Necrotizing fasciitis and gas gangrene are aggressive soft tissue infections that can cause rapid tissue destruction. Necrotizing fasciitis begins as a bacterial infection of the fascia and subcutaneous tissue, often following minor trauma or surgery. It spreads quickly along the fascial plane and can cause sepsis and organ failure if not treated promptly with extensive wound debridement and IV antibiotics. Gas gangrene is caused by Clostridium bacteria invading wounded muscle tissue. It leads to muscle necrosis, toxin production, and gas formation, with high mortality if not surgically treated. Cellulitis is a superficial skin infection that presents with erythema, pain, swelling and warmth over the affected area. It is usually

1. Necrotising fasciitis
Supervisor : Dr Dhanraj
Presenter
1.Lim Jing Ying
2.Tharshani Devi Srinivasagam

2. Necrotising fasciitis

3. Introduction
● Necrotizing fasciitis is a subset of the aggressive skin and soft tissue
infections (SSTIs) that cause necrosis of the fascia and subcutaneous
tissues.
● Travels rapidly along the fascial plane (poor blood supply) (2-3cm/H),
leaving the overlying tissues initially unaffected, potentially delaying
diagnosis and surgical intervention.
● Muscle tissues are frequently spared because of its generous blood
supply.

4. Etiology
• Follows an injury to the involved site
• Minor trauma
• Blunt trauma
• Insect bite
• surgical incision
• cuts
• injection site
• cutaneous ulcers
• burns

5. • Skin is the most common portal of entry
• 45% cases of unknown route
• Mostly involve extremities but may affect any body part
• infection of trunk and perineal region have higher mortality rate

8. Risk Factor
● Bacterial introduction:
○ Insect bites
○ Skin abrasions
○ Surgical procedure: abdominal, perineal surgeries or even a phlebotomy
○ IV drug user
● Immunosuppression:
○ DM
○ AIDS
○ Cancer
○ Organ transplant

9. CLINICAL PRESENTATION
● Pain
● Swelling
● Redness
● Fever

10. ● Early Signs
○ Tenderness (out of proportion)
○ Swelling
○ Skin induration
○ Patchy
discolouration/erythematous
without a defined margin

11. ● Late Signs
○ Necrotic patch of skin
○ Tense edema
○ Anaethesia
○ Bullous formation (initially clear to hemorrhagic)
○ Crepitus
○ Sepsis/multiorgan failure

12. Diagnosis
• Diagnosis is primarily clinical, and no test is as valuable as a high
degree of suspicion.
• Laboratory and radiologic evaluations can be helpful but are best
used for confirmation of the diagnosis.
• Pursuing such tests should never delay surgical intervention.
• Average time from onset of initial symptoms to diagnosis is 2 to 4
days, although some cases may take weeks to be correctly identified

13. Investigations
● FBC – haemoglobin level, TWC
● RP – sodium and creatinine level
● Blood glucose level
● CRP
● Blood gas
● Blood culture and sensitivity
● Plain X-ray
● USG

14. LRINEC score
- Laboratory Risk Indicator for
Necrotizing Fasciitis
- A tool for distinguishing necrotizing
fasciitis from other soft tissue
infections
- Cut off value is 6 points with positive
predictive value of 92% and negative
predictive value of 96%
- A score of 6 and above suggests NF

15. Finger probe Test
● Pt will be given LA
● Make 2-3cm incision in the skin large enough to insert index finger down
the deep fascia
● Lack of bleeding and /or “dishwasher pus” (grey coloured fluid )in the
wound seen
**SUGGESTIVE TO NECROTIZING FASCIITIS**

17. Management
- Early treatment is CRITICAL !
- What to do ?
- Treatment of shock (if any)
- Start IV broad spectrum antibiotics immediately
- Analgesics
- Extensive wound debridement
- Once cultured organism identified, start specific IV antibiotics

18. Choices of antibiotics

20. Prognosis
● Untreated NF has poor prognosis (severe morbidity eg limb loss are frequent
and death)
● Without appropriate treatment, mortality rate can be as high as 24-34%

21. Ddx: GAS GANGRENE

22. Gas Gangrene/ Clostridial myonecrosis
Epidemiology
• demographics
 male:female ratio – no sexual predilection
• risk factors
 posttraumatic (associated with C perfringens)
• car accidents (most common)
• crush injuries
• gunshot wounds with foreign bodies
• burns and frostbite
• IV drug abuse
 postoperative
• bowel resection or perforation
• premature wound closure
 spontaneous
• colon cancer (associated with C. septicum)
Pathophysiology
Clostridial species
• Clostridium perfringens (most common),
Clostridium novyi, Clostridium septicum,
Clostridium welschii
• Found in soil and gut flora
o Gain entry into the tissues through open
contaminated wound, esp in the muscles
• Gram-positive obligate anaerobic spore-
forming rods that produce exotoxins (e.g. C.
perfringens alpha toxin)
o causes muscle necrosis and vessel thrombosis
o can cause hemolysis and shock
• Incubation period <24h
• Gas produced by fermentation of glucose
o main component is nitrogen

