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Necrotizing Fasciitis-The Importance of Early Diagnosis and Debridement

December 20, 2005

By Schroeder, Janice L; Steinke, Elaine E

Necrotizing fasciitis (NF), is a life-threatening bacterial infection that causes rapid necrosis of deep subcutaneous tissue and fascia underlying the skin. French military hospitals and British naval surgeons in the 18th century, nurses in the Crimean war, and Confederate army surgeons all referred to NF in grim detail as hospital gangrene.1-3 In 1952, Bob Wilson, MD, was the first to describe the signs and symptoms of fascial necrosis and proposed the term necrotizing fasciitis. Publicity describing the condition as the “killer bug,”"flesh-eating bacteria,” and “galloping gangrene” during the past two decades has piqued public interest in this condition.1,2,4

CASE STUDY

Cassi Moore enjoyed the outdoors and spending weekends with her husband and three children ages 10, eight, and five. One Friday in June 1998 while on a camping trip, Moore sustained a small cut to her left thumb, which she immediately washed and bandaged. She also received a minor blow to her left lateral chest while practicing tae kwon do. On Sunday, Moore started to feel as though she were coming down with the flu.

By Monday afternoon, Moore was markedly worse, experiencing vomiting, diarrhea, fever, and pain on her left side. She went to her primary care physician, who diagnosed her with the flu and a pulled muscle based only on her verbal history. Her flu-like symptoms and left-side pain continued to increase, and Moore returned to her physician the next day complaining of extreme pain in her left side, much more than would be expected based on the appearance of her bruise. Again, based on her verbal report alone, the physician prescribed pain medication and sent her home. By Tuesday evening, the bruise on Moore’s chest was noticeably larger and darker.

Wednesday morning, Moore was very weak, and the medication she was taking did not stop the pain in her side. She was having difficulty breathing and was experiencing visual problems. By 11 AM on Wednesday, the bruise on her left side began to ulcerate and leak fluid and blood. By 1 PM, Moore was too weak to walk without assistance and was taken to the emergency department (ED).

On arrival in the ED, Moore had no detectable blood pressure and was in septic shock. Actions were quickly taken to stabilize her condition with IV fluids and medications. A computed tomography (CT) scan revealed gas in the soft tissues under her skin, which is a sign of necrotizing fasciitis. An infectious disease specialist and surgeon were consulted immediately, and Moore was rushed to the OR for emergency debridement of her left side and a portion of her left breast. Cultures obtained during surgery indicated the presence of group A Streptococcus (GAS). After surgery, Moore remained on a ventilator in the intensive care unit (ICU). Vasoconstricting medications kept blood flowing to her vital organs, and various IV antibiotics were administered in an effort to treat the NF.

Photographs courtesy of Cassi Moore and the National Necrotizing Fasciitis Foundation.

The day after surgery, it became apparent that Moore required hemodialysis, so she was transferred to a larger medical center with dialysis capabilities. At this point, Moore’s prognosis looked grim. She was in severe sepsis, and the effects of the vasoconstricting medications needed to keep her alive, combined with microvascular thrombosis from septic shock, were taking their toll on her hands and feet. Her fingers, toes, and parts of her right foot began to turn purple and black and started to shrivel. She eventually lost portions of all her fingers except her left thumb, which, surprisingly, was the thumb injured during the camping trip. Moore’s right leg was amputated below the knee and approximately one-third of her left foot also was amputated. The initial debridement of her left chest was followed by several smaller debridements in the ICU. After the infection in her side was gone, Moore underwent skin grafting procedures to her side, and later, reconstructive surgery to a portion of her side and left breast.

Approximately six weeks after the first surgery to debride her left side, Moore was strong enough to be transferred to a rehabilitation center for physical therapy, occupational therapy, and continued IV antibiotics. After 77 days in several hospitals and rehabilitation centers, Moore was discharged home.

