Vulvar infection and sepsis in a 42-year-old woman

L. Chesney Thompson

History of present illness

A 42-year-old gravida 2, para 2 woman presented to the emergency department with a history of several days of labial swelling and tenderness. She notes the discomfort was getting worse, which prompted her to seek medical care. She states her symptoms started from an “ingrown hair”after shaving. She does not describe any discharge or drainage. She thinks she may have a fever.

She is married and monogamous with no history of sexually transmitted infections. Her only surgery was a tubal ligation. She has type 1 diabetes and is on insulin therapy. She says her endocrinologist describes her control as“fair.”

Physical examination

General appearance: Overweight woman appearing fatigued and lethargic

Vital signs:

Temperature: 37.7°C Pulse: 90 beats/min

Blood pressure: 120/80 mmHg Respiratory rate: 18 breaths/min BMI: 38.1 kg/m2

Chest: Clear to auscultation bilaterally Cardiovascular: Regular rate and rhythm

Abdomen: Soft, obese, with normal bowel sounds and no tenderness

Pelvic:

Right labia with a swollen area measuring 6 × 10 cm with mild erythema extending 10 cm to the mons with moderate tenderness to palpation. There appears to be generalized edema and induration without any discrete mass or pointing abscess. There is no inguinal

adenopathy

Bimanual examination: Unremarkable. A marker was used to outline the erythema borders

Laboratory studies:

WBCs: 15 000/àL (normal 3500–12 500/àL), 75%

neutrophils

Glucose: 185 mg/dL (normal<135 mg/dL) CRP: 150 mg/L

The patient was presumed to have a vulvar cellulitis. She was admitted to the hospital given her poorly controlled diabetes

and concerns for developing sepsis, and started on intravenous cefazolin. After 12 hours the patient required more narcotic pain medications for labial discomfort. Despite antibiotics, the erythema became more progressive and extended beyond the original inked boundary markings from her earlier examin- ation onto the mons pubis. The patient noted marked tender- ness with palpation and there was evidence of epithelial separation with bullae formation (Fig. 17.1).

Vital signs 12 hours after admission:

Temperature: 39.4°C Pulse: 100 beats/min

Blood pressure: 110/60 mmHg Respiratory rate: 22 breaths/min

How would you manage this patient?

The patient was diagnosed with necrotizing fasciitis. She was taken to the operating room for examination under anesthesia and debridement. The bullae was aspirated and the contents were sent for culture and gram stain. The subcutaneous tissue was incised, and the fascial layers were easily separated with blunt manipulation. There was a lack of bleeding consistent with tissue necrosis. The tissue was dissected further to the

Acute Care and Emergency Gynecology, ed. David Chelmow, Christine R. Isaacs and Ashley Carroll. Published by Cambridge University Press.

© Cambridge University Press 2015.

Fig. 17.1 Expanding erythema and bullae formation.

abdominal wall and lateral to the thighs until the bleeding and viable tissue was identified, and the underlying muscle layer appeared healthy and uninfected (Figs 17.2&17.3). The tissue removed was submitted for histologic evaluation. Antibiotic therapy was expanded to ampicillin, gentamycin, and clinda- mycin. The patient was recovered in the ICU with aggressive fluid resuscitation and blood glucose management. The tissue pathology revealed inflammation with necrosis and a perivas- cular inflammatory infiltrates, which was consistent with the diagnosis of necrotizing fasciitis. The gram stain and culture revealed beta-hemolytic streptococci and Staphylococcus aur- eus. The patient required additional debridement in the oper- ating room on postoperative day 2 and responded to continued parenteral antibiotics and supportive care. She ultimately had a skin graft performed and recovered fully after a three-week hospital stay.

Necrotizing fasciitis

Necrotizing fasciitis is a soft tissue infection of the subcutane- ous fat and fascia overlying the muscle layer. The blood supply to this area is sparse, which limits defense against infection.

There are approximately 600–1200 cases of necrotizing fasciitis a year in the United States and they can involve any part of the body [1]. Morbidity and mortality are significant and dramatically increased with delay of initiating therapy.

Recognized predisposing risk factors include diabetes, immune-compromised status, obesity, recent trauma or sur- gery, intravenous drug use, kidney disease, and peripheral artery disease.

The infection is generally an opportunistic process facili- tated by diminished immunity and a breach of the integument.

The inciting event can be surgery or minor trauma such as scratches or insect bites. There are two types, depending on the organisms involved. Polymicrobial infections are classified as type I, and infections caused by group A streptococcus or other beta-hemolytic streptococci are classified as type II. Type I infections may commonly include anaerobic species such as Clostridia, Bacteroides, or Peptostreptococcus. Additional bacterial species such as Escherichia coli, Enterococcus, and Staphylococcusmay be involved. For this reason broad spec- trum antibiotics are best utilized. Methicillin-resistantStaphy- loccus aureus(MRSA) should also be considered, particularly when an abscess and purulent drainage is present.

A necrotizing fasciitis infection may spread over several days or progress more quickly, making the clinical presenta- tion either indolent or rapid. Because the infection resides under the skin, the appearance of skin manifestations may lag behind the subcutaneous infection and destruction. The patient may initially have more pain and tenderness than expected based on visiblefindings. Initial erythema and cellu- litis can be followed by more profound breakdown and necro- sis of the skin with bullae formation. Nerve destruction may cause the affected area to become less tender and painful as the process evolves. Crepitus may be present if a gas-producing Clostridiaspecies is involved.