23. Prognosis
Prognosis overall 25% mortality
50% mortality if bacteremic
100% mortality if treatment is delayed
poorer prognosis for older patients with comorbidities
prime site for gas gangrene infection is a dirty wound with dead muscle that has
been closed without adequate debridement. Toxins produced by the organisms
destroy the cell wall and rapidly lead to tissue necrosis, thus promoting the spread
of the disease,leading to toxaemia and shock

24. • Contamination with clostridial spores in posttraumatic or postoperative lesions establishes the initial stage of
infection.
• Local wound conditions are more important than the degree of clostridial contamination in the development
of gas gangrene. Disrupted or necrotic tissue provides the necessary enzymes and a low oxidation/reduction
potential, allowing for spore germination.
• Self-perpetuating destruction of tissue occurs via a rapidly multiplying microbial population and the
production of locally and systemically acting exotoxins.
• Local effects include necrosis of muscle and subcutaneous fat and thrombosis of blood vessels. Marked edema
may further compromise blood supply to the region. Fermentation of glucose is probably the main mechanism
of gas production in gas gangrene.
• Systemically, exotoxins may cause severe hemolysis. Hemoglobin levels may drop to very low levels and, when
occurring with hypotension, may cause acute tubular necrosis and renal failure. A rapidly progressive infection
can quickly result in shock.

25. Clinical Presentation
• Post trauma
• Sustain serious injury to skin / soft tissue
• open fracture
• Post operative
• Spontaneous : History of blood vessel disease (atherosclerosis, or
hardening of the arteries), diabetes, or colon cancer
• Sudden onset of pain  gradually worsen
• fever

26. Physical examination
• 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

27. Complications
• Massive hemolysis, which may require repeated blood transfusion
• Disseminated intravascular coagulation (DIC), which may cause severe bleeding
and may complicate aggressive surgical debridement
• Acute renal failure
• Acute respiratory distress syndrome
• Shock

28. Investigation
• Labs
• Elevated LDH
• Elevated/normal wbc
• neutrophillia
• high ESR
• Metabolic acidosis and renal failure
• Histology
• Gram positive bacteria
• Absence of neutrophils- lack of acute inflammatory response is hallmark of
gas gangrene
• Culture
- blood culture rarely grows Clostridial species
*it is extremely rare to confirm a spore with Gram staining. In
addition, C. perfringens is an anaerobic organism. Therefore, the
bacteria seldom grow in aerobic culture bottles.
Showing Gram +ve spore forming rods
consistent with C.perfringens

29. Imaging
• Radiography can help delineate the typical feathering pattern of gas in
soft tissue,however, gas may also not be present in some patients with
gas gangrene.
• CT scanning is also helpful, especially in abdominal cases of gas
gangrene.
• Studies on MRI to detect necrotizing soft tissue infection have reported
lower sensitivity (80-90%) and limited specificity. In addition, MRI is time
consuming.
• Ultrasound, although attractive as rapid bedside test, has not been well
studied in this clinical scenario.

30. Images

32. Treatment and management
excision of all the dead and devitalized muscle till normal healthy bleeding
muscle is seen is the most important measure to prevent gas gangrene.
Early diagnosis : key to life saving
• General measures : fluid replacement & high dose IV antibiotics, are started
immediately(Penicillin G and clindamycin)
• Mainstay treatment: prompt decompression of the wound & removal of all
dead tissue. Deep, penetrating wounds in muscular tissue are
dangerous,they should be explored, all dead tissue should be completely
excised and, if there is the slightest doubt about tissue viability, the wound
should be left open.
• In advanced case, amputation may be essential

33. • It is essential to distinguish gas gangrene, which is characterized by
myonecrosis, from anaerobic cellulitis, in which superficial gas
formation is abundant but toxaemia usually slight.
• Failure to recognize the difference may lead to unnecessary
amputation for the non-lethal cellulitis.

35. REFERENCES
• QJM: An International Journal of Medicine, Volume 109, Issue 11,
November 2016, Page
757, https://doi.org/10.1093/qjmed/hcw144
• https://emedicine.medscape.com/article/217943
• APLEY’S CONCISE SYSTEM OF ORTHOPAEDICS AND FRACTURES (E3)

36. CELLULITIS

37. CELLULITIS
• An acute, superficial, diffuse and spreading infection of the
skin.
• May refer to infection of the deeper dermis and adjacent
subcutaneous tissue.
PATHOPHYSIOLOGY

