Necrotizing Fasciitis

0899-5885/00 $15.00 + .00

Perioperative Critical Care

Necrotizing Fasciitis A Perioperative Case Study Lynn A. Sekeres, MSN , RN , CCRN , CPAN

Ms.

L was a healthy, slightly obese, 44-yearold woman who had been complaining of flulike symptoms with increasing fever and a lower extremity rash when she presented to the emergency room (ER). She was initially released but returned to the ER 3 days later with a deterioration of her condition that required an ICU admission. Her unfavorable prognosis required a prolonged ICU stay and extensive recovery on a patient care unit. What led to this nightmare?

Case Study Ms. L stated that she had been experiencing the flu . Her symptoms included a headache, fever, and myalgia. Her doctor prescribed ibuprofen, which helped to alleviate the symptoms. These symptoms initially resolved; then 10 days later she once again complained of increasing fever and a progressive lower extremity rash to the right groin with leg pain, followed by skin discoloration. Ms. L denied any injuries to her lower extremities. She went to the ER, where Doppler studies of the lower extremities were performed to rule out peripheral vascular disease; the results were normal. She was diagnosed with cellulitis of the right lower extremity and sent From the Post Anesthesia Ca re Unit, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania

home with a prescription for oral cephalexin (Keftex). The patient returned to the ER 3 days later with increased leg pain, edema, and bluish-black discoloration of both legs. She was unable to walk because of extreme pain, and she was hypotensive with a blood pressure of 80/ 50 mm Hg. She was treated with vasopressors (dopamine and norepinephrine) and a continuous infusion of fentanyl for pain control. Her lower extremities showed purpura with bullae and were tender to palpation and extremely edematous. Laboratory studies showed her to be thrombocytopenic and anetnic. She was also in acute renal failure and had elevated liver enzymes. Her white blood cell count, prothrombin time, and partial thromboplastin time were elevated. Urinalysis showed white cells and protein but no myoglobin. A CT scan was negative for fasciitis of the lower extremity. The tentative diagnosis at this time was septic shock, and treatment at this point included intravenous fluids and transfusion of platelets and packed red blood cells. The patient was also started on broad-spectrum intravenous antibiotic treatment of ceftriaxone and vancomycin. She was transferred to the intensive care unit (ICU). The next day her condition deteriorated further, and she had to be intubated and placed on mechanical ventilation because of noncardiogenic pulmonary edema. Her principal diagnosis was septic shock,

CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 I Number 2 I June 2000

181

182

SEKERES

which was caused by necrotizing fasciitis (NF) of the lower extremities. Secondary diagnoses included respiratory failure, renal and liver dysfunction secondary to sepsis, coagulopathy, and encephalopathy with mental status changes. Her condition was critical, and her family was aware of the unfavorable prognosis at this time. Within the first 2 days in the ICU, a plastic surgery consultation was obtained to evaluate the necrosis. Frequent wet-to-dry dressing changes were ordered. A tissue biopsy of her right knee wound was performed and cultured for aerobic and anaerobic bacteria and fungi. The culture showed no growth, and no organisms were present on Gram staining. Her abdomen had red-violet discoloration in the right lower quadrant and in the suprapubic region. Her lower extremities were worsening. The right leg had large purpuric lesions with bullae and areas of necrosis over the right thigh advancing to the right lateral abdomen. The left heel became necrotic with sloughing of the skin. After the first week in the ICU, the septic shock was resolved with antibiotics. She was taken off ventilatory support, and the vasopressor drips were discontinued. All blood cultures remained negative. The blood urea nitrogen and creatinine improved, indicating an improvement of renal function. Liver function tests and coagulation results were returning to normal values. She was weak but alert and oriented. Despite resolution of the septic shock, the necrotizing fasciitis of the lower extremities continued to progress, involving more area. The right leg from the groin to the ankle was ecchymotic with weeping bullae. Large areas of eschar developed on the right thigh. The left ankle was ecchymotic with bullae. Petroleum jelly gauze dressings were used to provide skin coverage. She lost significant amounts of protein and blood from her leg wounds and needed periodic transfusions of packed red blood cells to treat the anemia and total parenteral nutrition to improve her metabolic status. About 2 weeks after admission to the hospital, Ms. L was transferred to a patient unit on a nursing floor, and she had her first surgery to debride her legs. The culture result from this first debridement was positive for Candida. She required several debridement pro-

