Necrotizing Fasciitis - 2 Nursing CEs

Author: Brooke Baldwin-Rodriguez, RN, MSN

Written: February 8th, 2008

Updated: September 11, 2009

Course Description

Necrotizing fasciitis is a rare infection that spreads rapidly and can cause extensive damage to skin, tissue and muscle when not recognized and treated promptly. There are estimated to be 0.4 cases per 100,000. Increasing incidence in the 1990’s and reports on the news have led to fear of this invasive infection. Nurses play a crucial role in early identification of the signs and symptoms so that treatment can be initiated. This course will describe necrotizing fasciitis, identify the key signs and symptoms, and outline the treatment strategies that aim to minimize the devastating effects. The last part of this course will highlight the need for psychosocial support that patients and families have when facing a diagnosis like necrotizing fasciitis.

Course Objectives

Describe necrotizing fasciitis

Describe the three types of necrotizing fasciitis

Identify the different aerobic, anaerobic, and fungal organisms that may cause necrotizing fasciitis

List the risk factors that may precipitate a necrotizing fasciitis infection

Describe the pathophysiology of necrotizing fasciitis

Identify the main diagnostic criteria for a necrotizing fasciitis diagnosis

Identify early, advanced, and late signs and symptoms

List three clinical courses that necrotizing fasciitis follows

Identify and list the four main components of a treatment strategy for necrotizing fasciitis

Identify strategies for psychosocial support for the patient and family

Description and Etiology

The term necrotizing fasciitis conjures up images that scares the most experienced of nurses. The stories of bug bites that have “eaten” away at the flesh (aka, “flesh eating bacteria”), leading to significant tissue necrosis and the need to debride away a large percentage of body skin, subcutaneous tissue, and muscle have circulated not only throughout the healthcare community, but friends and neighbors as well. A high rate of mortality, up to 70%, reinforces the high risk associated with this infection. Although necrotizing fasciitis seems a relatively new phenomenon, cases have been documented by British naval surgeons in the 18th century, the Crimean war, and by Confederate army surgeons. This severe infection was referred to as hospital gangrene prior to 1952. In 1952 the term necrotizing fasciitis was first used; the term necrotizing fasciitis characterizes the key feature of this infection: fascial necrosis.

Necrotizing fasciitis is a bacterial infection that is life-threatening. It is a rapidly spreading infection of the subcutaneous tissue that results in extensive necrosis of the deep subcutaneous tissue and fascia. It expands along the deep fascial plane as it spreads throughout the body tissue. Necrotizing fasciitis is on the most severe end of the spectrum of necrotizing soft tissue infections (NSTIs). Less severe forms include necrotizing cellulitis, which is confined to the cutaneous layer.

Necrotizing fasciitis can be classified into three types based on the causative organism: types: Type 1, type 2, or type 3.

Type 1 involves a polymicrobial infection and includes aerobic gram-negative bacteria, anaerobic gram-negative bacteria, and anaerobic gram-positive bacteria.

Approximately 80% of necrotizing fasciitis is caused by type 1.

Common bacteria include:

Type	Organism
Aerobic	Group A streptococcus Group B streptococcus Staphylococcus aureus Escherichia coli Enterococcus Pseudomonas Klebsiella
Anaerobic	Bacteroides fragilis Clostridium Enterobacter
Fungi	Candida

Type 1 is often introduced at sites of surgery or trauma and is commonly found in the perineal and abdominal areas. Patients with diabetes mellitus and immunocompromised states with chronic debilitating diseases are more likely to present with type 1 necrotizing fasciitis.

Type 2 is caused by Group A streptococcus. Type 2 is generally community acquired and may also be called streptococcal gangrene. Type 2 most commonly affects the extremities.

Type 3 is associated with Vibrio vulnificus and enters the subcutaneous tissue via puncture wounds from fish or marine insects. This type is seen less commonly than either type 1 or type 2

Generally, necrotizing fasciitis can occur in patients of any age, but many conditions increase the risk:

• alcoholism or IV drug use

• diabetes mellitus

• immunocompromise

• obesity

• peripheral vascular disease

• smoking

• organ transplants

• neutropenia

When necrotizing fasciitis occurs in patients with relatively little risk it is usually attributed to more virulent strains that are resistant to antibiotics. Anything that impairs skin integrity also increases the risk. Trauma, lacerations, surgical wounds, skin biopsy, pressure ulcers, perirectal abscesses, psoriasis, chronic skin infection, boils, herpes zoster, and chronic venous leg ulcers, are a few of the noted breaks in skin that have lead to necrotizing fasciitis.

When untreated promptly, the patient afflicted with the disease can develop life-threatening sepsis and septic shock. Morbidity is increased in those patients who develop septic shock due to disseminated intravascular coagulation, respiratory failure, and multisystem organ failure. Identification and quick intervention is key to decreasing the risk of death.

