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Acute Kidney Injury - Outline

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Generalist Nursing Practice IV: Tertiary Care Across the Lifespan (NURS 4889)

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Temple University

Academic year: 2019/2020

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Acute Kidney Injury: - Acute kidney injury (AKI), previously known as acute kidney failure, is the term used to encompass the entire range of the syndrome, including a very slight deterioration in kidney function to severe impairment. - AKI is characterized by a rapid loss of kidney function. This loss is accompanied by a rise in serum creatinine level and/or a reduction in urine output. The severity of dysfunction can range from a small increase in serum creatinine or reduction in urine output to the development of azotemia (an accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood). - AKI can develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium, with or without a reduction in urine output.

Etiology and Pathophysiology: - Prerenal: o Due to reduced renal blood flow  Severe dehydration, heart failure, ↓ CO o Decreased glomerular filtration rate (GFR) o Causes oliguria - Intrarenal: o Direct damage to kidney tissue o Results from  Prolonged ischemia  Nephrotoxins  Hemoglobin released from hemolyzed RBCs  Myoglobin released from necrotic muscle cells o Acute tubular necrosis (ATN)* o Nephrotoxins can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules. o Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction. o Diseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI. - Postrenal: o Causes include  Benign prostatic hyperplasia (BPH)  Prostate cancer

 Calculi  Trauma  Extrarenal tumors o Postrenal causes of AKI involve mechanical obstruction in the outflow of urine. As the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function. o Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage that results in a progressive decline in kidney function. o If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. If it is not relieved after 12 weeks, recovery is unlikely.

Gerontologic Considerations: - Acute Kidney Injury: o More susceptible to AKI  Polypharmacy  Hypotension  Diuretic therapy  Aminoglycoside therapy

 Obstructive disorders  Surgery  Infection

o Older adults are at risk for the same causes of AKI as are younger adults. However, they are more susceptible to AKI.

o Dehydration is associated with polypharmacy (diuretics, laxatives, and drugs that suppress appetite or consciousness), acute febrile illnesses, and being bedridden. o Other common causes of AKI in older adults include hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders (e., prostatic hyperplasia), surgery, infection, and contrast media. o Impaired function of other organ systems from cardiovascular disease or diabetes mellitus can increase the risk of developing AKI. The aging kidney is less able to compensate for changes in fluid volume, solute load, and cardiac output.

Acute Kidney Injury: - Clinical Manifestations: o RIFLE classification – Stages of AKI  Risk (R)  Injury (I)  Failure (F)

 Loss (L)  End-stage kidney disease (E)  o Oliguric phase o Urinary changes  Urinary output less than 400 mL/day  Occurs within 1 to 7 days after injury  Lasts 10 to 14 days  Urinalysis may show casts, RBCs, WBCs o Urinary changes: Oliguria is a reduction in urine output to less than 400 mL/day. Oliguria usually occurs within 1 to 7 days of the injury to the kidneys. If the cause is ischemia, oliguria will often occur within 24 hours. o The duration of the oliguric phase lasts on average about 10 to 14 days but can last months in some cases. The longer the oliguric phase lasts, the poorer the prognosis for complete recovery of kidney function. o A urinalysis may show casts, RBCs, and white blood cells (WBCs). The casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules.

Oliguric Phase: - Hypovolemia may exacerbate AKI - Decreased urine output, fluid retention occurs o Neck veins distended o Bounding pulse

o Edema o Hypertension

Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions
Fluid volume: Hypovolemia (volume depletion) has the potential to exacerbate all forms of AKI. The reversal of hypovolemia with fluid replacement is often sufficient to treat many forms of AKI, especially those with prerenal causes. o When urinary output decreases, fluid retention occurs. The severity of the symptoms depends on the extent of the fluid overload. In the case of reduced urine output (anuria and oliguria), the neck veins may become distended with a bounding pulse. Edema and hypertension may develop. Fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions.
Metabolic acidosis o Serum bicarbonate level decreases o Severe acidosis develops  Kussmaul respirations o Metabolic acidosis: In kidney failure, the kidneys cannot synthesize ammonia (needed for hydrogen ion excretion) or excrete acid products of metabolism.

o Because of the large losses of fluid and electrolytes, the patient must be monitored for hyponatremia, hypokalemia, and dehydration. The diuretic phase may last 1 to 3 weeks. Near the end of this phase, the patient’s acid-base, electrolyte, and waste product (BUN, creatinine) values begin to normalize.

