**5. Decubitus (pressure ulcer or bedsore)**

Decubitus (pressure ulcer or bedsore) is formed as a result of long-term pressure, completely or partially blocking the skin blood flow [15]. The sites on a bony prominence are commonly affected, including the skin overlying the sacrum, the greater trochanter, the heel, and the scalp. Decubitus commonly develops in individuals who are on chronic bedrest or consistently use a wheelchair. Factors influencing the skin tolerance against pressure include malnutrition, skin wetness, diseases reducing the blood flow to the skin such as atherosclerosis, and diseases reducing the skin sensation such as paralysis or neuropathy. The advanced age, smoking, complicated diseases (atherosclerosis, diabetes mellitus, and secondary infection), and the use of anti-inflammatory drugs may hamper healing of decubitus.

There is a preceding erythematous stage before ulceration. The late stage presents as a black eschar form. The ulcer often deeply reaches the periosteal tissue. When a pocket is formed, secondary infection may become serious (**Figure 4**). Infection provokes slow or stalling healing and pale granulation tissue [16, 17]. Infected wounds may have a gangrenous odor. Bacterial biofilm formation leads to delayed healing of the decubital ulcer. Infected decubitus may progress to wet gangrene or clostridial/non-clostridial gas gangrene (**Figure 5**) [18], as described in Section 7. The colonization of *Staphylococcus aureus*, particularly methicillinresistant *Staphylococcus aureus* (MRSA), in the decubitus must be the important target of infection control [19]. It should be noted that the eradication of MRSA can be achieved only after healing of ulceration.

The National Pressure Ulcer Advisory Panel (NPUAP) in the United States proposed the staging of decubital ulcer [20].

**Stage I**: Intact skin with non-blanchable redness of a localized area usually over a bony prominence.

**Stage II**: A shallow open ulcer with a red, pink wound bed, without slough. **Stage III**: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, and muscle are not exposed. Slough may be present but does not obscure

*Non-clostridial gas gangrene caused by group A β-hemolytic streptococcal infection (gross and radiologic findings, H&E and Gram). Infected sacral decubitus seen in a 72-year-old diabetic female patient with a history of brain infarction progressed to gas gangrene. The arrowheads indicate the red-colored skin area with crepitation on touch. X-ray examination discloses gas formation in the soft tissue. Debridement tissue reveals*

*massive gangrenous inflammation with infection of Gram-positive cocci.*

*Large and deep decubiti with purulent exudation and pocket formation at the sacral region (two cases). Deep mining ulcers, so-called pockets, are noted. In the left case, the 40 40 mm pocket is indicated by dotted lines on the skin. Secondary infection is inevitable (the courtesy of Dr. Sandai Ohnishi at Hakuhokai Home Healthcare*

**Stage IV**: Full thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Undermining/tunneling

For the treatment purpose, the eschar stage decubitus can surgically be removed and skin-grafted (**Figure 6**). Histologically, the advanced lesion shows the fullthickness dermal necrosis with deep ulceration and abscess/gangrene formation.

the depth of tissue loss.

**Figure 5.**

**99**

**Figure 4.**

*Clinic, Nagoya, Japan).*

*Pathology of Gangrene*

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

(pocket formation) is often seen.

#### **Figure 3.**

*Pernio (H&E). Biopsy from the skin of sole demonstrates angiectasia of capillary vessels around the eccrine sweat gland (left) and fat necrobiosis (right). Loss of fat cell nuclei, membranous deposition in the cytoplasm, and focal stromal hyalinizing fibrosis are observed.*

#### **Figure 4.**

keratinocyte necrosis [12–14]. Representative features are displayed in **Figure 3**. These histopathologic pictures are seen in other vascular disorders, provoking a

