This document describes a case of necrotizing fasciitis in a 54-year-old man. The man presented with swelling and pain in his left lower leg, along with watery discharge and skin blisters. He had a history of an insect bite a month prior. Investigation revealed elevated white blood cell count and blood sugar. The patient was diagnosed with uncontrolled diabetes and necrotizing fasciitis. He underwent fasciotomy, debridement, and skin grafting. The wound culture grew Pseudomonas aeruginosa. With aggressive treatment including antibiotics, surgery, and control of his diabetes, the patient's condition improved.

1. Necrotizing Fasciitis
Dr. Shirish Silwal
House Officer
Dept. of General Surgery & Urology
B & B Hospital Pvt. Ltd.

2. Case 1
 Mr BKB, 54 years presented in the Emergency on
2070/3/31.
 Swelling and Pain in left lower leg .
 Watery discharge with skin blisters.
 H/O small wound due to insect bite a month ago.
 H/O Fever on and off for 3 days, not associated with chills or
rigor.
 Primary management done in other center took antibiotic for
1 day and Hot water bath taken.
 K/C/O HTN, NO PREVIOUS H/O DIABETES.

3. GENERAL EXAMINATION
General condition- Fair
JALCCOD - Nil ,
Vitals – T 97° F, BP 110/80 mm of Hg
SYSTEMIC EXAMINATION
 Per Abdominal Findings
Soft & non tender, bowel sound (+),
No organomegaly
 Respiratory system Findings
B/L vesicular breathe sound,
No added sound
 Other systemic findings NAD

4. LOCAL EXAMINATION OF LEFT LEG
 Inspection
• Discoloration of skin (+)
• Redness and swelling up to knee region
• Bulla with serous discharge present at the dorsum of foot
and ankle
• Movement of distal joint (+)
 Palpation
• Tenderness present
• Increased local temperature
• Neurovascular system not assessable due to edema

5. INVESTIGATION
 CBC
• WBC- 8400/Cumm
• Neutrophils - 85%
• Lymphocyte- 15%
• Platelets - 153000
 RFT
• Urea- 75mg/dl
• Creatinine- 1mg/dl
• Na+ 125mmol/L,
• K+ 2.5mmol/L
 Blood sugar- 230 mg/dl
 LIVER FUNCTION TEST
• Billirubin Total-1.0 mg/dl
• Billirubin Direct- 1.0 mg/dl
• SGPT/ALT- 39 IU/L
• SGOT/AST- 50 IU/L
• AlkalinePhosphatase- 128 IU/L
• URINE RME - NAD
• VENOUS DOPPLER - NORMAL

6. CULTURE
 Wound/pus culture:
 No growth (2070/3/31)
 No growth (2070/4/16)
 Heavy growth of pseudomonas sp.(2070/4/22)
 Pseudomonas aeroginosa(2070/4/24) national
reference lab.
 No growth after 48 hours(2070/4/28)

7. (2070/4/5) After Fasciotomy

11. (2070/4/11)- Continuous Debridement and hot
water bath

15. (2070/5/2)- After Skin Grafting

17. Treatment
 Diagnosed as uncontrolled diabetics with Cellulitis with
Necrotizing fasciitis
 Insulin on sliding scale
 IV antibiotics
 Gentamycin
 Metronidazole
 Penicillin
 Clindamycin
 Blood transfusion VIII bag

18. Surgery
 Fasciotomy done on (2070/4/2)
 Daily debridement, dressing and foot bath.
 Debridement with povidone iodine, washing powder,
Neosporin powder, placentex.
 Skin grafting on (2070/4/31)

19. Skin graft
 Requirement of survival
 Bed must be well vascularized.
 The contact between graft and recipient must be fully immobile.
 Low bacterial count at the site.
 Cause of failure
 Systemic Factors
 Malnutrition
 Sepsis
 Medical Conditions (Diabetes)
 Medications
 Steroids
 Antineoplastic agents
 Vasoconstrictors (e.g. nicotine)

20. Post-operative status
 Patient is stable and afebrile.
 Skin grafting 90% accepted.
 No foul smell from wound.
 Diabetes and Blood Pressure under control.

22. Necrotizing fasciitis

23. Past history
 Hippocrates in the 5th century BC noted
 known as malignant ulcer, gangrenous ulcer , putrid
ulcer, and hospital gangrene in the 18th century
 In 1871 after the Civil War was called hospital
gangrene by a war surgeon
 In 1924 called hemolytic streptococcal gangrene
 In 1952 called “necrotizing fasciitis”

24. Definition
 Characterized by fulminant destruction of tissue,
systemic signs of toxicity, and a high mortality rate.
 Pathologic features include extensive tissue
destruction, thrombosis of blood vessels, abundant
bacterial spread along fascial planes, and unimpressive
infiltration of acute inflammatory cells.