EPIDEMIOLOGY AND CAUSES OF NF

Necrotizing fasciitis can occur in any area of the body, but commonly occurs in the extremities, abdominal wall, and perineum as a result of a disruption to the skin (eg, insect bite, burn, surgical incision, injection, laceration).2-11 Necrotizing fasciitis also can be associated with varicella, blunt trauma,2,5-8 incarcerated hernias, and renal calculi.2 Nontraumatic hematogenous spread of toxin-producing bacteria, such as Streptococcus pharyngitis, can spread from a distant site of infection.2,7 The specific entry mode or cause of bacteria resulting in NF is not known in about 20% of cases.2,4,9-12

Necrotizing fasciitis can occur in patients of any age. Some preexisting conditions can increase the risk of NF. These include

* alcoholism or IV drug use,

* diabetes mellitus (DM),

* immunocompromise,

* obesity,

* peripheral vascular disease, and

* smoking.2-4,7,11-13

The cause of death from NF frequently is multiple organ system failure resulting from overwhelming sepsis. Morbidity and mortality rates reported in the literature vary from 6% to 80%,27,14 with Fournier’s gangrene, an infective gangrene of the scrotum or vulva, consistently reported as high as 75%.9 Most studies report an overall mortality rate of 28% to 30%.2,7-9 Regardless of the numbers, necrotizing fasciitis is a serious, life-threatening disease that requires prompt diagnosis and intervention.

TYPES OF NF

No single organism is responsible for all types of NF (Table 1). Based on the number and type of organisms present, NF can be divided into three types. Type INF is polymicrobial, involving aerobic gram- negative bacteria, anaerobic gramnegative bacteria, and anaerobic grampositive bacteria.2,5,8,11,15 Type INF usually is preceded by a break in the skin from a penetrating injury or surgical procedure. Patients with DM account for a disproportionately high percentage of people with type INF.5 Pain experienced by patients with type I NF statistically is less severe than in type II NF. This may be due to the neuropathy associated with DM. Patients in an immunocompromised state or who have chronic debilitating diseases also are more likely to exhibit type I NF.2,3,7,8,15

Type II NF is the most common type of NF, with reported cases occurring in all age groups. It usually is community-acquired, although 20% of the cases in an Ontario group A streptococcal study were nosocomial, and 50% had no obvious portal of entry.8 Type II NF occasionally is called streptococcal gangrene, or hemolytic streptococcal gangrene, with the offending organism being GAS alone or in combination with staphylococcus.2,7,8,15

Type III NF involves marine vibrio gram-negative rods. The usual portal of entry is a puncture wound from a fish or a cut or an insect bite that has been exposed to seawater or shellfish. These vibrios synthesize an extracellular toxin that mediates the soft- tissue damage in NF.2,15

PATHOPHYSIOLOGICAL MECHANISMS

The skin provides physical and physiological barriers to infection (ie, a first line of defense). Tight junctions of skin cells, the presence of antibacterial peptides, and the shedding of surface cells make it difficult for bacteria to colonize on intact skin. When the microbes penetrate the skin, physiological protection is activated through the inflammatory response. Chemical mediators are released that secrete pyrogenic endotoxins and exotoxins.16 Secretion of these fever-producing proteins begins a cascade of events that lead to tissue destruction. If the infection is not contained by the body’s neutrophils and platelets, continued release of cytokines damages endothelial cells. Increased vascular permeability of the damaged endothelial lining of vessels allows fluid to leak out into the extravascular spaces, adding to the endothelial cell dysfunction, inflammation, and edema.13 Decreased blood flow causes tissue hypoxemia and necrosis. Vasculitis and thrombosis in adjacent tissues cause further necrosis involving the subcutaneous nerves, which explains the clinical change from severe pain to numbness. Under hypoxic wound conditions, the polymorphonuclear neutrophil phagocytic function typically present early in the inflammatory process is severely hampered, allowing more anaerobic growth, which accelerates the necrotic process.3,9,13,17

