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• W3189346738 abstract "To the Editor: Vancomycin, a glycopeptide antibiotic, is commonly used in the practice of orthopedic surgery for the treatment of bone and joint infections, such as osteomyelitis and septic arthritis.1 It is the first-line drug for the management of methicillin-resistant Staphylococcus aureus and other gram-positive bacteria.1 However, it associated with adverse effects, including nephrotoxicity, phlebitis, hypersensitivity, tachycardia, and hypotension. Antibiotic-induced hypokalemia is a rare yet established complication of penicillin, amphotericin B, and aminoglycosides, particularly when combined or administered to patients with renal insufficiency.1 On the contrary, vancomycin-induced hypokalemia had been only reported in a few previous studies.2–4 we present an extremely rare phenomena of vancomycin-induced refractory hypokalemia in a pediatric patient with no other hypokalemia-related risk factors. A 12-year-old boy presented to our emergency department complaining of right knee swelling and pain. The pain was severe, insidious, nontraumatic, with no radiation, or diurnal variation. It was severe enough to restrain his ability to walk. The radiography demonstrated no bony injury. Initial laboratory evaluation showed an elevated C-reactive protein (211.7 mg/L; normal [NL], <5 mg/L), elevated erythrocyte sedimentation rate (118 mm/h; NL, 0–5 mm/h), high-normal white blood cell counts (8500/mm3; NL, 3500–11,000/mm3), normal serum creatinine (0.13 mg/dL), and normal serum electrolytes both potassium (4.4 mmol/L) and sodium (140 mmol/L), and he was diagnosed to have septic arthritis. Next morning, he underwent right knee debridement and started on empirical intravenous vancomycin. Over the next few days, vancomycin was tittered to 400 mg every 6 hours aiming to achieve a serum trough level of 15 to 20 μg/mL. Nine days later, he developed hypokalemia (2.8 mmol/L) but normal creatinine level. Intravenous potassium chloride 3 mEq was added to his maintenance intravenous fluid for 2 days. The serum potassium level was elevated to 3.3 mmol/L, which was slightly below the reference range, and he was maintained on the same vancomycin dose. One week after the initial correction, his serum potassium dropped again to 2.9 mmol/L, but the serum vancomycin level was within the therapeutic range and normal creatinine level. Once again, potassium correction was initiated. On the 21st day of the treatment, the intravenous vancomycin regimen was suspended, and the patient was discharged on oral cefuroxime for 2 weeks. One week after the suspension of vancomycin, the potassium levels were normalized (4.3 mmol/L) and remained stable thereafter (Fig. 1).FIGURE 1: Illustration of the changes in the potassium level over the treatment period.Vancomycin-related nephrotoxicity is uncommon and usually results in mild to moderate reversible damage. This toxic effect is more prominent in older patients, longer duration of therapy, and/or therapy with concomitant nephrotoxic agents. Children, on the other hand, tolerate vancomycin much better than older patients, because of infrequent baseline chronic diseases, lower possibility of concomitant nephrotoxic agent therapy, and intact renal function. Vancomycin-induced nephrotoxicity is generally due to either acute tubular necrosis or acute interstitial nephritis. The main factors responsible for the toxic effect include altered mitochondrial function and production of reactive oxygen species, especially in the proximal tubules.5 The first report to document vancomycin-induced hypokalemia was described by Siau,2 in which the patient developed hypokalemia-induced cardiac arrest in concomitant use of furosemide and vancomycin. They stated that the potassium depletion exacerbated by the addition of vancomycin.2 Another report described by Driemeyer et al,3 in which an elderly patient with no risk factors for hypokalemia developed vancomycin-induced hypokalemia. They described a strong temporal association between the use of vancomycin and the incidence of hypokalemia.3 In the previous cases, the patients were elderly with several comorbidities and polypharmacy. The clear association between the use of vancomycin and the depletion of potassium could not be ascertained, and it might be the result of concomitant drug use or drug-drug interactions. On the contrary, our patient was young with no chronic diseases, used no medicines, and maintained normal kidney function throughout the course of vancomycin therapy. In our case, we can correlate the incidence of hypokalemia solely to the use of vancomycin. This is further supported by the resolution of the hypokalemia several days after the suspension of vancomycin, and we agree with the proposed mechanism of potassium depletion through renal loss. In conclusion, vancomycin must be considered as a potential cause of reversal hypokalemia even if used as a monotherapy or in the absence of other hypokalemia risk factors. Potassium supplementation can partially correct the hypokalemia, whereas complete resolution can only be achieved with vancomycin suspension. Therefore, electrolytes monitoring during the course vancomycin therapy is recommended even in patients with no other risk factors. Mohammad A. Shahin, MDBaraa Mafrachi, MD School of Medicine, The University of Jordan Amman, JordanYazan Hammad, MD, MRCSI Division of Orthopaedics, Department of Special Surgery School of Medicine, The University of Jordan Amman, Jordan [email protected]Bassem I. Haddad, MDAbdel Rahman Mohammad Abuawad, MD Division of Orthopaedics, Department of Special Surgery School of Medicine, The University of Jordan Amman, JordanOsama Hussein El Khatib, MD Department of Internal Medicine, School of Medicine The University of Jordan Amman, Jordan" @default.
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• W3189346738 date "2021-08-02" @default.
• W3189346738 modified "2023-09-26" @default.
• W3189346738 title "Vancomycin-Induced Refractory Hypokalemia in a Pediatric Patient" @default.
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