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Necrotizing fasciitis



Necrotizing fasciitis
Classification & external resources
ICD-9 728.86
MedlinePlus 001443
eMedicine emerg/332  derm/743
MeSH C01.252.410.890.350

Necrotizing fasciitis or fasciitis necroticans, commonly known as “flesh-eating bacteria,” is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. Many types of bacteria can cause necrotizing fasciitis (eg. Group A streptococcus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis), of which Group A streptococcus (also known as Streptococcus pyogenes) is the most common cause.

Additional recommended knowledge

Contents

Symptoms

The infection begins locally, at a site of trauma, which may be severe (such as the result of surgery), minor, or even non-apparent. The affected skin is classically, at first, very painful without any grossly visible change. With progression of the disease, tissue becomes swollen, often within hours. Diarrhea and vomiting are common symptoms as well. Inflammation does not show signs right away if the bacteria is deep within the tissue. If it is not deep, signs of inflammation such as redness and swollen or hot skin show very quickly. Skin color may progress to violet and blisters may form, with subsequent necrosis (death) of the subcutaneous tissues. Patients with necrotizing fasciitis typically have a fever and appear very ill. More severe cases progress within hours, and the mortality rate can be over 70% if untreated.[1] Even with medical assistance, antibiotics take a great deal of time to affect the bacteria, allowing the infection to progress to a more serious state.[2]

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). These include streptococcal pyogenic exotoxins and other virulence factors. S. pyogenes produces an exotoxin known as a superantigen. This toxin is capable of activating T-cells non-specifically. This causes the over-production of cytokines that over-stimulate macrophages. The macrophages cause the actual tissue damage by releasing oxygen free radicals that are normally intended to destroy bacteria but are capable of damaging nearly any macromolecule they contact in the body.'''

Treatment

The diagnosis is confirmed by either blood cultures or aspiration of pus from tissue, but early medical treatment is crucial and often presumptive; thus, antibiotics should be started as soon as this condition is suspected. Initial treatment often includes a combination of intravenous antibiotics including penicillin, vancomycin and clindamycin. If necrotizing fasciitis is suspected, surgical exploration is always necessary, often resulting in aggressive debridement (removal of infected tissue). As in other maladies characterized by massive wounds or tissue destruction, hyperbaric oxygen treatment can be a valuable adjunctive therapy, but is not widely available. Amputation of the affected organ(s) may be necessary. Repeat explorations usually need to be done to remove additional necrotic tissue. Typically, this leaves a large open wound which often requires skin grafting. The associated systemic inflammatory response is usually profound, and most patients will require monitoring in an intensive care unit.

Prognosis

This disease is one of the fastest-spreading infections known, as it spreads easily across the fascial plane within the subcutaneous tissue. For this reason, it is popularly called the “flesh-eating disease,” and, although rare, it became well-known to the public in the 1990s. Even with modern medicine, the prognosis can be bleak, with a mortality rate of approximately 25% and severe disfigurement common in survivors.

Other bacterial strains

In February 2004, a rarer but even more serious form of the disease has been observed in increasing frequency, with several cases found specifically in California. In these cases, the bacterium causing it was a strain of Staphylococcus aureus (i.e. Staphylococcus, not Streptococcus as stated above) which is resistant against methicillin, the antibiotic usually used for treatment (see Methicillin-resistant Staphylococcus aureus for details). “Super Strep” appeared in Ohio and Texas in 1992 and 1993 and was contracted by approximately 140 people. It took under 12 hours to incapacitate most and caused 3 days of very high fevers. The death rate in 1993 was reported to be 10%, with a majority of the victims having mild to severe brain damage.

Well-known victims

  • Alicia Cole, an actress, contracted hospital-acquired necrotizing fasciitis following a routine myomectomy to remove uterine fibroids. She withstood multiple debridement surgeries which removed most of her abdomen and left buttock. The disease was finally contained, sparing her from amputating her left leg. [3]
  • David Walton, a leading economist in the UK and a member of the Bank of England’s Monetary Policy Committee which is responsible for setting interest rates, died of the disease within 24 hours of diagnosis on June 21, 2006.[4]
  • Lucien Bouchard, former premier of Québec, Canada, who became infected in 1994 while leader of the federal official opposition Bloc Québécois party. He lost a leg to the illness.[5]
  • Eric Allin Cornell, winner of the 2001 Nobel Prize in Physics, lost his left arm and shoulder to the disease in 2004.[6]
  • Melvin Franklin, bass singer for The Temptations. Though Franklin’s condition was diagnosed early enough to prevent complete amputation of his arm, he died from other health complications soon afterward in 1995.[citation needed]
  • Lana Coc-Kroft, a New Zealand television celebrity, was infected after she stepped on a coral reef in Fiji in 2005.[7]
  • Jan Peter Balkenende, Prime Minister of the Netherlands since 2002, was infected in 2004. He was in the hospital for several weeks, but recovered fully.[8]
  • Alan Coren, British writer and satirist, announced in his Christmas 2006 column for The Times that his long absence as a columnist has been due to contracting the disease while on holiday in France.[9]
  • Alexandru Marin, an experimental particle physicist, professor at MIT, Boston University and Harvard University, and researcher at CERN and JINR, died from the disease in 2005.[10]
  • Tommy Kwok Chin, Detention Enforcement Officer, United States Department of Justice, Immigration and Naturalization Service, Detention and Deportation. In October 1999, Agent Lee died after contracting the bacteria while detaining 151 illegal Chinese immigrants on a remote island off the coast of Washington state.
  • Barbara Miller-Roy, the mother of former NHL superstar goaltender Patrick Roy contracted the disease in October 2005.