TABLE 1

Types of Necrotizing Fasciitis (NF)1-3

Fascial layers beneath the skin are not well supplied with blood vessels. This poor blood supply inhibits the normal infection- fighting ability of the inflammatory re-sponse process and hampers the body’s ability to transmit antibiotics to the affected area. As infection and necrosis spread throughout the fascial layers, vasoconstriction and thrombosis lead to edema and further diminish circulation, resulting in hypoxemia and necrosis of the fascia, skin, soft tissue, and muscles. Progression of soft-tissue necrosis can \be as rapid as one inch per hour.11 The fastest and most effective way to reduce the bacterial load and stop the necrosis is with prompt surgical excision and debridement of all infected tissue.3,5,10,11

CLINICAL MANIFESTATIONS

Necrotizing fasciitis usually begins with flu-like symptoms, such as fever, chills, tachycardia, and aches. The skin becomes erythematous, tender, edematous, and warm, similar to cellulitis, with or without blisters, accompanied by localized pain. A hallmark of NF is pain out of proportion to the physical findings.2,3,5,11,12 Symptoms of pain and fever often are overlooked during initial visits to health care providers because the symptoms are mistaken for the flu, muscle strain, or cellulitis.3,5,11 The subcutaneous tissue may have a hard, almost wooden feel on palpation, extending beyond the obvious area of redness. A complete blood count reveals leukocytosis with a left shift within a few days of presenting symptoms. A left shift is an abnormally high number of bands (ie, immature neutrophils) on the differential count and is indicative of an ongoing bacterial infection.18 This first stage can progress over a matter of hours or may take several days.2,3,11

During stage two, the patient becomes systemically more ill and may exhibit deterioration in sensorium. The infection continues to spread over larger areas in spite of initiation of antibiotic therapy. Septic vasculitis and thrombosis impede antibiotic penetration, making antibiotic therapy only minimally effective. The skin starts changing color from red to a patchy, dusky blue-gray, and blisters may form. Laboratory results may reveal azotemia, hypocalcemia, hyponatremia, hypoproteinemia, thrombocytopenia, hematuria and elevated creatine kinase and sedimentation rates, and metabolic acidosis.3,7,8 Hypoalbuminemia, anemia, and hyperbilirubinemia are common.

If soft-tissue GAS is present, radiological scans may help establish the extent of the infection that cannot be detected by physical examination.2,3,11,13 The absence of soft-tissue GAS on scans does not rule out NF.2

In the third and final stage, bullae, an ominous sign, are seen in about 30% of cases. The bullae become filled with a hemorrhagic, foul-smelling fluid described as “dishwater pus.”2-4,7,11 Large areas of hemorrhagic bullae may cause the patient to become anemic.11,13 Normal appearing skin is undermined with necrosis while muscles remain intact. The large number of aerobic and anaerobic bacteria spreading along the fascial plane causes the vasculature of the skin to become inflamed and thrombosed, resulting in necrotic eschars that appear like deep thermal burns.2 If Enterobacter or Clostridiuni are responsible for the NF, crepitus due to bacterial gas production can be palpated. Nerve destruction replaces the severe pain with numbness.3 As toxins are released into the blood, the patient appears septic with a high fever, high white blood cell count, disorientation, or unconsciousness.2,3,11

PERIOPERATIVE IMPLICATIONS

The key to successful management of NF is early diagnosis and prompt debridement. A comprehensive history and physical examination of the patient presenting with pain that is out of proportion to the physical findings should cause a high degree of suspicion and prompt further investigation into the possibility of NF. Perioperative nurses should understand that initiating administration of broad- spectrum antibiotics and ensuring prompt surgical evaluation are critical for optimal patient outcomes.2,4,5,7,8,10,11

The physician can make a definitive diagnosis in the OR. The surgeon makes a 2-cm to 3-cm incision down to the deep fascial layer of skin where he or she obtains cultures. A lack of bleeding or a thin, brownish, murky fluid exuding from the wound is the first sign of possible NF. The surgeon then performs the “finger test” by gently inserting his or her index finger into the subcutaneous compartment between the fascia and dermis. If the tissues divide and fall apart easily, the finger test is considered positive for NF and prompt surgical debridement is imperative for positive patient outcomes.4,10,19

Perioperative nurses should ensure that surgical supplies specific to emergency NF debridement are immediately available, including

* aerobic and anaerobic culture swabs,

* instrumentation appropriate for the site to be debrided,

* pressure-vacuum irrigation equipment,

* standard set-up packs,

* standard skin preparation supplies,

* sterile specimen containers, and

* the surgeon’s antibiotic of choice for irrigation.

