1. Pt with systemic manifestation (fever, chills) should be treated with parenteral therapy.
 Cephalosporins
2. Pt with mild infection or have improved following initial treatment can treated with oral penicillin/ amoxicillin
3. Duration depend on clinical response (5-14 days)
 • An abscess is surrounded by an acute inflammatory response composed of a
fibrinous exudate, oedema and the cells of acute inflammation.

ETIOLOGY OF ABSCESS
The main cause of abscess are pyogenic bacteria such as_
-Sterptococcus spp
-Staphylococcus spp
-Pseudomonas aeruginosa
Cellulitis present
Swollen
Soft center
feels like fluid underneath
Painful
Tender
.Acute or hot abscess
2.Chronic or cold abscess
3.Superficial abscess
4.Deep abscess
5.Embolic abscess
6.Pyaemic or metastatic abscess.
Any breach in skin and mucous membrane
Pyogenic bacterial invasion
Formation of pyogenic membrane
Body immunity fails to fight
Finally abscess develops
o obesity

o diabetes

o atopic dermatitis

o chronic kidney disease

o malnutrition

o immune suppression/corticosteroids o IV drug use

o close contact with others with furuncles, e.g. sports teams

o hygiene•

Treatment: Incision and drainage, dry sterile dressings; antibiotics only if extensive
cellulitis or fever (systemic signs)
Necrotizing fasciitis is a rapidly progressive inflammatory infection of the fascia,
with secondary necrosis of the subcutaneous tissues.
Spread across soft tissue planes & flesh eating
• Surgical procedures that may cause local tissue injury and bacterial invasion (surgery for
intraperitoneal infections and drainage of perianal abscesses, IM injections and IV infusions)

• Minor insect bites

• Local ischemia and hypoxia can occur in patients with systemic illnesses (diabetes)
• Immune suppression
• Diabetes
• AIDS
• Cancer

• Bacterial introduction
• IV drug use
• Hypodermic therapeutic injections
• Insect bites
• skin abrasions
• abdominal and perineal surgery

• Associated conditions
• cellulitis
• Early findings
• localized abscess or cellulitis with rapid progression
• minimal swelling
• no trauma or discoloration
• late findings
• severe pain
• high fever, chills and rigors
• tachycardia
• skin bullae
• discoloration
• ischemic patches
• cutaneous gangrene
• swelling, edema
• dermal induration and erythema
• subcutaneous emphysema (gas producing organisms)
Left upper extremity shows necrotizing fasciitis in an individual who used illicit drugs. Cultures grew Streptococcus milleri
and anaerobes (Prevotella species). Patient would grease, or lick, the needle before injection.

Necrotizing fasciitis at a possible site of insulin injection in the left upper part of the thigh in a 50-year-old obese
woman with diabetes.
Photomicrograph of Fournier gangrene (necrotizing fasciitis), oil immersion at 1000X magnification. Note the acute
inflammatory cells in the necrotic tissue. Bacteria are located in the haziness of their cytoplasm. Courtesy of Billie Fife,
MD, and Thomas A. Santora, MD.
Left lower extremity in a 56-year-old patient with alcoholism who was found comatose after binge drinking. Surgical drainage
was performed to treat the pyomyositis-related, large, non–foul-smelling (sweetish) bullae. Gram staining showed the presence
of gram-positive rods. Cultures revealed Clostridium perfringens. The diagnosis was clostridial myonecrosis.
Sixty-year-old woman who had undergone postvaginal hysterectomy and repair of a rectal prolapse has a massive
perineal ulceration with foul-smelling discharge. Cultures revealed Escherichia coli and Bacteroides fragilis. The diagnosis
was perineal gangrene.

