**1. Introduction**

Gangrene is a lesion of ischemic tissue death. Typically, the acral skin of the hand and foot accompanies numbness, pain, coolness, swelling, and the skin color changes to reddish black. When severe infection is associated, fever and sepsis may follow. Risk factors of gangrene include diabetes mellitus, atherosclerosis, smoking, major trauma, alcoholism, liver cirrhosis, renal insufficiency, immunosuppression, acquired immunodeficiency syndrome (AIDS), drug abuse, malnutrition, and pernio. Clinically, the disease is divided into dry gangrene, wet gangrene, gas gangrene, internal gangrene, and necrotizing fasciitis. In all cases except for dry gangrene, the necrotic tissue is infected. Treatments include surgery, antibiotics administration, and efforts to control the underlying cause. Hyperbaric oxygen therapy can be tried. Amputation and debridement are performed as surgical treatments. Maggot therapy (artificial implantation of maggots in cavitated lesions) may be performed for digesting tissue debris of diabetic wet gangrene on the extremities.

In the present review article, pathologic features of varied gangrenous lesions are illustrated. In addition to gross findings, microscopic features are presented mainly with hematoxylin and eosin (H&E) and Gram stains. When needed, immunohistochemical approach is combined [1, 2]. Immunostaining using rabbit antisera raised against *Bacillus* Calmette-Guérin (BCG; *Mycobacterium bovis*), *Bacillus cereus*, *Treponema pallidum*, and *Escherichia coli* is employed. These low-specificity (widely cross-reactive) antimicrobial antisera effectively yield clear high-sensitivity signals with a low background [3, 4]. Please visit the author's Website at https://pathos223. com/en/ [5].

**3. Wet gangrene**

*Pathology of Gangrene*

*DOI: http://dx.doi.org/10.5772/intechopen.93505*

Wet or infected gangrene is featured by bacterial infection of the necrotic tissue,

and secondary sepsis accompanies a poor prognosis when compared with dry gangrene [9–11]. The affected part becomes markedly edematous, soft, rotten, and dark. Blisters filled with turbid fluid are formed on the discolored and cold-ontouch skin (**Figure 2**). Secondary infection of Gram-positive cocci is common. Infection of saprogenic (anaerobic) bacteria causes a foul smell. Gas formation is often associated, eliciting crepitation on touch. Causative bacteria are polymicrobial or monobacterial. In case of monobacterial infection by *Clostridium perfringens*, we call the status as clostridial gas gangrene. Wet gangrene rapidly progresses via the blockage of blood flow, and the hypoxic stagnant blood promotes rapid growth of anaerobic bacteria that often release exotoxins. The mortality rate of wet gangrene is high so that emergency salvage amputation is often necessary. Disseminated infection (sepsis) eventually leads the patient to death. The predisposing disorders for developing wet gangrene include diabetes mellitus, arteriosclerosis obliterans

(atherosclerotic arterial obstruction), and calciphylaxis/calcific uremic

wall calcification in patients with chronic renal failure under dialysis).

giant cells. The epidermis may reveal spongiosis, basal vacuolation, and

and *Aeromonas hydrophila* infection.

**4. Pernio (frostbite or chilblains)**

**Figure 2.**

**97**

arteriolopathy or "gray scale" (painful and intractable ulcers caused by arteriolar

Several lethal conditions described below are encompassed in the category of wet gangrene. These include polymicrobial necrotizing fasciitis, gas gangrene, Fournier's gangrene, fulminant streptococcal infection, *Vibrio vulnificu*s infection,

Pernio (frostbite or chilblains) is a vascular disease affecting small vessels of the peripheral skin. Persistent low temperature (cooling) or freezing of the skin causes pernio. Persistent hypoxia of the tissue eventually results in necrosis and ulceration. In a chronic stage, scleroderma-like change may follow. Histopathological features of pernio include mild inflammation around small vessels, peri-eccrine inflammation, and necrosis of the subcutaneous fat tissue with formation of multinucleated

*Wet gangrene (gross appearance of two cases and H&E). Infected deep irregular ulcers are formed in the back of the foot (left) and the base of the second toe after autoamputation (right). Histologically, Gram-positive cocci in the necrotic upper dermis are observed in the debridement specimen (the courtesy of Dr. Yasuhito Kaneko at*

*Department of Dermatology, Shimada Municipal Hospital, Shimada, Japan).*