The anesthesia care provider must be prepared to manage septic shock. Prompt access is essential to the surgical team.

The extent of infection often is underestimated on physical examination, so at the time of surgery, the surgeon must determine the extent of debridement needed. The surgeon must excise all necrotic tissue and expose all infection. He or she may determine that a repeat evaluation and further debridement of the area is needed after 24 to 48 hours. If the patient’s condition deteriorates clinically and hemodynamically with the continuing spread of necrosis, the patient should return to the OR sooner than the scheduled 24 to 48 hours. When an extremity is involved, amputation may be required if repeated attempts at debridement do not halt the progression of necrosis.10 During the hospital course, practitioners must perform frequent physical assessments to monitor the affected area for expansion of erythema, edema, pain, skin color changes, presence of bullae, and color and odor of drainage. Dressing changes may be excruciating, requiring premedication or sedation. During sedation, the practitioner thoroughly assesses the surrounding tissue with a sterile gloved hand to determine if the fascia can be separated. If the tissue can be loosened beyond the area of debridement, further surgical debridement may be necessary.10,13 It is common for patients to make multiple trips to the OR for repeat debridement procedures.

Anatomy of the skin

CONTROLLING PAIN

The use of patient-controlled analgesia (eg, morphine sulphate, meperidine, fentanyl) can provide adequate pain control. Assessing pain is important for both ensuring patient comfort and determining disease progression. Nerve necrosis may be developing if a patient reports a change from pain to numbness. Fever greater than 101 F (38.3 C), low hemoglobin and elevated hematocrit and blood urea nitrogen may indicate dehydration and the need for adjustment in fluid resuscitation. Extensive fat necrosis may cause hypocalcemia. Heparin therapy is initiated to decrease the risk and extent of vasculitis and thrombosis.13 Hyperbaric oxygen (HBO^sub 2^) therapy is advocated, particularly if the offending organism is anaerobic.3,5,12,13,20 One retrospective study reported a 35% mortality rate in a group of 33 patients who were treated with the standard antimicrobial and surgical protocol, compared to a 16% mortality rate in 30 patients who received HBO^sub 2^ in addition to the standard protocol.4 The anaerobic properties of bacteroides, Clostridium, Peptococais, and others make HBO^sub 2^ therapy an important adjunct to antimicrobial and surgical interventions. Hyperbaric oxygen is toxic to Clostridium in particular, blocking the production of alpha toxin. Hyperoxemia allows more efficient leukocyte function, increased red cell pliability, and termination of lipid peroxidation. The resulting reduction in edema aids in the preservation of marginally perfused tissue.4,5

PSYCHOSOCIAL CONSIDERATIONS

Psychological consequences of NF result from extreme pain, physical disfigurement, and emotional factors, such as anxiety, fear, worry, anger, and hopelessness. Emotional disharmony (eg, depression, anxiety) can slow the physical and emotional healing process. Appropriate dispensing of psychotropic and pain medications, optimal nutrition, and social services support for patients and their family members will help with the physical and emotional healing.”

DISCUSSION OF THE CASE STUDY

Moore’s experience follows the pattern of type II NF. An otherwise healthy adult, Moore was without the typical preexisting conditions often found in type I NF, such as DM or other debilitating diseases. The causative organism primarily was GAS. Although Moore had a small break in her skin on her left thumb, the site of’ NF was her left chest where she received blunt trauma. Her pain was out of proportion to her presenting symptoms, and she exhibited flu-like symptoms, including fever. Her symptoms progressed rapidly, from flu-like symptoms on Sunday to septic shock by Wednesday. Moore was fortunate that her surgeon did an immediate, thorough debridement, which prevented the need for repeat trips to the OR for further debridement. It was unfortunate that the microthrombotic component of septic shock therapy combined with the vasoconstricting agents needed to maintain vital organ perfusion caused necrosis of her fingers, toes, and right lower leg.