Necrotizing fascitis of entire thoracolumbar posterior area in 20-year-old patient with chronic myelogenous leukemia and
neutropenia (WBC count, 680/uL). Cultures revealed gram-negative Pseudomonas species and Bacteroides fragilis.
• Emergent frozen section can confirm diagnosis in early cases
• Technique:
• take 1x1x1cm tissue sample
• can be performed at bedside or in operating room
• surgical intervention should not be delayed to obtain
• Histological findings:
• necrosis of fascial layer
• microorganisms within fascial layer
• PMN infiltration
• fibrinous thrombi in arteries and veins and necrosis of arterial and venous walls
• CRP (mg/L) • Sodium (mmol/L)
• ≥150: 4 points • <135: 2 points
• WBC count (×103/mm3) • Creatinine (umol/L)
• <15: 0 points
• >141: 2 points
• 15–25: 1 point
• >25: 2 points • Glucose (mmol/L)
• Hemoglobin (g/dL) • >10: 1 point
• >13.5: 0 points
• 11–13.5: 1 point
• <11: 2 points
• The rapid and destructive clinical course of necrotizing fasciitis is thought to be due to
multibacterial symbiosis and synergy.
• Group A beta-hemolytic Streptococcus (GABS) has been identified as a major cause of
this infection.
• Usually associated with an underlying cause, such as diabetes, atherosclerotic vascular
disease, or venous insufficiency with edema.
• Usually polymicrobial rather than monomicrobial.
• Anaerobic bacteria are present in most necrotizing soft-tissue infections, usually in
combination with aerobic gram-negative organisms.
• Anaerobic organisms proliferate in an environment of local tissue hypoxia in those
patients with trauma, recent surgery, or medical compromise.
• Carbon dioxide and water are the end products of aerobic metabolism.
• Hydrogen, nitrogen, hydrogen sulfide, and methane are produced from the
combination of aerobic and anaerobic bacteria in a soft tissue infection.
• These gases, except carbon dioxide, accumulate in tissues because of reduced
water solubility.
• Organisms spread from the subcutaneous tissue along the superficial and deep
fascial planes, presumably facilitated by bacterial enzymes and toxins.
• This deep infection causes vascular occlusion, ischemia, and tissue necrosis.
Superficial nerves are damaged, producing the characteristic localized anesthesia.
Septicemia ensues with systemic toxicity.
• Important bacterial factors include surface protein expression and toxin
production. M-1 and M-3 surface proteins, which increase the adherence of the
streptococci to the tissues, also protect the bacteria against phagocytosis by
neutrophils.
• Operative treatment
• emergency radical debridement with broad-spectrum IV antibiotics post q
• Indications
• whenever suspicion for necrotizing fasciitis
• Operative findings
• liquefied subcutaneous fat
• dishwater pus
• muscle necrosis
• venous thrombosis
• Initial antibiotics
• start empirically with penicillin, clindamycin, metronidazole, and an aminoglycoside
• Definitive antibiotics
• Penicillin G: strep or clostridium
• Imipenem or doripenem or meropenem: polymicrobial
• + vancomycin or daptomycin if MRSA suspected
• Amputation
• low threshold for amputation when life threatening
Figure A is a clinical radiograph showing early necrotizing
fasciitis. Illustration A is a clinical photograph of a lower
extremity with necrotizing fasciitis and the classic signs of bullae,
tracking erythema, and swelling.
The clinical presentation is consistent with early necrotizing fasciitis. A biopsy with a
frozen section is effective at rapidly confirming an early diagnosis. If the biopsy is
performed in the operating room, and is positive, then their will be minimal time
delays in performing the required radical debridement.

Necrotizing fasciitis is characterized by hypotension, ascending rash, bullae and

fevers. Skin abrasions, prior surgical intervention, and any cause of open wounds in
the skin are all risk factors for the condition. The most common cultures are
polymicrobial. The management consists of immediate IV antibiotics and emergent
surgical debridement. Initial IV antiobiotics should be broad-spectrum to include
penicillin, an aminoglycoside, clindamycin, and metronidazole.

Incorrect Answers:
Answer 1 and 4: Although MRI and CT scans are useful adjuncts to demonstrate
edema in the soft tissue it does not provide the definitive diagnosis.
Answer 3: Needle aspiration has no use in the diagnosis of necrotizing fasciitis.
Answer 5: Ultrasound would be helpful if an abscess was suspected.
• The above clinical vignette is describing necrotizing fasciitis. Necrotizing fasciitis is
a rare and often fatal soft-tissue infection that requires high clinical suspicion and
prompt administration of broad-spectrum antibiotics and aggressive surgical
debridement (illustrations A). Fontes et al found that although polymicrobial
infections including gram-positive, gram-negative, aerobic, and anaerobic bacteria
were found most commonly in necrotizing fasciitis, Group A streptococcus was the
most common bacterial isolate. Wong et al also found the most isolated organism
to be group A streptococcus. In their study, the highest associated medical
comorbidity was diabetes mellitus (71%). They found that delay in surgery of more
than 24 hours was correlated with increased risk of death
• Infection of tissue by toxin producing clostridia
• Also known as clostridial myonecrosis
• Gas gangrene is most often caused by bacteria called Clostridium perfringens
• Clostridium is found nearly everywhere
• Gas gangrene develops suddenly. It usually occurs at the site of trauma or a recent
surgical wound
• People most at risk for gas gangrene usually have blood vessel disease
(atherosclerosis, or hardening of the arteries), diabetes, or colon cancer.
Most common causative agent: Clostridium perfringens
• Anaerobic organisms
• Survive & multiply only in tissue with low oxygen tension
• Example : dirty wound with dead muscle that has been closed without adequate debridement
• Incubation period <24h
Produce exotoxins (e.g. C. perfringens alpha toxin)
• Causes muscle necrosis and hemolysis
• Gas produced by fermentation of glucose
• Spread to blood stream and other tissue
• Post trauma
• Sustain serious injury to skin / soft tissue
• Experience open fracture
• Post operative
• History of blood vessel disease (atherosclerosis, or hardening of the arteries),
diabetes, or colon cancer
• Sudden onset of pain  gradually worsen
• Low grade fever
• Painful swelling
• Pale skin color, later becoming dusky and changing to dark red or purple
• When swollen area is pressed, gas can be felt as a crackly sensation (crepitus)
• Air under the skin (subcutaneous emphysema)
• Blisters filled with brown-red fluid
• Foul-smelling brown-red or bloody fluid (serosanguineous discharge)
• Tachycardia
• Fever
If the condition is not treated, the person can go into shock with decreased blood
pressure (hypotension), kidney failure, coma, and finally death
• Blood investigation
• Elevated white blood cells
• Neutrophilia
• High ESR
• Increased lactate dehydrogenase (LDH)
• Blood culture to determine the bacteria causing the infection