cedures over the next few weeks. An extensive amount of necrotic skin, subcutaneous tissue, and muscle were excised and then covered with petroleum jelly gauze, 4" X 4" gauze squares, and elastic wrap. While in the postanesthesia care unit, she developed a heart rate of 150 and a temperature of 38.9° C. She had a short return trip to the ICU to rule out recurrent sepsis. Her vital signs stabilized after 2 days in the ICU, and it was decided that she had a transient bacteremia. Eventually, gamma skin grafts were applied to her right lower extremity. The gamma graft is a synthetic graft used because of the large area of skin coverage needed before performing a split-thickness skin graft to limit the area of donor skin needed. The skin grafts healed slowly because of her poor nutritional status, prolonging her ICU stay. She was maintained on protein supplements and encouraged to ambulate as much as possible to promote graft and donor site healing and to strengthen muscles. Following the initial graft placement, her hemoglobin and hematocrit slowly improved. Ms. L was transferred to a transitional care unit approximately 5 weeks after the onset of her condition. Following the gamma grafts, she had a significant reduction in pain and made progress with her physical and occupational therapies but still had multiple denuded areas of muscle. She continued to receive a high-protein supplement by tube feedings to place her in an anabolic state in preparation for her split-thickness skin grafting. The final surgery was done almost 3 months after her admission to the ICU and included the application of the split-thickness skin graft, which was transferred from the left thigh to the right upper and lower leg. This grafting procedure was successful, and the patient was discharged to home approximately 3 months after her nightmare in the hospital began.

Clinical Presentation and Pathophysiology NF is a very serious and often life-threatening disease. 7• 19 It is a disease that involves rapidly spreading inflammation followed by necrosis of superficial fascia, subcutaneous fat, and in some cases, the muscle and epidermis.17 It is often associated with severe systemic toxicity.12 It must be diagnosed and treated early

NECROTIZING FASCllTIS

to have a positive outcome. Even the lay public has respect for this disease by calling it the flesh-eating disease. NF is uncommon, 12 but it has a high mortality rate of up to 74%. 5 It can progress very rapidly, consuming up to an inch of flesh an hour. 18Diagnosis often is difficult because the early symptoms can be suggestive of other types of skin infections. NF usually occurs in the abdomen, extremities, and perineum, but it can occur in several other areas of the body where fascia is present, 1· 2· 13 such as the Abdomen Extremities Perineum Genitourinary system Face and neck Scalp and periorbital area Catheter sites Data from Green RJ, Dafoe DC, Raffin TA: Necrotizing fasciitis. Chest 110:219-227, 1996; and Johns-Langford FP, Moon RE, Stolp BW, et al: Treatment of cervical necrotizing fasciitis with hyperbaric oxygen therapy. Otolaryngol Head Neck Surg 112:274-277, 1995.

There usually is some event, such as a laceration or local infection, that creates a break in the epidermis, resulting in a vulnerability to infection. 19 Lacerations, cuts, abrasions, contusions, burns, bites, subcutaneous injections, or operative incisions have been implicated as causative factors. 1 There are many conditions that put a patient at risk for NF, 1· 2· 5· 12· 18 including: Age greater than 50 Alcoholism Atherosclerosis Diabetes mellitus Hypertension Immunosuppression Intravenous drug use Malignancy Malnutrition Obesity Renal failure Surgery Trauma Data from Ault MJ, Geiderman J, Sokolov R: Rapid identification of group A streptococcus as the cause of necrotizing fasciitis. Ann Emerg Med 28:227-229, 1996; and Chapnick EK, Abter El: Necrotizing soft-tissue infections. Infect Dis Clin North Am 10:835-843, 1996.