Moore is again playing the guitar and keyboard with the help of finger extensions and is able to drive her car with modifications to the gas pedal that allows her to use her left foot on the gas. She is back at her job as a computer programmer and is again enjoying weekend outings with her family. Special prosthetics allow Moore to do almost everything she did before her ordeal with NF.

UNDERSTANDING NF

Necrotizing fasciitis is a rare, fast-spreading, life- threatening infection of the soft tissues underlying the skin. Early symptoms often are mistaken for cellulitis or other infections. The hallmark symptom of NF is pain that is out of proportion to presenting symptoms. Appropriate antibiotic therapy along with early and thorough debridement improves patient outcomes compared to delayed surgical debridement. Understanding the signs and symptoms, risk factors, and pathophysiologic process of NF increases the perioperative nurse’s a\bility to anticipate the surgical needs of the patient and facilitate a quick diagnosis and prompt treatment.

Editor’s note: The authors thank Cassi Moore for sharing her photographs and personal experience with necrotizing fasciitis. Readers can learn more about Moore’s experience by visiting the National Necrotizing Fasciitis Foundation web site at http:// www.nnff.org and clicking on “Survivor’s Stories.”

ABSTRACT

* NECROTIZING FASCIITIS (NF) is a potentially life-threatening bacterial infection of the skin, deep subcutaneous tissue, and fascia. Early symptoms may be misdiagnosed as cellulitis. A hallmark symptom that distinguishes NF from cellulitis is severe local pain that is out of proportion to the size and type of the wound present.

* EARLY DIAGNOSIS AND TREATMENT of NF is imperative for a patient’s survival. This article describes the pathophysiologic mechanisms, clinical manifestations, and treatment of NF, as well as implications for perioperative nursing. AORN J 82 (December 2005) 1031-1040.

The cause of death from necrotizing fasciitis frequently is multiple organ system failure resulting from overwhelming sepsis. Reported morbidity and mortality rates vary from 6% to 80%.

A hallmark of necrotizing fasciitis (NF) is pain that is out of proportion with the physical findings; NF usually begins with flu- like symptoms.

SIDEBAR

Common Definitions Used in Describing Necrotizing Fasciitis

Cytokines function as the messengers of the immune response by providing communication among macrophages and lymphocytes.1 They are divided into four major groups: interleukins, interferons, tumor necrosis factors, and transformation growth factors.2

Endotoxins are contained in the cell walls of gram-negative bacteria and are released during bacterial destruction.1 Endotoxin bacteria also are called pyrogenic bacteria because they activate the inflammatory process and produce fever. Endotoxins provoke the production of cytokines.3

Exotoxins are proteins released during bacterial growth.1 Very small quantities of exotoxin can be fatal.3

Fournier’s gangrene is an infective gangrene of the scrotum or vulva caused by anaerobic hemolytic strain of Streptococcus.1

Necrotizing fasciitis is a life-threatening bacterial infection that causes rapid necrosis of deep subcutaneous tissue and fascia underlying the skin.

Polymorphonuclear neutrophil is a predominant phagocytic cell in the early inflammatory response to injury.1

A pyrogenic substance or agent tends to cause a rise in body temperature, such as some bacterial toxins.

Thrombosis is an abnormal condition in which a clot (ie, thrombus) develops within a blood vessel.

Vasculitis is an inflammation of the blood vessels. It may be caused by a systemic disease or an allergic reaction.

1. S E Huether, K L McCance, Pathophysiology: The Biologic Basis of Disease in Adults & Children (St Louis: Mosby, 2002) 197-226.