38. CELLULITIS
EPIDEMIOLOGY
• Demographics: higher incidence among individuals aged 45-64 years. Can occur in all racial and ethnic groups and in geriatric
patients.
• Affected areas: affect any site, most often a limb (usually unilateral; bilateral is more often due to another condition. It can
occur by itself or complicate an underlying skin condition or wound.
RISK FACTORS
• Previous history of cellulitis.
• Fissuring of heels and toes
• Venous disease
• Current/prior injury: trauma, surgical wounds, radiotherapy
• Immunodeficiency: human immunodeficiency virus infection (HIV)
• Immune suppressive medications (Steroids: Prednisolone, Methotrexate)
• Diabetes
• Chronic kidney disease
• Chronic liver disease
• Obesity
• Pregnancy
• Alcoholism

39. PROGNOSIS
• Can be treated with oral antibiotics (
to which patient’s respond well) and
do not result in lasting sequelae.
• IV antibiotics are effective if oral
antibiotics therapy is unsuccessful.
• Uncontrolled cellulitis may progress
to serious illness through spread via
lymph/circulatory system.
COMPLICATIONS:
• Necrotising fasciitis - severe pain,
skin pallor, loss of sensation,
purpura, ulceration and necrosis.
• Gas gangrene.
• Severe sepsis (blood poisoning) -
fever, malaise, loss of appetite,
nausea, lethargy, headache, aching
muscles and joints.
• Infection of other organ (pneumonia,
osteomyelitis, meningitis)
• Endocarditis (heart valve infection).

40. AETIOLOGY
• Host factors – immunosuppressed patients ( elderly, diabetes, immunodeficiency, cancer, venous
stasis, chronic liver disease, peripheral arterial disease, and chronic kidney disease) have high risk.
• Procedures - venectomy, post-venectomy status following saphenous vein stripping and
lymphadenectomy following tumor excision, such as mastectomy.
• Concurrent use of IV/subcutaneous drugs.
• Bite wounds (most common: dog bites), lacerations, and puncture wounds
• Others: MRSA and Varicella infections
CAUSATIVE ORGANISMS
- Group A Beta hemolytic streptococcus
- Streptococcus pneumoniae
- Staphylococcus aureus
Venectomy* – excision of vein segment

41. CELLULITIS
HISTORY TAKING:
• History suggestive of trauma: Onset and duration of trauma
episode? Onset of cellulitis after trauma? Associated pain?
Progression of pain post trauma? Circumstances of the trauma?
• Underlying medical illness (DM, HTN, CKD, HIV, chronic liver
disease) or skin disorders (Dermatitis)
• Surgical history (Lymph node dissection, saphenous vein resection
from coronary bypass surgery) or presence of foreign bodies (in-
dwelling IV catheters, external orthopedic pins, and other surgical
devices).

42. CELLULITIS
Non-purulent cellulitis is associated with 4 cardinal signs of infection: erythema,
pain, swelling, and warmth.

43. CELLULITIS
LABORATORY INVESTIGATIONS
• Full blood count: Leucocytosis : Increased WCC in severe cases,
leucopenia may be present in severe disease (toxin-mediated
cellulitis).
• Inflammatory markers: Raised CRP, raised ESR.
• Blood C&S: for cellulitis of specific anatomic sites (e.g. facial and
especially ocular areas; in patients with a history of contact with
potentially contaminated water; in patients with malignancy on
chemotherapy, neutropenia, or severe cell-mediated
immunodeficiency; and in patients with animal bites) – identify
causative organism
• Ultrasound: For detection of occult abscess.
• CT scan: TRO necrotizing fasciitis.
• Gram stain & culture.
• Needle aspiration and biopsy.
• Skin biopsy.

44. TREATMENT & MANAGEMENT OF CELLULITIS
• Antibiotic regimens are effective in more than 90% of patients.
- Can be given by oral, injection or IV.
• Cellulitis is usually treated with a 1-week course of antibiotics (usually high-dose flucloxacillin
for 7 days, depending on severity, comorbidity, or site of infection)
• Management of cellulitis may be complicated because of the emergence of methicillin-
resistant Staphylococcus aureus (MRSA) and macrolide- or erythromycin-resistant
Streptococcus pyogenes.
• Non-severe cases of cellulitis may be treated empirically with semisynthetic penicillin, 1st/2nd
cephalosporins, macrolides, or clindamycin.
• Emollients/active treatment of fungal foot disease, are effective in people with skin disorders
that could predispose to cellulitis.
• For people with lymphoedema, strategies such as compression stockings or exercise may be
effective.
• Keep area clean/ apply dressings.
• Elevation of affected limb
• Adequate rest
• Analgesia.

46. CELLULITIS
DIFFERENTIAL DIAGNOSIS:
1. Necrotizing fasciitis
2. Burn Wound
3. Erysipelas
4. Erythema Multiforme
5. Impetigo
6. Insect Bites
7. Leukaemia Cutis
8. Lymphoma, Cutaneous T-Cell
9. Mycosis Fungoides
10.Myiasis
11.Osteomyelitis
12.Pyoderma Gangrenosum
13.Stevens-Johnson Syndrome
14.Wells Syndrome

47. THANK YOU