The more risk factors are present, the greater the chance of mortality. 7 It also has

183

been documented that there is a possible correlation between nonsteroidal anti-inflammatory drug use and NF. 7· 12 This disease also can occur in young, healthy patients, and it even has been reported in neonates.9 There is no single organism responsible for necrotizing faciitis disease. Gram-positive, gram-negative, anaerobic, marine vibrio, and fungi organisms have been identified in NF. The incidence of positive blood cultures ranges from 25% to 100%. 19 Idiopathic NF seems to be caused by group A streptococci, although a secondary NF can be caused by a variety of other potential organisms. 14 The bacteria most commonly cultured from NF wounds are species of streptococcus, staphylococcus, peptostreptococcus bacteroides, and clostridium. 10 The organisms most predominantly the cause are the /3-hemolytic Streptococcus pyogenes. These are the same organisms that cause strep throat, but they can be responsible for cellulitis, toxic shock syndrome, myositis, and NF. They are highly sensitive to antibiotics, but delays in treatment will result in increased morbidity and mortality.2 The necrosis occurs as a result of the thrombosis of surrounding vessels. 7The tissue damage and systemic toxicity of NF are believed to be caused by the release of bacterial toxins and endogenous cytokines. 12 Once in the bloodstream, the bacteria proliferate rapidly, producing toxins and abnormally high levels of enzymes that destroy tissue by breaking down protein. The toxin release can lead to septic shock and multisystem organ failure , often within a week. 17 Signs and Symptoms

The signs and symptoms of NF are very vague and can be mistaken for other conditions. A reddened, tender, swollen area of cellulitis accompanied by local pain and fever is usually the first sign of NF. 15 Early NF is very painful. The classic suspicious symptom is severe pain out of proportion to local findings . This pain may be the only clue to the diagnosis of NF in patients who have no predisposing factors. Erythema, edema, and ecchymosis are the general signs. Following these initial changes, the erythema spreads quickly over large areas. Within a few days the skin darkens to bluish purple with areas of blisters,

184

SEKERES

and bullae develop. NF should be suspected strongly once the purple bullae are identified. These bullae initially are fluid filled and eventually become hemorrhagic, often leaving the patient anemic.12 Once the bullae are present, the disease is well established in the subcutaneous space. The necrosis occurs in the superficial fascia and fat, producing a watery, thin, and often foul-smelling fluid known as "dishwater pus." Hypocalcemia is common because of extensive fat necrosis. 19 A lowgrade fever of 38°C to 38.5°C and accompanying tachycardia of often more than 120 beats per minute can be present. 18 Serious changes to the skin are delayed, but serious necrosis is occurring underneath the skin.7 Fascia! and subcutaneous fat necrosis is widespread, with relative sparing of skin and underlying muscle.12 Skin can act as a barrier for keeping pathogens out of the body but also is effective at keeping them in, allowing for the quick spread of organisms underneath the skin. 10 Distinct margins are absent, with the diseased area gradually fading into normal skin. Four or five days later, it is evident that the purplish skin is becoming gangrenous. The disease affects the subcutaneous nerves, and these areas become anesthetized. As toxins are released into the bloodstream, signs and symptoms of sepsis develop. During the second week of the disease, the skin sloughs off. This disease can be fatal if left untreated. In a few documented cases, however, untreated patients spontaneously recovered after the sloughing of necrotic skin. 12

Early diagnosis is critical to the treatment of NF. Once NF is suspected, antibiotics and surgical debridement should be started immediately. High doses of broad-spectrum antibiotics (e.g., cefazolin, clindamycin, gentamicin, penicillin, or metronidazole) have been used in NF before the invading organism is identified.16 Penicillin is the drug of choice if the identified organism is group A streptococci. In some cases, several broad-spectrum agents are prescribed at once. 18 It is crucial to initiate surgical excision as soon as NF is recognized or suspected. 7 Prompt excision of all infected or devitalized tissue is performed. It is necessary to remove necrotic tissue because any remaining tissue will continue the infection process. This could involve daily surgical debridement. In extreme cases, the extremity may have to be amputated.16 Hyperbaric oxygen therapy (HBO) can be used in conjunction with antibiotics and surgical debridement as a treatment for NF. With HBO therapy, the patient is placed in a chamber containing higher than atmospheric pressure. HBO may inhibit the formation of toxins, increase oxygenation and epithelialization, strengthen the ability of white blood cells to oppose invasive microorganisms, and promote the formation of new blood vessels. It does not destroy toxins that have already been produced. 13· 17· 18 HBO is not available in all hospital facilities. The patient must be stable to be transferred to a facility with HBO.