25. Risk Factors
 Drug use
 Diabetes mellitus
 Obesity
 Immunosuppression
 Renal failure

26. Types of Necrotizing Infection
 Necrotizing cellulitis
 Clostridial cellulitis
 Nonclostridial anaerobic cellulitis
 Meleney’s synergistic gangrene
 Synergistic necrotizing cellulitis
 Necrotizing fasciitis
 Type I
 Type II

27. Type I Necrotizing Fasciitis
 Mixed aerobic and anaerobic infection
 Bacteria almost always isolated
 Staphylococcus aureus, Streptococci, Enterococci,
E.coli, Peptostreptococcus species, Prevotella,
Porphyromonas, bacteroides fragilis and Clostridium
species.
 More common in diabetics, post op patients, and
patients with peripheral vascular disease.

28. Type I
 Cervical necrotizing fasciitis
 Ludwig’s angina
 Fournier’s gangrene
 Caused by penetration of the GI or urethral mucosa
by enteric organisms

29. Type II Necrotizing Fasciitis
 Monomicrobial
 Group A Strep
 ORSA
 Can occur in any age group and in healthy patients
 Risk factors
 H/o blunt trauma or laceration
 Varicella
 Injection drug use
 Post operative
 Post partum
 Burns
 Exposure to a case
 ?NSAIDs

30. Type II
 Can result from hematogenous translocation from GAS
in throat
 NSAIDs thought to inhibit neutrophil function or mask
symptoms and delay diagnosis

31. Pathophysiology
 "Flesh-eating bacteria" is a misnomer, as the bacteria
do not actually "eat" the tissue. They cause the
destruction of skin and muscle by releasing toxins
(virulence factors), which include streptococcal
pyogenic exotoxins.
 Streptococcus pyogenes produces an exotoxin known
as a superantigen. This toxin is capable of activating T-
cells non-specifically, which causes the overproduction
of cytokines and severe systemic illness (Toxic shock
syndrome).

32. Clinical Manifestations
• Unexplained/disproportionate pain
• Blister and bullae formation
• Signs of systemic toxicity fever
tachycardia hypotension
• Tense edema outside the involved
skin
• Crepitus/subcutaneous gas

33. Why it is so aggressive?
 Toxins-host releases
cytokines, including
interleukin-2, tumor necrosis
factor and gamma-interferon.
resulting in shock
 substances cause vascular
thrombosis and ischemic
gangrene
 tissue is consumed at 1 inch
per hour
 inoculation from
subcutaneous tissue
 hematogenous spread from
distant site
 found in post op
complications of fecal
contaminated wound
 shock & multi system organ
failure, ARDS

34. Risk Score
1) Serum CRP >= 150mg/L (4 pt)
2) WBC 15K-25K (1 pt) or > 25K (2 pt)
3) Hb 11-13.5 (1 pt) or <= 11 (2 pt)
4) Na < 135 (2 pt)
5) Cr >1.6 (2 pt)
6) Glucose >180 (1 pt)
 Score >/= 6 should raise suspicion for NF
 >/= 8 highly predictive of NF

35. Diagnosis
 Imaging
 Soft tissue X-rays, CT, MRI
 Can reveal gas in the tissues, but not as good as direct surgical
exploration
 Role of Doppler these techniques showed changes in
subcutaneous adipose tissue , fascia and muscle.
 Cultures
 Blood Culture positive in 60% with type II, 20% with type I
 Surgical wound cultures almost always positive

39. Treatment
 Early and aggressive surgical exploration and debridement
 Re exploration should be performed with in 24 hrs
 Antibiotic therapy
 Type I: Ampicillin or Unasyn(Ampicillin + Sulbactam)
with
clindamycin or metronidazole
If recent hospitalization, use Zosyn (Piperacillin and Tazobactam Injection)or Timentin
(Ticarcillin and Clavulanate) instead of Unasyn.
 Type II: Penicillin G and clindamycin; vancomycin
 Hemodynamic support
 Intravenous immunoglobulin (currently under investigation, but not
recommended) well an attempt to reduce hyper proliferation of T cells inhibit
production of tumor necrosis factor
 Hyperbaric oxygen therapy

40. Role of Surgery
Necrotizing fasciitis is a surgical
emergency,
the patient should be admitted
immediately to a surgical intensive care
unit in a setting such as a regional burn
center or trauma center, where the
surgical staff is skilled in performing
extensive debridement and reconstructive
surgery.

41. Prognosis
• Aggressive treatment- mortality 30%
• Delayed treatment- mortality 92%
• Patient with predisposing factor- mortality 80%
• Ineffective debridement- mortality 83%
• Death cause by sepsis and multi organ failure
• Predictor for mortality
WBC >30k,Creatinine>2
Clostridia infection
Presence of heart disease during admission

42. Conclusion
 Necrotizing fasciities is a aggressive disease.
 Rapid identification and rapid treatment is essential for
recovery from this aggressive disease.
 Aggressive disease should be treated aggressively.
Tit For Tat.

43. Thank You