Recovery phase: The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to plateau and then decrease. Although the major improvements occur in the first 1 to 2 weeks of this phase, kidney function may take up to 12 months to stabilize. o The outcome of AKI is influenced by the patient’s overall health, the severity of kidney failure, and the number and type of complications.

Diagnostic Studies: - Thorough history - Serum creatinine - Urinalysis - Kidney ultrasonography

Renal scan
Computed tomography (CT) scan
Renal biopsy
A thorough history is essential for diagnosing the etiology of AKI. Consider prerenal causes when there is a history of dehydration, blood loss, or severe heart disease.
An increase in serum creatinine may not be evident until there is a loss of more than 50% of kidney function.
Urinalysis is an important diagnostic test. The urine osmolality, sodium content, and specific gravity are measured, and urine sediment, hematuria, pyuria, and crystals may be seen.
Kidney ultrasonography is often the first test done because it provides imaging without exposure to potentially nephrotoxic contrast agents.
A renal scan can help assess abnormalities in kidney blood flow, tubular function, and the collecting system.
A computed tomographic (CT) scan can identify lesions and masses, as well as obstructions and vascular anomalies.
Renal biopsy is considered the best method for confirming intrarenal causes of AKI.
Contraindicated o Magnetic resonance angiography (MRA) with gadolinium contrast medium  Nephrogenic systemic fibrosis  Contrast-induced nephropathy (CIN) o Administration of gadolinium has been associated with the development of a devastating and potentially lethal disorder, nephrogenic systemic fibrosis, in patients with kidney failure. o In patients with kidney failure, contrast-induced nephropathy (CIN) can occur when contrast medium for diagnostic studies causes nephrotoxic injury.

Collaborative Care: - Primary goals o Eliminate the cause o Manage signs and symptoms o Prevent complications - Ensure adequate intravascular volume and cardiac output o Force fluids (early) o Loop diuretics (e., furosemide [Lasix]) o Osmotic diuretics (e., mannitol) - Closely monitor fluid intake during oliguric phase - If AKI is already established, forcing fluids and diuretics will not be effective and may, in fact, be harmful. - Closely monitor fluid intake during the oliguric phase of AKI. The general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e., urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e., respiration, diaphoresis).

Hyperkalemia: Risk of Life-threatening Dysrhythmias: - Peaked T-waves o Different from ST elevation (full segment): associated with MI o Peaked, enlarged o After peaked T’s, QRS widens -> pt can go asystolic if not treated

Regular Insulin IV: o Potassium moves into cells when insulin is given o IV glucose is given concurrently to prevent hypoglycemia o When effects of insulin diminish, potassium shifts back out of cells
Sodium bicarbonate o D50 to prevent hypoglycemia o Bicarb: Metabolic acidosis  Correct acidosis and cause a shift of potassium into cells o 1amp IV push
Calcium gluconate IV o Generally used in advanced cardiac toxicity (With evidence of hyperkalemic ECG changes) o Calcium raises the threshold for excitation, resulting in dysrhythmias
Sodium polystyrene sulfonate (Kayexalate) o Cation-exchange resin is administered by mouth or retention enema o When resin is in bowel, potassium is exchanged for sodium o Therapy removes 1 meq of potassium per gram of drug o It is mixed in water with sorbitol to produce osmotic diarrhea, allowing for evacuation of potassium-rich stool from body o Assess bowel sounds
Hemodialysis: o Most effective therapy to remove potassium o Works within a short period of time o Cardiac monitoring
Dietary Restriction: o Potassium intake is limited to 40meq/day o Primarily used to prevent recurrent elevation, not used for acute elevation
Hyperkalemia is one of the most serious complications in AKI because it can cause life-threatening cardiac dysrhythmias.
The various therapies used to treat elevated potassium levels are listed in Table 47-5. Both insulin and sodium bicarbonate serve as a temporary measure for treatment of hyperkalemia by promoting a shift of potassium into the cells, but potassium will eventually be released.
Calcium gluconate raises the threshold at which dysrhythmias will occur, serving to temporarily stabilize the myocardium.
Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually remove potassium from the body.
Never give this drug to a patient with a paralytic ileus because bowel necrosis can occur.