Diagnosis

Discussion of Case Study

NF can be surgically diagnosed by exploration, with the skin readily separating from the underlying fascia . Normally the skin is bound tightly to the fascia. 12· 15 Radiographic studies are not always helpful in making a diagnosis unless soft-tissue gas is present. CT or MR imaging can be helpful by revealing small pockets of soft-tissue gas and by establishing the extent of infection that cannot be detected by physical examination. 19 Gas is present in the majority of cases. 15 The only way of isolating the causative organism is by tissue biopsy from the border of infection. 15

As the case study illustrated, NF often is difficult to diagnose. Ms. L's clinical picture was not completely consistent with NF. It could be argued that perhaps Ms. L did not have NF but had another form of necrotizing skin infection. Many terms are used interchangeably with NF, including: Acute dermal gangrene Fournier's gangrene Hemolytic streptococcal gangrene Necrotizing cellulitis Necrotizing erysipelas Necrotizing myositis

Treatment

NECROTIZING FASCllTIS

Progressive synergistic bacterial gangrene Suppurative fasciitis Data from Shindo ML, Nalbone VP, Dougherty WR: Necrotizing

fasciitis of the face. Laryngoscope 107:1071-1079, 1997.

There are other disease processes similar to NF, such as toxic shock syndrome, progressive bacterial gangrene, and myosis. 14 When Ms. L presented to the ER the first time, she was diagnosed with cellulitis and sent home with a broad-spectrum oral antibiotic. She had Doppler studies done, and NF was not suspected. When patients do not respond well to antibiotics or if they develop intense and severe local pain, NF rather than cellulitis must be considered. 3 If NF had been suspected, a course of broad-spectrum intravenous antibiotics could have been begun immediately. In Ms. L's case, because of the delayed diagnosis, intravenous antibiotics were not started until 3 days later. The symptoms of NF, including increased leg pain, edema, and bluish-black skin discoloration of both legs, were present in Ms. L's case when she returned to the ER. She had the classic suspicious symptom of severe pain out of proportion to local findings. At this point, the broad-spectrum intravenous antibiotics ceftriaxone and vancomycin were administered immediately. Her extremities developed bullae, which are strongly suggestive of NF. 11 The rapid progression of the disease from Ms. L's ankle into her abdomen along with tissue necrosis and sloughing also were characteristic of NF. The ER nurses had to act quickly to assess Ms. L's condition. This assessment had to occur quickly and continuously because her condition was critical on admission to the ER. Her vital signs had to be stabilized. Blood specimens for immediate analysis were drawn, and multiple blood products were administered. It is difficult to determine a diagnosis of NF, but suspicions should occur because of the clinical picture. Although the literature suggests that it is crucial to initiate excision as soon as NF is identified or suspected, 13 Ms. L did not have her debridement until 2 weeks after admission. Tissue biopsy of her right knee wound was performed, but the culture showed no growth. Many organisms have been attributed to NF,9 but there is no documentation of a diagnosis of NF with no organism present. After her first surgical debridement 2 weeks

185

after admission to the hospital, the culture was positive for candida. At this time, she was not treated with an antifungal medication nor was HBO used for her treatment, although this hospital did own an HBO chamber. Ms. L spent 2 weeks in the ICU. She was diagnosed with septic shock caused by NF of the lower extremities. She was immediately started on a course of antibiotics and vasopressors for a blood pressure of 80/ 50 mm Hg. It is suggested in the literature that vasopressors should be avoided if possible because peripheral vasoconstriction will further diminish perfusion of damaged tissue17 ; however, the vasopressors were effective in maintaining her blood pressure. The ICU nurses were responsible for frequently monitoring her vital signs, hemodynamic status, and laboratory results; titrating her vasopressors; and administering blood products, total parenteral nutrition, and antibiotics. Nursing care of this patient also included frequent, astute assessment and management of her wounds. In addition to accurately assessing, describing, and documenting the appearance of the wounds,4 nurses should mark the borders of the wound, actually marking the skin to obtain objective measurements of spread.14 Because a moist healing environment generates the most rapid healing,10 Ms. L's wet-to-dry dressings were changed every 4 hours as ordered. These dressing changes must be performed with care because wet-to-dry dressings can remove healthy as well as necrotic tissue. 4 In addition to her continuous fentanyl drip, Ms. L required premedication with morphine sulfate before these painful dressing changes. ICU patients frequently are inactive and immobile because of medical conditions, surgical and diagnostic procedures, and the need to maintain various catheter lines and tubes.4 The ICU nurses applied an air-mattress overlay to Ms. L's bed and provided turning and repositioning as possible to prevent skin breakdown. Ms. L had multiple surgical procedures for debridement of her wounds, for which spinal anesthesia was administered. Care was taken to properly position the patient on the operative bed. This patient was going to be immobile in the OR while anesthetized. Bony prominences had to be padded to prevent further breakdown, and extremities had to be se-