• Tissue and fluid cultures to test for bacteria including clostridial species
• X-ray, CT scan, or MRI of the area may show gas in the tissues
• Fluid replacement
• Antibiotic therapy
• Wound debridement
• Amputation
• Hyperbaric oxygen treatment
• Clean any skin injury thoroughly
• Watch for signs of infection (such as redness, pain, drainage, or swelling around a
wound
• Deep, penetrating wound in muscular tissue are dangerous
• All dead tissue should be completely excised
• There is no effective antitoxin against Clostridium perfringens
By: Vinoota
• Tetanus is a nervous system disorder characterized by muscle spasms that is caused
by the toxin-producing anaerobe Clostridium tetani
• Unvacinated or inadequadely immunised
• Entirely preventable disease if immunization is given
• Hot and damp climate with soil rich in organic matter
• Developing and underdeveloped country
Clostridium tetani
• Gram positive
• Anaerobic however spores can live in oxygen rich area
• Rod shape
• tennis / drumstick shape
• Motile
• Incubation varies from few days to weeks
• Soil,animal feces and occasionally human feces
• Not from person-person
• Through acute wound or chronic skin lesions
• Open fracture, trivial injuries, burns, gangrene, animal or insect bite, abscess,
parenteral drug use, neonates via infected umbilical stumps
 C.Tetani enters body through wound

Stays as sporulated form until optimal anaerobic condition is achieved

Germinates under anaerobic condition and multiply

Produce tetanospasmin a potent nuerotoxin

Tetanospasmin travels through bloodstream and lymphatics and attach to motor nueron

Travels via axons to spinal cord

Binds to specific sites which are responsible to inhibit skeletal muscle contraction
• General malaise
• Trismus (lockjaw)- masseter muscle
• Risus sardonicus(Grinning expressions)- facial muscle
• Severe – painful reflex spasm 24-72 hr of initial symptom
• Laryngeal spams- respiration problem
• Oesophageal spasm – dysphagia
• Urinary retention
• Opisthotonus - arching of neck and back muscle
• Autonomic dysfunction – tachycardia, labile blood pressure, sweating, cardiac
arrhythmia
Trismus

Risus sardonicus

Opisthotonus
• Short incubation period
• Short onset time
• Extremes of age
• Death due to- aspiration, hypoxia, respiratory failure, cardiac arrest
 TYPE
Localized tetanus
Cephalic tetanus
Neonatal tetanus
Opthalmoplegic tetanus
DESCRIPTION
 Mild
 Pain and stiffness confined to the wound area with
increase tone of surrounding muscles
 Recovery usually occur
 Uncommon but fatal
 When portal of entry of C.Tetani is middle ear.
 Cranial nerve abnormabilty usually CN VII
 Generalise tetanus present / absent
 Infection of umbilical stump
 Failure to thrive, poor suckling, grimacing, irritabilty,
intense rigidity and spasm
 100% mortality
 Penetrate through eye injuries
 CN III palsy and ptosis
• By clinical findings
• Gram stainning
• Culture – Robertson’s cooked meat medium
• Differential diagnosis
1. Phenothiazine overdose
2. Strychnine poisoning
3. Meningitis
4. Tetany
 SUSPECTED TETANUS ESTABLISHED TETANUS
 Any wound must be clean  Place patient in quiet, isolated, well
and debrided if necessary ventilated and darkroom
 Human tetanus IG 250  Benzodiazepines- control spasm and
unit + IM tetanus toxoid sedate patient
 If patient already  Intubation and mechanical ventilation-
protected- single booster respiratory compromise
dose of toxoid  Magnesium sulphate infusion-
 If not three doses must be decrease need of antispasmodics
given  IV metronidazole/ penicilin/
cephalosporin
 IM HTIG 500 IU – neutralize
circulating toxin
 If not IM immune equine tetanus IG10
000 IU – severe allergic reaction
 After patient recover active
immunization should be administered
PREVENTION
 Preventable disease
 All individuals should be
immunise regardless of age
 Active immunization with
alum-adsorbed toxoid
 Boosters at 10 year interval
for those at risk
 Passive - equine / HTIG are
short lived and last for only 2
weeks
• https://www.medicinenet.com/cellulitis/article.htm#cellulitis_facts

• Essential of Kumar & Clark’s Clinical Medicine, 5th ed, Anna Ballinger, 2011

• Browse’s Introduction to the Symptoms and Signs of Surgical Disease, 5th ed, Kevin G
Burnand, 2015
• Uptodate