Acute Kidney Injury Case Study
1. AKI can be prerenal, intrarenal, and postrenal. Prerenal is a decrease in blood flow to the kidneys and this leads to a decrease in glomerulus perfusion and filtration. During prerenal, Azotemia occurs and is the accumulation of nitrogenous waste in the blood. This results in a reduction in sodium excretion, increased sodium and water retention, and decreased urine output. Intrarenal has direct damage to the kidney. Nephrotoxins can cause structures to crystallize and cause damage to the cells, also hemoglobin and myoglobin can block the tubules. Acute tubular necrosis is the main cause and this is when ischemia disrupts the basement membrane and causes patchy destruction. Postrenal there is a mechanical obstruction to the flow of urine. Prolonged obstruction can cause tubular atrophy and irreversible kidney fibrosis. 2. a. The first stage is the oliguric stage. During this stage, there are urinary changes were there is a reduction in the urinary output to less than 400ml/day, this is called oliguria. This occurs within 1 to 7 days after an injury to the kidneys and can last up to 10 to 14 days. Also, during the oliguric stage there is hypovolemia, which can be corrected by fluid replacement or hypervolemia with the symptoms of edema, bounding pulse, and neck veins distention. The kidneys can’t synthesize ammonia and this causes metabolic acidosis. During this stage, Sodium decreases (hyponatremia) and potassium increases (hyperkalemia). Hematologic disorders and neurologic disorders may occur. b. The second stage is the diuretic phase. During this stage, the patient will have 1 to 3 L fluids caused by osmotic diuresis from high urea concentration. Due to large fluids being loss in this stage monitor for hyponatremia, hypokalemia, and dehydration. This phase can last up to 3 weeks. c. The last stage is the recovery phase. This phase begins when the GFR increases, causing the BUN and creatinine to plateau and then decrease. This may take up to 12 months for kidney function to stabilize. 3. Oliguria is when a patient has a urine output of less than 400ml/day. It is mainly seen prerenal causes, such as hypovolemia, decreased cardiac output, decreased vascular resistance, and decreased renovascular blood flow. Nonoliguria is when there is a urine output greater than 400ml/day. It is mainly seen with interstitial nephritis and acute tubular necrosis. Both oliguria and nonoliguria will be seen in the oliguric phase of acute kidney failure. 4. …show more content…
Initially, the elevated creatinine and BUN lab values show that she may have ARF. In addition to the lab values, she had a history of congestive heart failure, which is a common cause of prerenal heart failure. Also, she had signs of being in the oliguric stage, such as her nonoliguric output of 510ml/day, her pitting edema, jugular vein distension, crackles bilaterally in the lungs, and changes in potassium (causing longer prolonged QRS and peaked T waves). After her diagnosis, she began to improve because she was in the recovery phase of ARF, where the BUN and creatinine levels begin to fall and CAVHD was no longer needed. 5. A cause of bowel perforation is abdominal surgery, which she had received. Due to the elevated WBC, I believe the bowel perforation resulted in an infection and the doctor proscribed gentamicin sulfate (Garamycin) and piperacillin sodium (pipracil) to treat the infection. Gentamicin however, is a nephrotoxin. 6. …show more content…
Risk factors for nephrotoxicity: comorbidities, volume depletion, liver dysfunction, sepsis, renal dysfunction, hypokalemia, hypomagnesemia, and advanced age ii. Prevention: prevent the accumulation of aminoglycosides in the kidney, lower dosage, and alternative medication
b. Amphotericin B – antifungal
i. Risk factors for nephrotoxicity: therapy with other nephrotoxins and higher dose of amphotericin B ii. Prevention: lower dosages and alternative medication
c. NSAIDs- anti-inflammatory
i. Risk factors for nephrotoxicity: advanced age, liver issues, higher dose of NSAID, and cardiovascular disease ii. Prevention: alternative medication and lower dosages of medication
7. Dopamine is used to improve blood flow and treat symptoms of shock. It could have been prescribed because she was continuously deteriorating and dopamine would help to increase the blood flow to the kidneys and help if she started to go into shock.