186

SEKERES

cured with no compression of underlyling nerves.16 After surgery, the patient was transferred to the postanesthesia care unit. Because she had spinal anesthesia, care focused on padding the bony prominences because there was a block of motor and sensory function. She was repositioned at least every 2 hours to prevent breakdown. Because she was immobile, frequent coughing and deep breathing were encouraged to promote full lung

expansion to prevent atelectasis. Frequent vital signs were recorded. Hypotension can occur because of sympathetic blockade from a spinal anesthesia. 8 The treatment chosen for Ms. L did not necessarily fit all the recommended treatment as described in the literature for NF. This case report, however, shows that proper nursing interventions aided Ms. L's recovery. She beat the odds and survived her case of NF.

SUMMARY NF involves rapidly spreading inflammation with necrosis of superficial fascia , fat, and possibly muscle and epidermis. Severe systemic toxicity can be associated with NF and mortality rates can reach 74% with this so called flesh eating disease. Treatment modalities include antibiotics, surgical intervention, and other therapies such as hyperbaric oxygen. Successful treatment of NF can be facilitated with diligent nursing assessment and intervention.

REFERENCES l. Ardire L, Mrowczynski E: Necrotizing fasciitis: Case study of a nursing dilemma. Ostomy/Wound Management 43:30- 45, 1997 2. AultMJ , Geidermanj, Sokolov R: Rapid identification of group A streptococcus as the cause of necrotizing fasc iitis. Ann Emerg Med 28:227-229, 1996 3. Bisno AL, Hacker SM, Roaten SP: Today's strategies for bacterial skin infections. Patient Care 31: 78-94, 1997 4. Boynton PR, Paustian C: Wound assessment and decision-making options. Critical Care Nursing Clinics of North America 8:125-138, 1996 5. Chapnick EK, Abter EI: Necrotizing soft-tissue infections. Infect Dis Clin North Am 10:835-843, 1996 6. Deresinski SC, Khan A, Koster F, et al: Emerging infections: Beyond the media hype. Patient Care 29:29-55, 1995 7. Douglas M: Necrotizing fasciitis: A nursing perspective. J Adv Nurs 24:162-166, 1996 8. Drain C: The Post Anesthesia Care Unit, ed 3. Philadelphia, WB Saunders, 1994 9. Epps C, Brown M: Necrotizing fasciitis: A case study. Neonatal Network 16:19-25, 1997

10. Freeman Z, Rivers], VanCouwenberghe C: Necrotizing fasciitis: A cautionary tale . Am J Nurs 97:34- 36, 1997 11 . Greehan OM, Penberton LB: Management of wounds and wound infections in the intensive care unit. Critical Care Nursing Quarterly 20:69-78, 1997 12. Green RJ, Dafoe DC, Raffin TA: Necrotizing fasciitis. Chest 110:219-227, 1996 13. johns-Langford FP, Moon RE, Stolp BW, et al: Treatment of cervical necrotizing fasciitis with hyperbaric oxygen therapy. Otolaryngol Head Neck Surg 112:274-277, 1995 14. McHenry CR, Brandt CP, Piotrowski JJ, et al: Idiopathic necrotizing fasciitis: Recognition , incidence, and outcome of therapy. Am Surg 60:490-494, 1994 15. Neal M: Wound care: Necrotizing infections: Nursing Times 90:53-59, 1994 16. Nelson-Conley CL: Necrotizing fasciitis. AORN J 63:1119-1122, 1996 17. Redfield D, Hayes T: Orthopedic infections. Critical Care Nursing Quarterly 21:24-35, 1998 18. Ruth-Sahd LA, Pirrung M: The infection that eats patients alive. RN 60:28-34, 1997 19. Shindo ML, Nalbone VP, Dougherty WR: Necrotizing fasciitis of the face. Laryngoscope 107:1071-1079, 1997

Address reprint requests to Lynn A. Sekeres, MSN, RN, CCRN, CPAN 9242 Highmeadow Road Allison Park, PA 15101