NSTI.pptx

NECROTIZING SOFT TISSUE INFECTION

1. NECROTISING SOFT TISSUE INFECTION WITH INFECTIVE ENDOCARDITIS DR. MANISH KUMAR SR, SURGERY UNIT IV VMMC & SAFDARJUNG HOSPITAL, NEW DELHI

2. NECROTIZING SOFT TISSUE INFECTIONS (NSTI) NSTI are rapidly progressing skin and soft tissue infections associated with necrosis of the dermis, subcutaneous tissue, superficial fascia, deep fascia, or muscle. This definition includes a variety of conditions, such as Fournier gangrene affecting the perineum and genitalia, Meleney streptococcal gangrene, and clostridial myonecrosis.

3. Anatomy Most bacteria and fungi can multiply within viable tissue, but fibrous attachments or “boundaries” between subcutaneous tissues and fascia (e.g., scalp, hands) can help limit the spread of infection. The natural lack of fibrous attachments in the larger areas of the body (e.g., trunk, extremities) facilitates widespread infection.

4. From the surface down and forming concentric circles, we find the skin (epidermis and dermis), superficial fascia or subcutaneous tissue (hypodermis), the deep fascia, and muscles. The deep fascia continues with the epimysium (connective tissue surrounding muscles), and sends prolongations (intermuscular septa) that divide the different muscle compartments.

5. Since the fascia is a continuum from the surface to the endomysium muscles, it is the route by which a surface process spreads to muscles or bones and vice versa. Diagram showing the names of the infections corresponding to the different layers from the skin to the muscle. NSTI necrotizing soft tissue infections

6. NSTIs are rarely “idiopathic”; a minor wound or injury almost always precedes the devastating infection, often by several weeks.

7. Risk factors and precipitating events related to necrotizing soft tissue infections (NSTI) Risk factors Precipitating events Diabetes Surgery Alcohol abuse Minor invasive procedures Immunosuppression Intravenous drug use Malnutrition/obesity Penetrating injuries Age >60 years Soft tissue infection Peripheral vascular disease Underlying malignancy Intravenous drug misuse

8. Streptococci and clostridia - fulminant course with rapid onset of symptoms and worsening over days or even hours and may be rapidly progressing to death if untreated. Infections caused by mixed flora, staphylococcus, and gram-negative organisms - indolent course over days to weeks, which may mislead clinicians into not considering the diagnosis of NSTI.

9. Pathophysiology Microbial invasion of the subcutaneous tissues (SCT) occurs either through external trauma or from direct spread from perforated viscera. After that, microorganisms proliferate and generate toxins and enzymes like hyaluronidase, enabling horizontal extension through deep fascial planes.

10. As this process progresses, thrombosis of the perforating nutrient vessels causes progressive dermis and skin ischemia, leading to bullae formation, ulceration, and skin necrosis. Ischemia and necrosis generate an inflammatory response and cytokine

11. Diagnosis The gold standard modality for the diagnosis of NSTI remains operative exploration, and it is also the mandatory live-saving treatment. Erythema, warmth, and pain - 90% of cases Crepitus, skin necrosis, and bullae are much more specific to NSTI - less than 40% (1) Signs and symptoms of systemic illness (i.e., sepsis) Fever, hypotension, organ failure such as renal failure or hypoxia

12. Imaging Plain radiography Most radiographic findings are similar to those for cellulitis, with increased soft-tissue thickness and opacity. Frequently, films are unremarkable until the infection and necrosis are advanced and subcutaneous air can be identified. Radiographic evidence of air in the soft tissue may be present before clinical crepitus is detected [34].

13. Plain X-ray film of the pelvis with NF showing ectopic air in the subcutaneous tissue of the right thigh (arrow)

14. USG Suggestive ultrasound features are thickening and distortion of the deep fascia (>4 mm; fasciitis), turbid fluid collections along the deep fascia, features of myositis, i.e., muscle hypo- or hyperechogenic swelling, findings of cellulitis, i.e., swelling of the subcutaneous tissue, including cobblestone appearance (hyperechogenic subcutaneous tissue traversed by hypoechoic strands of fluid).

15. Increased Doppler hyperemia or thrombosed small blood vessels [36, 37] can also be seen. In the case of Fournier gangrene, the main ultrasound findings are a thickened edematous scrotal wall that may contain hyperechoic foci with reverberation artifacts (gas). The testes and epididymis are often normal in size and echotexture owing to their direct aorta branch blood supply.

16. CT - gas in the soft tissues (the easiest finding for nonradiologists to diagnose and the most specific), multiple fluid collections, absence or heterogeneity of tissue enhancement by intravenous (IV) contrast, and significant inflammatory changes under the fascia.

