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Zorluk: ZorInfectious Diseases

A 32-year-old man is admitted to the hospital with a 1-week history of fever, chills, and profound fatigue. He has a history of intravenous drug use and was treated for a skin abscess two months ago. His temperature is 38.8°C (101.8°F), blood pressure is 110/70 mm Hg, and pulse is 108/min. Physical examination reveals a new grade 3/6 holosystolic murmur best heard at the cardiac apex. Transesophageal echocardiography demonstrates a 1.2-cm mobile vegetation on the mitral valve. Three sets of blood cultures obtained on admission grow *Enterococcus faecalis* that is susceptible to ampicillin, vancomycin, gentamicin, and linezolid. The patient is initiated on continuous intravenous ampicillin and every-8-hour intravenous gentamicin. Over the next 48 hours, his clinical symptoms improve and his temperature decreases to 37.9°C (100.2°F). However, laboratory studies show his serum creatinine has increased from 0.8 mg/dL on admission to 2.5 mg/dL, and his urine output has been 350 mL over the past 24 hours. Which of the following is the most appropriate modification to this patient's antimicrobial regimen?

  1. Discontinue gentamicin and add intravenous ceftriaxoneCevap
  2. B
    Discontinue gentamicin and continue ampicillin monotherapy
  3. C
    Discontinue the current regimen and initiate intravenous vancomycin
  4. D
    Discontinue the current regimen and initiate intravenous linezolid
  5. E
    Continue the current regimen and adjust the gentamicin dose based on serum trough levels

Cevap

Discontinue gentamicin and add intravenous ceftriaxone
The most appropriate modification to this patient's regimen is to discontinue gentamicin and add intravenous ceftriaxone. This patient has *Enterococcus faecalis* infective endocarditis and has developed severe acute kidney injury (AKI) secondary to gentamicin toxicity. Enterococci are intrinsically tolerant to the bactericidal effects of cell-wall active agents (like penicillins) when used alone. To achieve the bactericidal activity required to cure endocarditis, synergistic combination therapy is necessary. The standard first-line regimens are ampicillin plus an aminoglycoside (e.g., gentamicin) or ampicillin plus ceftriaxone. Although ceftriaxone has no clinically significant activity against enterococci on its own, it saturates specific penicillin-binding proteins (PBPs, primarily PBP 2 and 3), which works synergistically with ampicillin (which binds PBP 4) to provide bactericidal activity. Because the ampicillin plus ceftriaxone regimen is equally effective as ampicillin plus gentamicin but entirely avoids aminoglycoside-associated nephrotoxicity, it is the treatment of choice for *E. faecalis* endocarditis in patients who develop AKI during therapy or those with preexisting renal dysfunction.

Adım Adım Çözüm

1
Identify the patient's primary diagnosis and current clinical status.
The patient has Enterococcus faecalis infective endocarditis and has developed oliguric acute kidney injury (AKI) while receiving ampicillin and gentamicin.
Establishing the current complication is necessary to determine the appropriate next step in management.
2
Evaluate the current antimicrobial regimen's role in the patient's complication.
Gentamicin is a well-known nephrotoxic agent and is the most likely cause of the acute kidney injury.
Identifying the offending agent allows for targeted modification of the regimen.
3
Determine the optimal alternative therapy that maintains efficacy while avoiding further toxicity.
Substituting ceftriaxone for gentamicin provides the necessary bactericidal synergy against E. faecalis without causing further nephrotoxicity.
Endocarditis requires bactericidal therapy, and the ampicillin-ceftriaxone combination achieves this synergy through complementary binding of penicillin-binding proteins.

Anahtar Kavram

Management of Enterococcus faecalis infective endocarditis in the setting of aminoglycoside-induced acute kidney injury.
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Infectious Diseases

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