Decubitus (pressure ulcer or bedsore) is formed as a result of long-term pressure, completely or partially blocking the skin blood flow [15]. The sites on a bony prominence are commonly affected, including the skin overlying the sacrum, the greater trochanter, the heel, and the scalp. Decubitus commonly develops in individuals who are on chronic bedrest or consistently use a wheelchair. Factors influencing the skin tolerance against pressure include malnutrition, skin wetness, diseases reducing the blood flow to the skin such as atherosclerosis, and diseases reducing the skin sensation such as paralysis or neuropathy. The advanced age, smoking, complicated diseases (atherosclerosis, diabetes mellitus, and secondary infection), and the use of anti-inflammatory drugs may hamper healing of

There is a preceding erythematous stage before ulceration. The late stage presents as a black eschar form. The ulcer often deeply reaches the periosteal tissue. When a pocket is formed, secondary infection may become serious (**Figure 4**). Infection provokes slow or stalling healing and pale granulation tissue [16, 17]. Infected wounds may have a gangrenous odor. Bacterial biofilm formation leads to delayed healing of the decubital ulcer. Infected decubitus may progress to wet gangrene or clostridial/non-clostridial gas gangrene (**Figure 5**) [18], as described in Section 7. The colonization of *Staphylococcus aureus*, particularly methicillinresistant *Staphylococcus aureus* (MRSA), in the decubitus must be the important target of infection control [19]. It should be noted that the eradication of MRSA can

The National Pressure Ulcer Advisory Panel (NPUAP) in the United States

*Pernio (H&E). Biopsy from the skin of sole demonstrates angiectasia of capillary vessels around the eccrine sweat gland (left) and fat necrobiosis (right). Loss of fat cell nuclei, membranous deposition in the cytoplasm,*

**Stage I**: Intact skin with non-blanchable redness of a localized area usually over a

chronic irritative process of the skin.

*Pathogenic Bacteria*

decubitus.

bony prominence.

**Figure 3.**

**98**

**5. Decubitus (pressure ulcer or bedsore)**

be achieved only after healing of ulceration.

proposed the staging of decubital ulcer [20].

*and focal stromal hyalinizing fibrosis are observed.*

*Large and deep decubiti with purulent exudation and pocket formation at the sacral region (two cases). Deep mining ulcers, so-called pockets, are noted. In the left case, the 40 40 mm pocket is indicated by dotted lines on the skin. Secondary infection is inevitable (the courtesy of Dr. Sandai Ohnishi at Hakuhokai Home Healthcare Clinic, Nagoya, Japan).*

#### **Figure 5.**

*Non-clostridial gas gangrene caused by group A β-hemolytic streptococcal infection (gross and radiologic findings, H&E and Gram). Infected sacral decubitus seen in a 72-year-old diabetic female patient with a history of brain infarction progressed to gas gangrene. The arrowheads indicate the red-colored skin area with crepitation on touch. X-ray examination discloses gas formation in the soft tissue. Debridement tissue reveals massive gangrenous inflammation with infection of Gram-positive cocci.*

**Stage II**: A shallow open ulcer with a red, pink wound bed, without slough.

**Stage III**: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, and muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss.

**Stage IV**: Full thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Undermining/tunneling (pocket formation) is often seen.

For the treatment purpose, the eschar stage decubitus can surgically be removed and skin-grafted (**Figure 6**). Histologically, the advanced lesion shows the fullthickness dermal necrosis with deep ulceration and abscess/gangrene formation.

#### **Figure 6.**

*Surgical removal of a large decubital ulcer covered with black eschar at the trochanter region. Surgical treatment was effective in this intractable ulceration (the courtesy of Dr. Sandai Ohnishi, Nagoya, Japan).*

Patterns of bacterial infection are often unique. *Staphylococcus aureus*, including MRSA, mainly colonizes the superficial layer (**Figure 7**), while Gram-negative rods, including *Pseudomonas aeruginosa* and *Escherichia coli*, are observed in the deep layer (**Figures 8** and **9**) [2].

The phenotype of MRSA can be demonstrated immunohistochemically in routinely formalin-fixed, paraffin-embedded lesions [21]. *S. aureus* is immunoreactive not only for staphylococcal antigens but also for protein A, an immunoglobulinbinding protein specifically expressed on the cell wall of *S. aureus*. The multidrug resistance of MRSA, determined by the expression of penicillin-binding protein 2<sup>0</sup> (PBP2<sup>0</sup> ) encoded by the *mecA* gene, can be immunophenotyped with monoclonal antibodies. Representative findings are demonstrated in **Figure 10**.