Pathophysiology

The bacteria under the skin begin to eat away at the subcutaneous layer between the skin and muscle. The bacteria is either a result of a direct break in the skin or the result from a distant site of infection. Bacterial toxins and enzymes, such as collagenase, streptokinase, and lipase, help the pathogen spread and cause necrosis. The immune system mounts a large, exaggerated attack. The cytokines increase vascular permeability and damaged endothelial lining of the vessels and leads to inflammation and edema. Vasodilation is followed by vasoconstriction and thrombosis result due to the cytokines and other inflammatory mediators (endotoxins and exotoxins) blocking the blood vessels. The fascial layer, where the infection occurs is not well supplied by blood flow which inhibits the body’s normal response and the body’s ability to transport antibiotics to the area. Decreased blood flow leads to hypoxemia and hypoxia; cell death ensues due to the decrease in blood flow to the tissue. Decreased blood flow to the area decreases the flow of neutrophils to the area. Since the infectious process occurs in the area of the subcutaneous tissues, delayed diagnosis often occurs because there are no obvious signs and symptoms.

Diagnosis

Rapid diagnosis is imperative because the tissue necrosis can progress as fast as 1 inch and hour. Diagnosis of necrotizing fasciitis is usually the result of clinical diagnosis rather than laboratory diagnosis. The diagnosis of necrotizing fasciitis is often delayed because it mimics many other conditions. Necrotizing fasciitis is often first assessed as cellulitis, phlebitis, or deep vein thrombosis. Initial vague symptoms described by the patient also lead to incorrect diagnosis. Initially, the patient may complain of flu-like symptoms: diarrhea, thirst, gastric symptoms, chills, and tachycardia. A lesion that appears red, erythemateous, with no clear borders that may be attributed to cellulitis is usually present. The hallmark sign of the condition should promote a high index of suspicion: pain out of proportion to the apparent severity, or the physical findings. Symptoms can be classified as early, advanced, and late. However, caution should be noted due to the rapid progression from early to. Late signs and symptoms in these types of patients.

Early signs and symptoms

• Localized heat

• Localized erythema

• Localized edema

Advanced signs and symptoms

• Malaise

• Thirst

• Diarrhea

• Stomach pain

• Vesicle formation

Late signs and symptoms

• Confusion

• Hypotension

• Tachycardia

• Shock

Diagnostic Criteria for Necrotizing Fasciitis

1.   Mental status changes 2.  Generalized malaise, tachycardia 3.  Systemic toxic reaction: fever, increased white blood cell count, positive blood cultures 4.  Focal necrosis, microvascular thrombosis, and leukocyte identified from involved tissue samples 5.   Extensive necrosis of the superficial; fascia in the absence of microvascular occlusion 6.  Pain that is out of proportion to the visual assessment 7.   Little or no resolution of the signs an symptoms after treatment with antibiotics   Ruth-Sahd &  Gonzales (2006)

Most commonly, lesions will appear on the extremities or abdominal area. When the lesions are located on the perineum or genitalia it is called Fournier’s gangrene.

Necrotizing fasciitis can also be categorized into three groups based on clinical course:

1.   Acute

2.  Fulminant

3.  Subacute

Acute necrotizing fasciitis occurs when the skin turns from red to purple-black in 3 to 4 days. As tissue necrosis continues the skin begins to slough off. Blister and bullae may develop with gray, foul-smelling that is termed “dishwater pus”. Patients may complain of increased levels of pain not relieved with Opiods.

Fulminant necrotizing fasciitis has an extremely rapid progression and presents with severe sepsis, multiple organ failure, and shock within 24 hours. 100% chance of mortality is inevitable unless extensive debridement and, perhaps, amputation is performed.

Subacute necrotizing fasciitis presents over weeks to months. The progression begins with a less extensive area and symptoms may be present for an extended period. However, even with subacute type, rapid deterioration may occur after the long incubation period.

Laboratory tests, histopathology, and radiographic studies help aid in the diagnosis of necrotizing fasciitis. Laboratory tests like a complete blood count show leukocytes with a left shift within a few days of presenting symptoms. The first stage can progress over a few hours to days. Elevated sedimentation rate and elevated creatinine kinase levels can be seen as well. Elevated creatinine signals renal involvement. Blood cultures can identify the causative organism and aid in the choice of antibiotics. Biopsy will show infiltration of the fascia by polymorphonuclear leukocytes. Other laboratory values that may indicate necrotizing fasciitis include: hypocalcemia, hyponatremia, hpoproteinemia, thrombocytopenia, and metabolic acidosis.

Computed topography and/or magnetic resonance imaging identifies pockets of air and gas and can reveal the extent of the affected area. MRI is superior to CT in differentiating healthy and necrotic tissue. It must be noted that negative results on either MRI or CT do not rule out a necrotizing fasciitis diagnosis. Diagnosis may not be confirmed until surgical debridement is done. Surgical exploration is the fastest way to definitive diagnosis. If the skin separates or lifts from the underlying necrotic tissue, during surgical exploration diagnosis is confirmed.

