A 32-year-old previously healthy man presents with fevers and hypotension. He was bitten by a dog 4 days ago with deep puncture wounds that required operative closure. He has a history of anaphylaxis to penicillin and cephalosporins and has been receiving trimethoprim-sulfamethoxazole since surgery. Tetanus toxoid was administered and his other immunizations are up to date. On examination, his wound shows evidence of cellulitis.
Which of the following changes to his antibiotic regimen is most appropriate?
Correct Answer: C
Prophylactic antibiotics are not typically required after animal bites. However, they reduce the rate of infection of high-risk bites:
Amoxicillin-clavulanate for 3 to 5 days is the preferred prophylactic agent. Alternatives in patients with cephalosporin allergies should have activity against both Pasteurella multocida (ie, trimethoprim-sulfamethoxazole, doxycycline, levofloxacin) and anaerobes (clindamycin, metronidazole). Thus, this patient has untreated anaerobic infection and would benefit from the addition of clindamycin. Changing to levofloxacin or adding vancomycin would not give the appropriate coverage. Tetanus toxoid should also be administered to all patients who have completed primary immunization but who’s booster has been 5 years of greater.
Reference:
A 20-year-old female college student presents with fever and a painful left knee for the last 3 days. She denies any recent trauma and was treated last week for a urinary tract infection. Her vital signs are T 38.8°C, HR 112 beats/min, RR 24 breaths/min, BP 78/42 mm Hg, and O2 saturation 98% on RA. Physical examination reveals a swollen and erythematous knee with decreased range of motion. Joint aspiration demonstrates white blood cell (WBC) 20,000, with 80% neutrophils and calcium pyrophosphate crystals, and no organism are seen on gram stain. In addition to fluid administration, which of the following interventions is most appropriate?
Correct Answer: B
In patients who present with an acutely painful and swollen joint, prompt identification and treatment of septic arthritis can substantially reduce morbidity and mortality. An associated skin, urinary tract, or respiratory infection should provide insight to the likely pathogen. Definitive diagnosis is established by identification of bacteria in the synovial fluid. Gram stain is positive in many cases, but the absence of bacteria on initial gram stain should be considered conclusive evidence of the absence of infection. Empiric IV antibiotic therapy should be administered while awaiting culture results. Antibiotic therapy should cover (1) methicillin-resistant Staphylococcus aureus (which can be treated with vancomycin) and (2) gram-negative organisms such as Klebsiella pneumoniae and Neisseria gonorrhoeae (which are typically treated with ceftriaxone or thirdgeneration cephalosporin). In addition to antibiotic therapy, patients with septic arthritis should have orthopedic evaluation for irrigation and debridement. Septic arthritis can cause the release of calcium pyrophosphate crystals from cartilage, so the finding of such crystals does not rule out infection. Intra-articular steroids or indomethacin would relieve acute joint inflammation but would not treat the underlying infection nor be immediately appropriate treatment.
References:
A 55-year-old male with non–insulin-dependent diabetes mellitus presents with lower leg swelling and severe pain. He fell while gardening yesterday and has a laceration on his heel. On examination has a fever of 39.4°C and is mildly confused. He has erythema, edema, and crepitus up to the midcalf. Notable laboratory values are a WBC count of 22,000 cells/mm2 and lactate 3.9.
What is the most appropriate next step in treatment?
Necrotizing fasciitis (NF) is a bacterial infection characterized by friability of the superficial fascia, dishwater-gray exudate, and a notable absence of pus. It can occur after major traumatic injuries, as well as after minor breaches of the skin or mucosa or nonpenetrating soft-tissue injuries (eg, muscle strain or contusion). It is more common in immunocompromised patients. Necrotizing infections can result in widespread tissue destruction, which may extend from the epidermis to the deep musculature.
Clinical manifestations of NF include soft-tissue edema, erythema, severe pain and tenderness, fever, and skin bullae or necrosis. Factors that can differentiate NF from cellulitis include pain out of proportion to clinical signs, hypotension, and shock. Patients who are immunosuppressed may present without these typical findings.
NF can be subdivided into three types based on the pathogenic organisms involved:
For patients with aggressive soft-tissue infection, prompt surgical exploration is essential to determine the extent of infection, to assess the need for debridement, and to obtain specimens for gram staining and culture. No single clinical laboratory test or group of tests can adequately replace surgical inspection for diagnosis of these infections. In addition to prompt surgical intervention, appropriate antibiotic treatment and supportive care are essential to reduce morbidity and mortality.
