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Gangrene affecting toes.
Classification and external resources
ICD-10 R02, I70.2, E10.2, I73.9
ICD-9 040.0, 785.4
DiseasesDB 19273
MedlinePlus 007218
eMedicine article/217943 article/782709 article/214992 article/438994 article/2028899 article/2051157
Patient UK Gangrene
MeSH D005734

Gangrene is a potentially life-threatening condition caused by a critically insufficient blood supply (necrosis).[1][2] This may occur after an injury or infection, or in people suffering from any chronic health problem affecting blood circulation.[2] The primary cause of gangrene is reduced blood supply to the affected tissues, which results in cell death.[3] Diabetes and long-term smoking increase the risk of suffering from gangrene.[2][3]

There are different types of gangrene with different symptoms, such as dry gangrene, wet gangrene, gas gangrene, internal gangrene and necrotizing fasciitis.[1][2] Treatment depends on the underlying cause, and can include resection, debridement (or, in severe cases, amputation) of the affected body parts, antibiotics, revascularization (via a vascular bypass or angioplasty), or hyperbaric oxygen therapy.[4]


Gangrene is caused by a critically insufficient blood supply (e.g., peripheral vascular disease) or infection.[3][5][6] It is associated with diabetes[7] and long-term tobacco smoking. This condition is most common in the lower extremities (legs and feet).



Dry gangrene is a form of coagulative necrosis that develops in ischemic tissue, where the blood supply is inadequate to keep tissue viable. Dry gangrene is often due to Peripheral artery disease, but can be due to Acute limb ischemia. The limited oxygen in the ischemic limb limits putrefaction and bacteria fail to survive. The affected part is dry, shrunken and dark reddish-black, resembling mummified flesh. The dark coloration is due to liberation of hemoglobin from hemolyzed red blood cells, which is acted upon by hydrogen sulfide (H2S) produced by bacteria, resulting in formation of black iron sulfide that remains in the tissues.[citation needed] The line of separation usually brings about complete separation, with eventual falling off of the gangrenous tissue if it is not removed surgically, a process called autoamputation.

Dry gangrene is the end result of chronic ischemia. If ischemia is detected early, the process can be treated by revascularization (via vascular bypass or angioplasty). However, once gangrene has developed, the affected tissue are not salvageable.

Diabetes mellitus is a risk-factor for peripheral vascular disease and thus for dry gangrene, but also a risk factor for wet gangrene.


Wet gangrene occurs in naturally moist tissue and organs such as the mouth, bowel, lungs, cervix, and vulva.[citation needed] Bedsores occurring on body parts such as the sacrum, buttocks, and heels — although not necessarily moist areas — are also wet gangrene infections.[citation needed] This condition is characterized by thriving bacteria and has a poor prognosis (compared to dry gangrene) due to septicemia resulting from the free communication between infected fluid and circulatory fluid. In wet gangrene, the tissue is infected by saprogenic microorganisms (Clostridium perfringens or Bacillus fusiformis, for example), which cause tissue to swell and emit a fetid smell. Wet gangrene usually develops rapidly due to blockage of venous (mainly) and/or arterial blood flow. The affected part is saturated with stagnant blood, which promotes the rapid growth of bacteria. The toxic products formed by bacteria are absorbed, causing systemic manifestation of septicemia and finally death. The affected part is edematous, soft, putrid, rotten and dark. The darkness in wet gangrene occurs due to the same mechanism as in dry gangrene.


Main article: Gas gangrene

Gas gangrene is a bacterial infection that produces gas within tissues. It can be caused by Clostridium, most commonly alpha toxin producing Clostridium perfringens, or various non-clostridial species.[6][8] Infection spreads rapidly as the gases produced by bacteria expand and infiltrate healthy tissue in the vicinity. Because of its ability to quickly spread to surrounding tissues, gas gangrene should be treated as a medical emergency.

Gas gangrene is caused by a bacterial exotoxin-producing clostridial species, which are mostly found in soil, and other anaerobes such as Bacteroides and anaerobic streptococci. These environmental bacteria may enter the muscle through a wound and subsequently proliferate in necrotic tissue and secrete powerful toxins. These toxins destroy nearby tissue, generating gas at the same time. A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen, and 16.1% oxygen was reported in one clinical case.[9]

Gas gangrene can cause necrosis, gas production, and sepsis. Progression to toxemia and shock is often very rapid.



The method of treatment is generally determined by the location of affected tissue and extent of tissue loss. The best treatment for gangrene is revascularization (i.e., restoration of blood flow) of the afflicted organ, which can reverse some of the effects of necrosis and allow healing. Other treatments include antibiotic therapy, wound care, debridement and surgical amputation.

"Most amputations are performed for ischemic disease of the lower extremity. Of dysvascular amputations, 15-28% of patients undergo contralateral limb amputations within 3 years. Of elderly persons who undergo amputations, 50% survive the first 3 years."[12]

In the United States, 30,000–40,000 amputations are performed annually. There were an estimated 1.6 million individuals living with the loss of a limb in 2005; these estimates are expected to more than double to 3.6 million such individuals by the year 2050.[13] Antibiotics alone are not effective because they may not penetrate infected tissues sufficiently.[14] Hyperbaric oxygen therapy (HBOT) treatment is used to treat gas gangrene. HBOT increases pressure and oxygen content to allow blood to carry more oxygen to inhibit anaerobic organism growth and reproduction.[15] A regenerative medicine therapy was developed by Dr. Peter DeMarco to treat gangrene using procaine and PVP. He applied his therapy to diabetic patients to avoid amputations. Growth factors, hormones and skin grafts have also been used to accelerate healing for gangrene and other chronic wounds.[citation needed]

Angioplasty should be considered if severe blockage in lower leg vessels (tibial and peroneal artery) leads to gangrene.[16]


American Civil War soldier lies in bed with a gangrenous amputated arm

As early as 1028 fly maggots were commonly[citation needed] used to treat chronic wounds or ulcers to prevent or arrest necrotic spread, as some species of maggots consume only dead flesh, leaving nearby living tissue unaffected. This practice largely died out after the introduction of antibiotics, acetonitrile[citation needed] and enzyme to the range of treatments for wounds. In recent times, however, maggot therapy has regained some credibility and is sometimes employed with great efficacy in cases of chronic tissue necrosis.