8.
a. Diuretics can be given if there is a decrease in urine output, because low urine output is accompanied by fluid retention. The diuretic will remove the fluid that the patient is
1. AKI can be prerenal, intrarenal, and postrenal. Prerenal is a decrease in blood flow to the kidneys and this leads to a decrease in glomerulus perfusion and filtration. During prerenal, Azotemia occurs and is the accumulation of nitrogenous waste in the blood. This results in a reduction in sodium excretion, increased sodium and water retention, and decreased urine output. Intrarenal has direct damage to the kidney. Nephrotoxins can cause structures to crystallize and cause damage to the cells, also hemoglobin and myoglobin can block the tubules. Acute tubular necrosis is the main cause and this is when ischemia disrupts the basement membrane and causes patchy destruction. Postrenal there is a mechanical obstruction to the flow of urine. Prolonged obstruction can cause tubular atrophy and irreversible kidney fibrosis. 2. a. The first stage is the oliguric stage. During this stage, there are urinary changes were there is a reduction in the urinary output to less than 400ml/day, this is called oliguria. This occurs within 1 to 7 days after an injury to the kidneys and can last up to 10 to 14 days. Also, during the oliguric stage there is hypovolemia, which can be corrected by fluid replacement or hypervolemia with the symptoms of edema, bounding pulse, and neck veins distention. The kidneys can’t synthesize ammonia and this causes metabolic acidosis. During this stage, Sodium decreases (hyponatremia) and potassium increases (hyperkalemia). Hematologic disorders and neurologic disorders may occur. b. The second stage is the diuretic phase. During this stage, the patient will have 1 to 3 L fluids caused by osmotic diuresis from high urea concentration. Due to large fluids being loss in this stage monitor for hyponatremia, hypokalemia, and dehydration. This phase can last up to 3 weeks. c. The last stage is the recovery phase. This phase begins when the GFR increases, causing the BUN and creatinine to plateau and then decrease. This may take up to 12 months for kidney function to stabilize. 3. Oliguria is when a patient has a urine output of less than 400ml/day. It is mainly seen prerenal causes, such as hypovolemia, decreased cardiac output, decreased vascular resistance, and decreased renovascular blood flow. Nonoliguria is when there is a urine output greater than 400ml/day. It is mainly seen with interstitial nephritis and acute tubular necrosis. Both oliguria and nonoliguria will be seen in the oliguric phase of acute kidney failure. 4. …show more content…
Initially, the elevated creatinine and BUN lab values show that she may have ARF. In addition to the lab values, she had a history of congestive heart failure, which is a common cause of prerenal heart failure. Also, she had signs of being in the oliguric stage, such as her nonoliguric output of 510ml/day, her pitting edema, jugular vein distension, crackles bilaterally in the lungs, and changes in potassium (causing longer prolonged QRS and peaked T waves). After her diagnosis, she began to improve because she was in the recovery phase of ARF, where the BUN and creatinine levels begin to fall and CAVHD was no longer needed. 5. A cause of bowel perforation is abdominal surgery, which she had received. Due to the elevated WBC, I believe the bowel perforation resulted in an infection and the doctor proscribed gentamicin sulfate (Garamycin) and piperacillin sodium (pipracil) to treat the infection. Gentamicin however, is a nephrotoxin. 6. …show more content…
Risk factors for nephrotoxicity: comorbidities, volume depletion, liver dysfunction, sepsis, renal dysfunction, hypokalemia, hypomagnesemia, and advanced age ii. Prevention: prevent the accumulation of aminoglycosides in the kidney, lower dosage, and alternative medication
b. Amphotericin B – antifungal
i. Risk factors for nephrotoxicity: therapy with other nephrotoxins and higher dose of amphotericin B ii. Prevention: lower dosages and alternative medication
c. NSAIDs- anti-inflammatory
i. Risk factors for nephrotoxicity: advanced age, liver issues, higher dose of NSAID, and cardiovascular disease ii. Prevention: alternative medication and lower dosages of medication
7. Dopamine is used to improve blood flow and treat symptoms of shock. It could have been prescribed because she was continuously deteriorating and dopamine would help to increase the blood flow to the kidneys and help if she started to go into shock.
8.
a. Diuretics can be given if there is a decrease in urine output, because low urine output is accompanied by fluid retention. The diuretic will remove the fluid that the patient is