Renal Replacement Therapy (RRT): - Indications for (RRT): (Most common CVVH) o Volume overload* o Elevated serum potassium level* o Metabolic acidosis o BUN level higher than 120 mg/dL (43 mmol/L) o Significant change in mental status o Pericarditis, pericardial effusion, or cardiac tamponade - Peritoneal dialysis (PD) - Intermittent hemodialysis (HD)

o In some situations when immediate vascular access is required, percutaneous cannulation of the internal jugular or femoral vein is performed.

Procedure: o Before treatment, nurse should  Complete assessment of fluid status, condition of access, temperature, skin condition o During treatment, nurse should  Be alert to changes in condition  Measure vital signs every 30 to 60 minutes o Effectiveness and Adaptation o Cannot fully replace normal functions of kidneys o Can ease many of the symptoms o Can prevent certain complications

Continuous Renal Replacement Therapy: - Alternative or adjunctive method for treating AKI - Means by which uremic toxins and fluids are removed - Acid-base status/electrolyte balance adjusted slowly and continuously - Contraindication o Presence of manifestations of uremia that necessitate rapid resolution - Continued for 30 to 40 days - Most common approaches: venovenous - Continuous venovenous hemofiltration (CVVH) - Continuous venovenous hemodialysis (CVVHD) o Not only fluids - Hemofilter change every 24 to 48 hours - Ultrafiltrate should be clear yellow - Specimens may be obtained for evaluation

Continuous Vevovenous Hemofiltration Dialysis (CVVHD): - Large volumes fluid removed hourly, then replaced - Fluid replacement dependent on stability/individualized needs of patient - Dialysate bags attached to distal end of hemofilter - Highly permeable, hollow fiber hemofilter - Removes plasma water and nonprotein solutes - Basic schematic of continuous venovenous therapies. - Blood pump is required to pump blood through the circuit. - Replacement ports are used for CVVH and CVVHD only and can be given before or after filtration. - Dialysate port is used for CVVHD only. Regardless of modality, ultrafiltrate is drained via the ultrafiltration drain port.

Peritoneal Dialysis: - Peritoneal access is obtained by inserting a catheter through the anterior abdominal wall - Technique for catheter placement varies - Usually done via surgery - Watch for peritonitis o Fluid should be clear, not cloudy (sign of infection) o Fever, discomfort - Dialysis Solutions and Cycles: o Three phases of PD cycle  Inflow (fill)  Dwell (equilibration)  Drain

o Called an exchange

Inflow o Prescribed amount of solution infused through established catheter over about 10 minutes o After solution infused, inflow clamp closed to prevent air from entering tubing
Dwell o Also known as equilibration o Diffusion and osmosis occur between patient’s blood and peritoneal cavity o Duration of time varies, depending on method
Drain o Lasts 15 to 30 minutes o May be facilitated by gently massaging abdomen or changing position
The cycle starts again with the infusion of another 2 L of solution. For manual PD, a period of about 30 to 50 minutes is necessary to complete an exchange.
Ultrafiltration (fluid removal) during PD depends on osmotic forces; glucose is the most effective osmotic agent currently available. Dextrose remains the most commonly used osmotic agent available in PD solutions.
Systems: o Automated peritoneal dialysis (APD)  Cycler delivers the dialysate  Times and controls fill, dwell, and drain o Continuous ambulatory peritoneal dialysis (CAPD)  Manual exchange o APD is the most popular form of PD because it allows patients to accomplish dialysis while they sleep. The machine cycles four or more exchanges per night with 1 to 2 hours per exchange. o {See next slide for APD figure.} o It is difficult to achieve the required solute and fluid clearance solely with nighttime APD. Therefore, one or two daytime manual exchanges may also be prescribed to ensure adequate dialysis. o CAPD: Exchanges are carried out manually with 1 to 3 L of peritoneal dialysate at least four times daily, with dwell times averaging 4 hours. For example, one schedule exchanges at 7: AM, 12:00 noon, 5:00 PM, and 10:00 PM.
Complications: o Exit site infection* o Peritonitis * o Hernias o Lower back problems o Bleeding o Pulmonary complications o Protein loss o Infection of the peritoneal catheter exit site is most commonly caused by Staphylococcus aureus or Staphylococcus epidermidis (from skin flora). o Most frequently, peritonitis occurs because of improper technique in making or breaking connections for exchanges. o Because of increased intraabdominal pressure secondary to the dialysate infusion, hernias can develop in predisposed individuals such as multiparous women and older men.