**6. Gas gangrene (clostridial myonecrosis)**

Gas gangrene caused by infection of *Clostridium perfringens* (formerly called *C. welchii*) is a life-threatening emergency, as a representative and grave form of wet gangrene [22–25]. *C. perfringens* is an obligate anaerobic Gram-positive bacillus forming spores on culture plates. Traumatic skin invasion of the microbe results in

*Another decubital ulcer with massive colonization of Gram-negative rods in the deep gangrenous tissue (H&E and immunostain). Gas formation is associated. A monoclonal antibody (J5) against lipopolysaccharide*

*common in* Enterobacteriaceae *illustrates an advanced infective process in the decubitus.*

Pseudomonas *infection in the deep part of the decubitus (H&E and immunostain). In the subcutaneous abscess (arrow), immunostaining using a monoclonal antibody against* Pseudomonas aeruginosa *demonstrates phagocytized microbes in neutrophils.* E. coli *antigens are negative. Arrowhead indicates superficially colonized*

**6.1 Traumatic gas gangrene**

**Figure 8.**

*Pathology of Gangrene*

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

**Figure 9.**

**101**

Staphylococcus aureus*, as shown in Figure 7.*

#### **Figure 7.**

*Microscopic double-layered appearance of the resected decubital ulcer (H&E, Gram and immunostain). Colonization of* Staphylococcus aureus*, probably MRSA, is observed along the eroded surface and clearly illustrated by Gram stain and immunostaining for staphylococcal antigens. Abscess formation with ischemic gangrene is noted in the deep zone.*

#### **Figure 8.**

Patterns of bacterial infection are often unique. *Staphylococcus aureus*, including MRSA, mainly colonizes the superficial layer (**Figure 7**), while Gram-negative rods, including *Pseudomonas aeruginosa* and *Escherichia coli*, are observed in the deep layer

*Surgical removal of a large decubital ulcer covered with black eschar at the trochanter region. Surgical treatment was effective in this intractable ulceration (the courtesy of Dr. Sandai Ohnishi, Nagoya, Japan).*

The phenotype of MRSA can be demonstrated immunohistochemically in routinely formalin-fixed, paraffin-embedded lesions [21]. *S. aureus* is immunoreactive not only for staphylococcal antigens but also for protein A, an immunoglobulinbinding protein specifically expressed on the cell wall of *S. aureus*. The multidrug resistance of MRSA, determined by the expression of penicillin-binding protein 2<sup>0</sup>

) encoded by the *mecA* gene, can be immunophenotyped with monoclonal

*Microscopic double-layered appearance of the resected decubital ulcer (H&E, Gram and immunostain). Colonization of* Staphylococcus aureus*, probably MRSA, is observed along the eroded surface and clearly illustrated by Gram stain and immunostaining for staphylococcal antigens. Abscess formation with ischemic*

antibodies. Representative findings are demonstrated in **Figure 10**.

(**Figures 8** and **9**) [2].

(PBP2<sup>0</sup>

**Figure 7.**

**100**

*gangrene is noted in the deep zone.*

**Figure 6.**

*Pathogenic Bacteria*

Pseudomonas *infection in the deep part of the decubitus (H&E and immunostain). In the subcutaneous abscess (arrow), immunostaining using a monoclonal antibody against* Pseudomonas aeruginosa *demonstrates phagocytized microbes in neutrophils.* E. coli *antigens are negative. Arrowhead indicates superficially colonized* Staphylococcus aureus*, as shown in Figure 7.*

#### **Figure 9.**

*Another decubital ulcer with massive colonization of Gram-negative rods in the deep gangrenous tissue (H&E and immunostain). Gas formation is associated. A monoclonal antibody (J5) against lipopolysaccharide common in* Enterobacteriaceae *illustrates an advanced infective process in the decubitus.*
