Acute tubular necrosis primary prevention: Difference between revisions
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==Overview== | ==Overview== | ||
Effective measures for the primary prevention of acute tubular necrosis include identification of individuals who are at high risk, maintain volume status and adequate renal perfusion by proper hydration, isotonic fluid administration, monitoring urine output and serum creatinine levels regular intervals to ensure normal renal function and avoiding or decreasing dose of nephrotoxins and contrast media. | Effective measures for the primary prevention of acute tubular necrosis include identification of individuals who are at high risk and prompt treatment for underlying conditions, maintain volume status and adequate renal perfusion by proper hydration, isotonic fluid administration, monitoring urine output and serum creatinine levels regular intervals to ensure normal renal function and avoiding or decreasing dose of nephrotoxins and contrast media. | ||
==Primary Prevention== | ==Primary Prevention== | ||
*Effective measures for the primary prevention of acute tubular necrosis include: | *Effective measures for the primary prevention of acute tubular necrosis include: | ||
** Identifying individuals who are at risk for developing acute tubular necrosis. | ** Identifying individuals who are at risk for developing acute tubular necrosis. Promptly treating conditions that can lead to decreased renal perfusion and/or decreased oxygen to the [[Kidney|kidneys]] can reduce the risk of acute tubular necrosis. These include: | ||
*** Patients who are undergoing for major surgery such as cardiac or abdominal surgery | *** Patients who are undergoing for major surgery such as cardiac or abdominal surgery | ||
*** Marked hypovolemia | *** Marked hypovolemia | ||
Revision as of 17:46, 31 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
Effective measures for the primary prevention of acute tubular necrosis include identification of individuals who are at high risk and prompt treatment for underlying conditions, maintain volume status and adequate renal perfusion by proper hydration, isotonic fluid administration, monitoring urine output and serum creatinine levels regular intervals to ensure normal renal function and avoiding or decreasing dose of nephrotoxins and contrast media.
Primary Prevention
- Effective measures for the primary prevention of acute tubular necrosis include:
- Identifying individuals who are at risk for developing acute tubular necrosis. Promptly treating conditions that can lead to decreased renal perfusion and/or decreased oxygen to the kidneys can reduce the risk of acute tubular necrosis. These include:
- Patients who are undergoing for major surgery such as cardiac or abdominal surgery
- Marked hypovolemia
- Severe hypotension
- Acute pancreatitis
- shock and sepsis
- Chronic renal disease
- Critically ill and hospitalized individuals
- Diabetes mellitus
- Monitor serum creatinine and urine output regularly in high-risk individuals.
- Avoiding or decreasing daily dose of nephrotoxins[1]
- Maintain volume status to ensure adequate renal blood flow by proper hydration or isotonic fluid administration.
- Contrast media-induced acute tubular necrosis may be prevented with administration of isotonic saline along with radiocontrast substance.[2]
- Identifying individuals who are at risk for developing acute tubular necrosis. Promptly treating conditions that can lead to decreased renal perfusion and/or decreased oxygen to the kidneys can reduce the risk of acute tubular necrosis. These include:
References
- ↑ Pazhayattil GS, Shirali AC (2014). "Drug-induced impairment of renal function". Int J Nephrol Renovasc Dis. 7: 457–68. doi:10.2147/IJNRD.S39747. PMC 4270362. PMID 25540591.
- ↑ Mueller C, Buerkle G, Buettner HJ, Petersen J, Perruchoud AP, Eriksson U, Marsch S, Roskamm H (February 2002). "Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty". Arch. Intern. Med. 162 (3): 329–36. PMID 11822926.