Nursing Management: - Nursing assessment o Measure vital signs

A primary nutritional goal in AKI is to maintain adequate caloric intake (providing 30 to 35 kcal/kg and 0. to 1 g of protein per kilogram of desired body weight) to prevent the further breakdown of body protein for energy purposes.
Adequate energy should be primarily from carbohydrate and fat sources to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. Supplementation of essential amino acids can be given for amino acid replacement.
Sodium is restricted as needed to prevent edema, hypertension, and heart failure.
Dietary fat intake is increased so that the patient receives at least 30% to 40% of total calories from fat. Fat emulsion IV infusions given as a nutritional supplement provide a good source of nonprotein calories (see Chapter 40).
If a patient cannot maintain adequate oral intake, enteral nutrition is the preferred route for nutritional support (see Chapter 40).
When the gastrointestinal (GI) tract is not functional, parenteral nutrition is necessary to provide adequate nutrition. The patient treated with parenteral nutrition may need daily HD or CRRT to remove the excess fluid. Concentrated formulas of parenteral nutrition are available to minimize fluid volume.

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Acute Kidney Injury - Outline

Course: Generalist Nursing Practice IV: Tertiary Care Across the Lifespan (NURS 4889)

30 Documents

Students shared 30 documents in this course

University: Temple University

Was this document helpful?

Acute Kidney Injury:

-Acute kidney injury (AKI), previously known as acute kidney failure, is the term used to encompass the

entire range of the syndrome, including a very slight deterioration in kidney function to severe

impairment.

-AKI is characterized by a rapid loss of kidney function. This loss is accompanied by a rise in serum

creatinine level and/or a reduction in urine output. The severity of dysfunction can range from a small

increase in serum creatinine or reduction in urine output to the development of azotemia (an

accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood).

-AKI can develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine,

and potassium, with or without a reduction in urine output.

Etiology and Pathophysiology:

-Prerenal:

oDue to reduced renal blood flow

Severe dehydration, heart failure, ↓ CO

oDecreased glomerular filtration rate (GFR)

oCauses oliguria

-Intrarenal:

oDirect damage to kidney tissue

oResults from

Prolonged ischemia

Nephrotoxins

Hemoglobin released from hemolyzed RBCs

Myoglobin released from necrotic muscle cells

oAcute tubular necrosis (ATN)*

oNephrotoxins can cause obstruction of intrarenal structures by crystallization or by causing

damage to the epithelial cells of the tubules.

oHemoglobin and myoglobin can block the tubules and cause renal vasoconstriction.

oDiseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may

also cause AKI.

-Postrenal:

oCauses include

Benign prostatic

hyperplasia (BPH)

Prostate cancer

Calculi

Trauma

Extrarenal tumors

oPostrenal causes of AKI involve mechanical obstruction in the outflow of urine. As the flow of

urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function.

oBilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic

pressure, and tubular blockage that results in a progressive decline in kidney function.

oIf bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. If it is not

relieved after 12 weeks, recovery is unlikely.

Gerontologic Considerations:

-Acute Kidney Injury:

oMore susceptible to AKI

Polypharmacy

Hypotension

Diuretic therapy

Aminoglycoside therapy

Obstructive disorders

Surgery

Infection

oOlder adults are at risk for the same causes of AKI as are younger adults. However, they are more

susceptible to AKI.

Acute Kidney Injury - Outline

Generalist Nursing Practice IV: Tertiary Care Across the Lifespan (NURS 4889)

Temple University

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Acute Kidney Injury - Outline

Course: Generalist Nursing Practice IV: Tertiary Care Across the Lifespan (NURS 4889)

University: Temple University

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