Treatment

Four general principles in treatment of necrotizing fasciitis include:

1.   early diagnosis and surgical debridement

2.  early administration of broad-spectrum antibiotics

3.  aggressive resuscitation

4.  aggressive nutritional support

Early Diagnosis and Surgical Debridement

Early diagnosis and debridement are essential components of successful treatment for patients with necrotizing fasciitis. Debridement should be aggressive and radical. The rationale for aggressive debridement is to ensure that no bacteria are left behind. Many patients require multiple trips to the operating room for debridement. Return trips to the operating room are often deemed necessary when the patient’s condition deteriorates and the patient becomes hemodynamically unstable. If an extremity is involved, amputation is often necessary if debridement does not halt the progression of necrosis. Skin and muscle grafts are generally required after the infection has cleared.

Early Administration of Antibiotics

Broad-spectrum antibiotics are used for the beginning of treatment and then adjusted based on culture and gram stain results. Penicillin, clindamydcin, or metronidazole, and aminoglycoside or third-generation cephalosporin are started. There is usually more than one bacteria associated with necrotizing fasciitis which prompts treatment with more than one antibiotic. Antibiotics do not stop the progression of necrosis and surgical removal is absolutely necessary. Diligent evaluation for the presence of secondary infection is required.

Aggressive Fluid Resuscitation Due to the large wounds that these patients typically have and the high potential of developing septic shock, aggressive resuscitation is necessary. Low hemoglobin and hemotocrit laboratory values and rising blood urea nitrogen may indicate dehydration and a need to adjust fluid resuscitation.

Aggressive Nutritional Support

Nutritional support is absolutely essential for the healing process of such large wounds. Increased protein requirements and increased caloric needs necessitate nutritional support in these patients. Collaboration with nutritional support services is critical in determine the caloric and protein requirements as nutritional requirements often double.

Other Treatment Modalities

Hyperbaric oxygen therapy may be considered as a modality of treatment, especially if the organism is anaerobic. Patients must be hemodynamically stable enough to undergo this treatment. The rationale behind hyperbaric oxygen therapy is that it increases tissue oxygenation and epithelialization, strengthens the ability of the white blood cells to fight infection, and promotes the formation of new blood vessels.

Nursing Direct Treatment

Nursing directed treatment is aimed at pain control during dressing changes and identifying psychosocial needs of the patient and family. Dressing changes are often painful and require premedication and/or sedation. Patient controlled analgesia (PCA) like morphine sulphate, meperidine, or fentanyl are commonly used analgesics in controlling pain. Since the extent of the injury is usually large, the dressing changes are time and labor intensive. More that one nurse is usually needed to complete the dressing changes. Negative-pressure vacuum-assisted devices may be ordered by the physician, but the large surface area of these wounds may make application difficult. Nurses are vital in monitoring changes in patient condition and alerting physicians when the condition changes. Serial assessments and changes in assessment must be promptly recorded and reported.

Desired Outcomes/Goals of Care

Patients with necrotizing fasciitis require special pain management and psychosocial management. The goal is to provide care that support rehabilitation and return to daily activities and psychosocial adjustment to the condition.

Extreme pain, physical disfigurement, and anxiety, fear, anger, and hopelessness increase the value of psychosocial support for patients and families experiencing treatment associated with necrotizing fasciitis. Nurses can facilitate coping mechanisms by envolving social service support at an early stage in the treatment. Psychological support and medications help to achieve the desired outcomes.

References

Marini, J., J. MD. Wheeler, A., P. (2009). Critical care medicine: the essentials. (4th ed.). Lippincott, Williams & Wilkins. Philadelphia

Hargrove-Huttel, R., A. (2008). Lippincott’s review series: medical-surgical nursing. (2nd ed.). Lippincott, Williams & Wilkens. Philadelphia

Cainzos, M. & Gonzalez-Rodriguez, F.J. (2007). Necrotizing Soft Tissue Infections. Current Opinion in Critical Care, 13: 433-439.

Endorf, F.W., Supple, K.G. & Gamelli, R.L. (2004). The Evolving Characteristics and Care of Necrotizing Soft-Tissue Infections. Burns, 31: 260-273.

McGee, E.J. (2005). Necrotizing Fasciitis: Review of pathophysiology, diagnosis, and treatment. Critical Care Nursing Quarterly, 28(1), 80-84.

Ruth-Sahd, L. (2006). Multiple Dimensions of Caring for a Patient with Acute Necrotizing Fasciitis. Dimensions in Critical Care Nursing, 25(1), 15-21. 

Salcido, R. (2007). Necrotizing Fasciitis: Reviewing the causes and treatment strategies. Advances in Skin & Wound Care, 20: 288-293.

Schroeder, J.L & Steinke, E.E. (2005). Necrotizing Fasciitis: The importance of early diagnosis and debridement. Association of Operating Room Nurses Journal, 82(6), 1031-1040.