17. Stranding of the fat of the subcutaneous tissue and skin thickening (cellulitis; asterisk), thickening and blurring of the left sternocleidomastoid and platysma muscles (myositis; thick arrow). Asymmetrical thickening of the superficial and deep fascial layers (fasciitis; thin arrow) and stranding of the fat of the subcutaneous tissue and skin thickening (cellulitis; asterisk).

18. Axial images of a CT of a. the pelvis and b. the lower extremities show stranding of the fat of the subcutaneous tissue, thickening of the skin (cellulitis), and thickening of the superficial and deep fascial layers (fasciitis; asterisk). Subcutaneous emphysema (thick arrow) is also noted. A continuity solution in the right gluteus is seen, indicating a decubitus ulcer (thin arrow)

19. MRI Hyperintense signal in subcutaneous tissue in fluid-sensitive sequences (cellulitis), deep fascial thickening (fasciitis), deep fascial fluid collections, and hyperintense T2 signal within the muscles [11-16]. The involvement of three or more compartments in one extremity has also been described as an NSTI indicator [15].

20. Gas in the deep fascial planes is inconstant and characterized by signal voids, is best seen on gradient echo sequences, and is a hallmark of NF [12, 13, 15, 17]. A thick (>3 mm) abnormal perifascial signal hyperintensity on fat-suppressed (FS) T2-weighted images is seen more frequently in NSTI and explained as purulent perifascial fluid and edema [15]. This feature, independent of the thickness, has been described as a sensitive, albeit nonspecific, feature [12].

21. a.Fatsuppressed T2-weighted axial image shows areas of high signal intensity in nearly all fasciae surrounding the muscles of the antero-medial and posterior compartments ( fasciitis±fluid collections; thin arrows), hyperintensity in the subcutaneous tissue (cellulitis; asterisk) and within the muscles (myositis; thick arrow). b. Fatsuppressed T1-weighted axial image shows the same findings as T2, stranding of subcutaneous tissue (cellulitis) and the thickness of the deep fasciae (fasciitis and fluid collections). c. Post-contrast fat-suppressed T1-weighted axial image and d. post-contrast subtraction T1-weighted axial image show enhancement in some of the hyperintense fasciae seen in a (arrows)

22. Local Exploration A 2-cm elliptical excision on an extremity will usually suffice and can be performed under local anesthesia at the bedside. Visually inspect for tissue necrosis, dishwater fluid or purulence, greyish discoloration of tissues.

23. The tissue at the edges of the incision should be firm and resist pressure—the “push” test. If the surgeon is able to dissect more than a centimeter subcutaneously with blunt finger pressure alone, this is considered a positive finding and wide debridement in the operating room is indicated.

24. Any fluid encountered should be collected and sent for immediate Gram stain and culture in addition to at least 1 cm3 of skin and subcutaneous tissue and samples from fascia and muscle.

25. Treatment of Necrotizing Soft Tissue Infections Surgery All affected tissue should be sharply excised with at least 1 cm rim of normal tissue Bleeding is not an indication of tissue viability, since the presence of active infection will often cause these areas to be hyperemic. All questionable tissue should be resected at the initial operation; the need for multiple operations and the spread of infection both increase the risk of mortality.(2)

26. Antibiotics Broad-spectrum antibiotics - effective against most gram-positive and gram-negative organisms and ensure Methicillin-resistant S. aureus coverage and good anaerobic coverage. Clindamycin has toxin-neutralization properties, especially in streptococcal and clostridial infections.

27. Resuscitation Sepsis and septic shock should be managed in an intensive care unit (ICU) Goal-directed resuscitation with isotonic fluids, vasopressor support as needed with norepinephrine and vasopressin, and control of hyperglycemia Recent studies suggest that IV thiamine, vitamin C, and hydrocortisone in combination might improve outcomes in sepsis.(3)

28. Adjunctive treatment Hyperbaric oxygen treatment (HBO) Patient is placed in a high-pressure chamber, resulting in delivery of oxygen at 2-3 times atmospheric pressure. This leads to arterial oxygen tension as high as 2000 mm Hg with resulting tissue oxygen tension of 300 mm Hg. This compares with arterial oxygen tension of 300 mm Hg and tissue oxygen tension of 75 mm Hg when breathing 100% oxygen at normal atmospheric pressure.

29. The use of HBO is based on animal and human studies showing that elevated levels of oxygen at the tissue level reduce edema, stimulate fibroblast growth, increase the killing ability of leukocytes by augmenting the oxidative burst, have independent cytotoxic effects on some anaerobes, inhibit bacterial toxin elaboration and release, and enhance antibiotic efficacy.4-8

30. Multiple studies have examined the use of HBO in the treatment of NSTIs with mixed results. its use should only be considered in hemodynamically stable patients in whom HBO therapy will not delay surgical debridement.