John M. Trombold wrote: "Middleton Goldsmith, a surgeon in the Union Army during the American Civil War, meticulously studied hospital gangrene and developed a revolutionary treatment regimen. The cumulative Civil War hospital gangrene mortality was 45 percent. Goldsmith's method, which he applied to over 330 cases, yielded a mortality under 3 percent."[17] Goldsmith advocated the use of debridement and topical and injected bromide solutions on infected wounds to reduce the incidence and virulence of “poisoned miasma.” Copies of his book were issued to Union surgeons to encourage the use of his methods.[18]


The etymology of gangrene derives from the Latin word gangraena and from the Greek gangraina (γάγγραινα), which means "putrefaction of tissues". It has no etymological connection with the word green, despite the affected areas turning black and/or green and/or yellowish brown. It is coincidence that, in Lowland Scots the words "gang green" (go green) can be said to be an eggcorn for gangrene, as it describes the symptoms of the affliction.

See also[edit]


  1. ^ a b Porth, Carol (2007). Essentials of pathophysiology. Lippincott Williams & Wilkins. p. 41. ISBN 978-0-7817-7087-3. Retrieved 2010-06-15. 
  2. ^ a b c d "Gangrene – Introduction". NHS Health A–Z. NHS. Retrieved 2010-06-15. 
  3. ^ a b c "Gangrene – Causes". NHS Health A–Z. National Health Service (England). Retrieved 2010-06-15. 
  4. ^ "Gangrene – Treatment". NHS Health A–Z. National Health Service (England). Retrieved 2010-06-15. 
  5. ^ Gardner, AW; Afaq, A (November–December 2008). "Management of lower extremity peripheral arterial disease". Journal of cardiopulmonary rehabilitation and prevention 28 (6): 349–357. doi:10.1097/HCR.0b013e31818c3b96. PMC 2743684. PMID 19008688. 
  6. ^ a b Yang, Z.; Hu, J.; Qu, Y.; Sun, F.; Leng, X.; Li, H.; Zhan, S. (2013). "Interventions for treating gas gangrene (Protocol)". Cochrane Database of Systematic Reviews (6): Article number: CD010577. doi:10.1002/14651858.CD010577. 
  7. ^ Korzon-Burakowska, A; Dziemidok, P (December 2011). "Diabetic foot-the need for comprehensive multidisciplinary approach.". Annals of agricultural and environmental medicine 18 (2): 314–317. PMID 22216805. 
  8. ^ Sakurai, J.; Nagahama, M.; Oda, M. (November 2004). "Clostridium perfringens alpha-toxin: characterization and mode of action". Journal of Biochemistry 136 (5): 569–574. doi:10.1093/jb/mvh161. PMID 15632295. 
  9. ^ Chi CH, Chen KW, Huang JJ, Chuang YC, Wu MH (December 1995). "Gas composition in Clostridium septicum gas gangrene". Journal of the Formosan Medical Association 94 (12): 757–9. PMID 8541740. 
  10. ^ Levenson, RB; Singh, AK; Novelline, RA (March–April 2008). "Fournier gangrene: role of imaging.". Radiographics 28 (2): 519–528. doi:10.1148/rg.282075048. PMID 18349455. 
  11. ^ Warkentin, TE (August 2010). "Agents for the treatment of heparin-induced thrombocytopenia.". Hematology/Oncology clinics of North America 24 (4): 755–775. doi:10.1016/j.hoc.2010.05.009. PMID 20659659. 
  12. ^ Amputations of the Lower Extremity at eMedicine
  13. ^ Ziegler-Graham K, MacKenzie EJ, Ephraim PL, Travison TG, Brookmeyer R (March 2008). "Estimating the prevalence of limb loss in the United States: 2005 to 2050". Arch Phys Med Rehabil 89 (3): 422–9. doi:10.1016/j.apmr.2007.11.005. PMID 18295618. 
  14. ^ Lipsky BA (December 1999). "Evidence-based antibiotic therapy of diabetic foot infections". FEMS Immunol. Med. Microbiol. 26 (3-4): 267–76. doi:10.1016/s0928-8244(99)00143-1. PMID 10575138. 
  15. ^ Slack WK (May 1976). "Hyperbaric oxygen therapy in anaerobic infections: gas gangrene". Proceedings of the Royal Society of Medicine 69 (5): 326–7. PMC 1864235. PMID 1273078. 
  16. ^ "Angioplasty and stent placement - peripheral arteries". Retrieved July 24, 2013. 
  17. ^ Gangrene therapy and antisepsis before lister: the civil war contributions of Middleton Goldsmith of Louisville. PubMed - NCBI
  18. ^ Watson, Dr. Scott. "Hospital Gangrene During The Civil War - Civil War Medicine". Retrieved 2014-04-15. 

External links[edit]

Media related to Gangrene at Wikimedia Commons