See also

References

  1. ^ http://www.medscape.com/viewarticle/444061
  2. ^ http://www.webmd.com/a-to-z-guides/Necrotizing-Fasciitis-Flesh-Eating-Bacteria-Topic-Overview
  3. ^ [1]
  4. ^ Flesh-eating bug killed top economist in 24 hours
  5. ^ The Once and Future Scourge
  6. ^ Cornell Discusses His Recovery from Necrotizing Fasciitis with Reporters
  7. ^ Authorities on alert for flesh-eating bug
  8. ^ PM: foot infection could have been fatal
  9. ^ Before I was so rudely interrupted
  10. ^ "In Memoriam - Alexandru A. Marin (1945 - 2005)", ATLAS eNews, December 2005 (accessed 5 November 2007).

(2)Tiu,A et al,ANZ J Surg. 2005 Jan-Feb;75(1-2):32-4

acquired deformities of fingers and toes (Boutonniere deformity, Bunion, Hallux rigidus, Hallux varus, Hammer toe) - other acquired deformities of limbs (Valgus deformity, Varus deformity, Wrist drop, Foot drop, Flat feet, Club foot, Unequal leg length, Winged scapula)

patella (Luxating patella, Chondromalacia patellae)

Protrusio acetabuli - Hemarthrosis - Arthralgia - Osteophyte
Systemic connective
tissue
disorders
Polyarteritis nodosa - Churg-Strauss syndrome - Kawasaki disease - Hypersensitivity vasculitis - Goodpasture's syndrome - Wegener's granulomatosis - Arteritis (Takayasu's arteritis, Temporal arteritis) - Microscopic polyangiitis - Systemic lupus erythematosus (Drug-induced) - Dermatomyositis (Juvenile dermatomyositis) - Polymyositis - Scleroderma - Sjögren's syndrome - Behçet's disease - Polymyalgia rheumatica - Eosinophilic fasciitis - Hypermobility
DorsopathiesKyphosis - Lordosis - Scoliosis - Scheuermann's disease - Spondylolysis - Torticollis - Spondylolisthesis - Spondylopathies (Ankylosing spondylitis, Spondylosis, Spinal stenosis) - Schmorl's nodes - Degenerative disc disease - Coccydynia - Back pain (Radiculopathy, Neck pain, Sciatica, Low back pain)
Soft tissue disordersmuscle: Myositis - Myositis ossificans (Fibrodysplasia ossificans progressiva)

synovium and tendon: Synovitis - Tenosynovitis (Stenosing tenosynovitis, Trigger finger, DeQuervain's syndrome)

bursitis (Olecranon, Prepatellar, Trochanteric)

fibroblastic (Dupuytren's contracture, Plantar fasciitis, Nodular fasciitis, Necrotizing fasciitis, Fasciitis, Fibromatosis)

enthesopathies (Iliotibial band syndrome, Achilles tendinitis, Patellar tendinitis, Golfer's elbow, Tennis elbow, Metatarsalgia, Bone spur, Tendinitis)

other, NEC: Muscle weakness - Rheumatism - Myalgia - Neuralgia - Neuritis - Panniculitis - Fibromyalgia
Osteopathiesdisorders of bone density and structure: Osteoporosis - Osteomalacia - continuity of bone (Pseudarthrosis, Stress fracture) - Monostotic fibrous dysplasia - Skeletal fluorosis - Aneurysmal bone cyst - Hyperostosis - Osteosclerosis
Osteomyelitis - Avascular necrosis - Paget's disease of bone - Algoneurodystrophy - Osteolysis - Infantile cortical hyperostosis
ChondropathiesJuvenile osteochondrosis (Legg-Calvé-Perthes syndrome, Osgood-Schlatter disease, Köhler disease, Sever's disease) - Osteochondritis - Tietze's syndrome
See also congenital conditions (Q65-Q79, 754-756)
  This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Necrotizing_fasciitis". A list of authors is available in Wikipedia.
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