Abstract
Ceftriaxone is having many uses and useful “third-generation” cephalosporin that necessitates being given every day. Ceftriaxone acts as binds to one or many of the penicillin-binding proteins which inhibit the final transpeptidoglycan step of peptidoglycan synthesis in the bacterial cell wall, thus inhibiting biosynthesis and arresting cell wall assembly resulting in bacterial cell death. Ceftriaxone-associated biliary adverse events in children less than eighteen years cause biliary pseudolithiasis and scarcely nephrolithiasis often happen in children less than eighteen years after receiving overdoses of ceftriaxone. Ceftriaxone perhaps binds with calcium and figure insoluble chelation leading to biliary pseudolithiasis. Cholelithiasis, increased biliary thickness, and pseudolithiasis rarely happen in a period of being a child, but there are two modes of distribu¬tion described by two peaks, the first being at an early stage of development and the second is a period of life when a child develops into an adult. Hyperbilirubinemia is significantly contraindicated for neonates administrated ceftriaxone, particularly premature neonates, because of the displacement of bilirubin from albumin-binding sites and increase in blood concentrations of free bilirubin. A child than one month old and a child less than twelve-month old in special are at great risk of poor results because of bilirubin encephalopathy. Coincident administrations of ceftriaxone with aminoglycosides such as gentamycin and loop diuretics (furosemide) perhaps increase the risk of nephrotoxicity (rapid degeneration in the kidney function to the toxic outcome of double or triple medications). Coincident administrations of ceftriaxone with anticoagulant medications such as warfarin are associated with bleeding due to increased prothrombin times, which is reversible with vitamin K.

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