2. B Bullock, R Henze, Focus on Pathophysiology (Philadelphia: Lippincott, 2002) 271-291.

3. B Bullock, R Henze, Focus on Pathophysiology (Philadelphia: Lippincott, 2002) 223-251.

NOTES

1. I Loudon, “Before our time: Necrotizing fasciitis, hospital gangrene, and phagedema,” Lancet 344 (Nov 19, 1994) 1416-1419.

2. R J Green, D C Dafoe, T A Raffin, “Necrotixing fasciitis,” Chest 110 (July 1996) 219-227.

3. S D Fritzsche, “Soft-tissue infection: Necrotizing fasciitis,” Plastic Surgical Nursing 23 (Winter 2003) 155-139.

4. T J Andreasen, S D Green, B J Childres, “Massive infectious soft-tissue injury: Diagnosis and management of necrotizing fasciitis and purpura fulminans,” Plastic and Reconstructs Surgery 107 (April 2001) 1025-1035.

5. W Guo, S Steinberg, “Infections of skin, muscle, and soft tissue,” in Textbook far Critical Care, fifth ed, J M Vincent et al, eds (Philadelphia: Elsevier Saunders, 2005) 1309-1312.

6. S Nseir et al, “Fatal streptococcal necrotizing fasciitis as a complication of axillary brachial plexus block,” British journal of Anesthesia 92 (March 2004) 427-429.

7. D Purnell, T Hazlett, S L Alexander, “A new weapon against severe sepsis related to necrotizing fasciitis,” Dimensions of Critical Care Nursing 23 (January/February 2004) 18-23.

8. D Stevens, “Necrotizing infections of the skin and fascia,” Up to date, htty://www .nptodate.com (accessed 1 Jan 2005).

9. M Maynor, “Necrotizing fasciitis,” eMedicme,http:// www.emedicine.com/emerg /topic332.htm (accessed 6 Oct 2005).

10. B Oelschlager, E P Dellinger, “Necrotizing soft-tissue infections,” Contemporary Surgery 57 suppl (August 2001) S26-S31.

11. L A Sekeres, “Necrotizing fasciitis: A perioperative case study,” Critical Care Nursing Clinics of North America 12 (June 2000) 181-186.

12. B W Walker, “Putting the breaks on necrotizing fasciitis,” Nursing 34 (October 2004) 40-41.

13. A Fink, G DeLuca, “Necrotizing fasciitis: Pathophysiology and treatment,” Dermatology Nursing 14 (October 2002) 324-327.

14. L Braun et al, “A sepsis review: Epidemiology, economics, and disease characteristics,” Dimensions of Critical Care Nursing 22 (May/June 2003) 117-124.

15. J Blanchard, “Necrotizing fasciitis; cleaning hospital toys; disinfecting noncritical items; clinical practice patterns; barrier protection,” AORN Journal 81 (March 2005) 608.

16. B Bullock, R Henze, Focus on Patliophysiology (Philadelphia: Lippincott, 2002) 223-251.

17. S E Huether, K L McCance, Pathophysiology: The Biologic Basis of Disease in Adults & Children (St Louis: Mosby, 2002) 197-226.

18. K D Pagana, R J Pagana, Mosby’s Diagnostic and Laboratory Test Reference, 7th ed (St Louis: Elsevier Mosby, 2005).

19. L Tierney et al, 2005 Current Medical Diagnosis and Treatment (New York: McGraw-Hill, 2005) 1350-1392.

20. D Levy, “Medical encyclopedia: Necrotizing soft tissue infection,” MedlinePlus, http://ipuno.nlm.nih.gov/med lineplus/ency/ article/001443.htm (accessed 18 Oct 2005).

Janice L. Schroeder, RN; Elaine E. Steinke, RN

Janice L. Schroeder, RN, BSN, CNOR, CRNFA, is a private first assistant at Hutchinson Medical Center, Hutchinson, Kan.

Elaine E. Steinke, RN, PhD, ARNP, is a professor at Wichita State University, School of Nursing, Wichita, Kan.

Copyright Association of Operating Room Nurses, Inc. Dec 2005




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