The benefits of hyperbaric oxygen therapy for treatment of NF remain controversial. Surgical debridement should not be delayed in order to pursue hyperbaric oxygen treatment. The rationale for using IVIG in patients with NF is based on its ability to neutralize extracellular toxins that mediate pathogenesis. Clinical studies supporting its efficacy have had serious limitations, and a consensus supporting its use has not been reached.
Efforts to inhibit bacterial superantigens involved in the pathogenesis of necrotizing infections are ongoing but have not shown clinical success to date.
A 28-year-old woman is admitted to the ICU with septic shock due to a soft-tissue infection. Three days prior to admission, she fell while riding her bicycle and sustained lacerations to her legs which she self-treated. Within the ICU, she undergoes fluid resuscitation, receives vasopressor support and broad-spectrum antibiotics, and is taken for surgical debridement. Tissue and blood cultures grow Streptococcus pyogenes and antibiotics are narrowed to penicillin and clindamycin. Two days later, she remains febrile, and vasopressor dependent, has a generalized rash, develops acute kidney injury requiring renal replacement therapy as well as elevated transaminases and jaundice. Sensitivity testing shows no antimicrobial resistance and no further organisms.
Which of the following interventions is MOST likely to be beneficial for treatment of this patient?
Correct Answer: A
Group A Streptococcus (S. pyogenes) can produce exotoxins and superantigens that lead to streptococcal toxic shock syndrome characterized by rapidly progressive soft-tissue destruction, shock, and multiple organ failure. Although there is mixed evidence, several studies show benefit of IVIG in cases of streptococcal toxic shock syndrome. IVIG may raise antibody levels by passive immunity in the setting of overwhelming infection. It may contribute neutralizing antibodies against streptococcal exotoxins—however these may differ by specific manufacturer preparations. Hyperbaric oxygen has been studied to varying effect in necrotizing infection, but there is no indication that it would have any direct benefit in this patient. Clinical trials have not demonstrated a benefit of anti-TNF antibody administration in patients with septic shock. There is no role for changing antibiotic regimen in this patient with pansusceptible S. pyogenes, and no polymicrobial infection.
A 61-year-old man presented with fever, malaise, and a blistering red rash 5 days after undergoing a laparoscopic cholecystectomy. Per report, the rash started at his port insertion sites but has progressed and now involves his face, trunk, and extremities. His medical history includes end-stage renal disease on intermittent hemodialysis, hypertension, and diabetes mellitus. Vital signs are T 38.7°C, HR 76 beats/min, BP 150/80 mm Hg, RR 26 breaths/min, and oxygen saturation of 97% on room air. Examination reveals red, blistering, tender skin, warm-to-touch and peels with gentle stroking. The rash is accentuated in the flexor creases. Perioral crusting is present but mucous membranes are spared.
What is the MOST likely etiology of this condition?
The patient’s presentation is consistent with staphylococcal scalded skin syndrome (SSSS). SSSS is a localized S. aureus infection that produces exfoliative exotoxins (exfoliatin). These cause the breakdown of desmosomes and detachment of the epidermal layer. Skin biopsy shows separation within the superficial layer of the epidermis—in contrast to toxic epidermal necrolysis (TEN) which has skin separation at the dermoepidermal junction. SSSS is a disease usually seen in infancy but may appear in older, immunosuppressed patients with renal failure (as the toxins are cleared renally). The skin typically appears burnt, with fluid-filled bullae that easily rupture, with exfoliation of the epidermis under gentle pressure (positive Nikolsky sign). The rash often begins centrally, is sandpaper-like, progressing into a wrinkled appearance, and accentuated in flexor creases. Accompanying signs and symptoms include fever, tenderness and warmth to palpation, facial edema, conjunctivitis, and perioral crusting, but mucous membranes are spared. Dehydration may be present and significant.
Antibiotic treatment depends on whether the isolated pathogen is methicillin-resistant. Supportive treatment includes IV hydration to replace fluid losses, and aggressive skin care with petroleum jelly or similar agent to maintain moisture. A systemic infection with circulating endotoxins is characteristic of bacteremia and sepsis. Drug-induced keratinocyte necrosis is typical of toxic epidermal necrolysis and is noninfectious. Fascial bacterial infection alone would not cause the characteristic skin blistering described here.
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