As in our case, there may be little signs of sepsis early in the disease process. With progression, fever, tachycardia, and hypotension can develop. Necrotizing fasciitis should be sus- pected if cellulitis persists despite appropriate antibiotics.

Fig. 17.2 Surgical debridement showing dissection of infected tissue and

healthy underlying muscle. Fig. 17.3 Postoperative healing wound showing extent of dissection.

Diagnostic evaluation should be primarily driven by history and physicalfindings in the context of risk factors, and may be augmented by laboratory testing. It is particularly important to suspect the diagnosis if vital signs begin to suggest systemic inflammatory response syndrome (SIRS) or sepsis. The white blood cell count is typically elevated and includes a left shift.

C-reactive protein (CRP) is typically elevated. Creatinine kinase (CK) may be elevated particularly with muscle involve- ment (myonecrosis). Blood cultures are generally positive, but typically, results are not available when initial management decisions must be made. Wound culture and gram stain can be helpful for antibiotic management but are not available for initial management decisions. Recommendations for radiog- raphy using CT or MRI imaging have been suggested and may help establish the extent of the process, including whether there is muscle involvement or the presence of gas or an abscess. There is little evidence, however, to support its routine use, and patient management should not be significantly changed or delayed based on radiologic testing.

Initiating the treatment as early as possible is critical to the patient’s survival, and morbidity and mortality increase with delayed intervention. The laboratory risk indicator for necro- tizing fasciitis (LRINEC) assessment tool attempts to discern necrotizing fasciitis from less aggressive soft tissue infections [2,3]. A score is generated based on laboratory tests and vital signs. Based on a cutoffvalue, those at risk are candidates for more aggressive management including diagnostic imaging (if not previously utilized) or surgery. Another proposed pre- operative measure to direct possible surgical intervention is needle aspiration of the leading edges of the infection with gram stain. If the gram stain is positive for organisms, surgery should be considered. An alternative is to make a small inci- sion with local anesthesia and to use afinger to assess the lack of resistance to blunt dissection, degree of bleeding, and the appearance of “dishwater” pus. Recommendations have also been made to collect a biopsy for frozen section during this exam. Some clinicians feel the diagnosis is grossly apparent if all thesefindings are present, limiting the need for microscopic diagnosis. Most frequently, the diagnosis and decision to inter- vene are based on clinical suspicion.

Unfortunately, there are no well-designed studies and consequently no standardized protocols for the management of necrotizing fasciitis. Aggressive management is necessary.

Surgical debridement is the mainstay of therapy. While broad

spectrum antibiotics are essential, they will not be curative alone. Mortality rates approach 100% without surgery. Aggres- sive surgical and antibiotic therapy significantly reduces mor- bidity and mortality. Fluid resuscitation and hemodynamic support are also necessary. The goal of surgical therapy is to remove all of the infected, devitalized tissue until healthy viable tissue is reached. The area of debridement may be quite exten- sive, as in our case. Tissue should be sent for histology as well as gram stain, and cultures should be obtained from the wound. Antibiotics must provide broad spectrum coverage of gram-positive and negative bacteria as well as anaerobic organisms. A reasonable regimen would include penicillin for gram-positive organisms, gentamycin or a quinolone for gram-negative bacteria, and clindamycin for anaerobic cover- age. Surgical debridement should be repeated as needed until the wound appears healthy with granulation tissue. Antibiotics may be withdrawn after the infection appears resolved. Small studies of intravenous gamma-globulin (IVIG) have not con- sistently demonstrated benefit. IVIG may be appropriate in cases involving streptococcal toxic shock. Hyperbaric oxygen therapy has received attention and support, but consistent evidence to promote its use is lacking. Management of these extremely sick patients requires interdisciplinary teams of surgeons with training in extensive debridement and skin grafting, and critical care specialists.

Key teaching points

A high index of suspicion is key to early diagnosis of necrotizing fasciitis.

Risk factors for necrotizing fasciitis include diabetes, immune compromise, obesity, recent trauma or surgery, intravenous drug use, kidney disease, and peripheral artery disease.

Signs of necrotizing fasciitis may include: pain disproportionate to examinationfindings, deep tissue induration beyond the margins of skin involvement, painless or anesthetic areas, bullae or skin necrosis, crepitus, orfindings of systemic inflammatory response syndrome (SIRS) or sepsis.

Aggressive surgical debridement is essential to recovery and survival.

Treatment requires broad spectrum antibiotics and aggressive management of medical comorbidities.

References

1. Trent JT, Kirsner RS. Diagnosing necrotizing fasciitis.Adv Skin Wound Care2002;15:135–8.

2. Wong Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (laboratory

risk indicator for necrotizing fasciitis) score: A tool for distinguishing necrotizing fasciitis from other soft tissues infections.Crit Care Med 2004;32:1535–42.

3. Barie PS. The laboratory risk indicator for necrotizing fasciitis (LRINEC) score: Useful tool or paralysis by analysis?Crit Care Med2004;32:

1618–19.

Case 17: Vulvar infection and sepsis in a 42-year-old woman