31. Intravenous immunoglobulin (IVIg) Involves the administration of pooled IVIg from human donors. Its use in the treatment of NSTI is based on the theory that it binds exotoxins produced by staphylococcal and streptococcal bacterial infections and subsequently limits systemic inflammatory response.9,10 Consideration of IVIg therapy be limited to critically ill patients with only staphylococcal or streptococcal NSTIs or both.

32. Wound Care and Reconstruction Once the infection is resolved - negative pressure vacuum dressing and reconstructive procedures, usually a skin graft, is planned in 2 to 4 weeks. Rehabilitation with physical therapy and optimal nutrition. The inclusion of tissue substitutes such as acellular dermal matrix and regeneration templates in reconstruction may improve cosmetic and functional outcomes, although this increases cost significantly.

33. REFERENCES Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85-A:1454–1460. Kobayashi L, Konstantinidis A, Shackelford S, et  al. Necrotizing soft tissue infections: delayed surgical treatment is associated with increased number of surgical debridements and morbidity. J Trauma. 2011;71:1400–1405. Marik PE, Khangoora V, Rivera R, et  al. Hydrocortisone, vitamin C, and thiamine for the treatment of severe sepsis and septic shock: a retrospective before-after study. Chest. 2017;151:1229–1238.

34. 4. Kaye D. Effect of hyperbaric oxygen on aerobic bacteria in vitro and in vivo. Proc Soc Exp Biol Med. 1967; 124(4):1090–1093. [PubMed: 4381602] 5. Park MK, Muhvich KH, Myers RA, Marzella L. Hyperoxia prolongs the aminoglycoside-induced postantibiotic effect in Pseudomonas aeruginosa. Antimicrob Agents Chemother . 1991; 35(4): 691–695. [PubMed: 1906262] 6. Mader JT, Brown GL, Guckian JC, Wells CH, Reinarz JA. A mechanism for the amelioration by hyperbaric oxygen of experimental staphylococcal osteomyelitis in rabbits. J Infect Dis. 1980; 142(6):915–922. [PubMed: 7462700]

35. 7. Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic. A comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg. 1986; 121(2):191–195. [PubMed: 3511888] 8. Korhonen K, Kuttila K, Niinikoski J. Tissue gas tensions in patients with necrotising fasciitis and healthy controls during treatment with hyperbaric oxygen: a clinical study. Eur J Surg. 2000; 166(7):530–534. [PubMed: 10965830]

36. 9. Takei S, Arora Y, Walker S. Intravenous immunoglobulin contains specific antibodies inhibitory to activation of T-cells by staphylococcal toxin superantigens. J Clin Invest. 1993; 91:602–607. [PubMed: 8432865] 10. Norrby-Teglund A, Kaul R, Low D. Plasma from patients with severe invasive group A streptococcal infections treated with normal polyspecific IgG inhibits stretococcal superantigeninduced T cell proliferation and cytokine production. J Immunol. 1996; 156:3057–3064. [PubMed: 8609429]

37. 11. Wong CH, Wang YS. The diagnosis of necrotizing fasciitis. Curr Opin Infect Dis. 2005;18(2):101–6. 12. Yu JS, Habib P. MR imaging of urgent inflammatory and infectious conditions affecting the soft tissues of the musculoskeletal system. Emerg Radiol . 2009;16(4):267–76. 13. Schmid MR, Kossmann T, Duewell S. Differentiation of necrotizing fasciitis and cellulitis using MR imaging. AJR Am J Roentgenol . 1998;170(3):615–20.

38. 14. Seok JH, Jee WH, Chun KA, Kim JY, Jung CK, Kim YR, et al. Necrotizing fasciitis versus pyomyositis: discrimination with using MR imaging. Korean J Radiol . 2009;10(2):121–8. 15. Kim KT, Kim YJ, Won Lee J, Kim YJ, Park SW, Lim MK, et al. Can necrotizing infectious fasciitis be differentiated from nonnecrotizing infectious fasciitis with MR imaging? Radiology. 2011;259(3):816–24. 16. Revelon G, Rahmouni A, Jazaerli N, Godeau B, Chosidow O, Authier J, et al. Acute swelling of the limbs: magnetic resonance pictorial review of fascial and muscle signal changes. Emerg Radiol . 1999;30(1):11–21.

39. 17. Turecki MB, Taljanovic MS, Stubbs AY, Graham AR, Holden DA, Hunter TB, et al. Imaging of musculoskeletal soft tissue infections. Skeletal Radiol . 2010;39(10):957–71.

40. Thank you