Transcript Acute Tubular Necrosis

Acute Tubular Necrosis (ATN)
Dr. Belal Hijji, RN, PhD
December 14 & 17, 2011
Learning Outcomes
At the end of this lecture, students will be able to:
• Explain the common causes of acute tubular necrosis.
• Identify the four phases of ATN and their characteristics.
• Discuss assessment and diagnostic findings of ATN.
• Identify disease states that increase the risk of ATN.
• Discuss the importance of hemodynamic monitoring and fluid
balance in a patient with ATN.
• Discuss the medical, pharmacological, and nutritional
management of ATN.
• Discuss the nursing management of a patient with ATN.
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This is the typical appearance of the blood vessels (vasculature)
and urine flow pattern in the kidney. The blood vessels are shown
in red and the urine flow pattern in yellow.
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Causes of ATN
• ATN is the most common cause of acute renal failure (ARF); it
results from nephrotoxic or ischemic injury that damages the
kidney tubular epithelium.
• Damage to the kidney cells prevents normal concentration of
urine, filtration of wastes, and regulation of acid-base,
electrolytes, and water balance.
– Ischemic acute tubular necrosis: Ischemic damage occurs as a result
of vasodilation associated with sepsis and when hypotension is
prolonged (Pre-renal low perfusion).
– Toxic acute tubular necrosis: Nephrotoxic damage results from
injury by drugs (gentamicin, amikacin, vancomycin) and chemicals
(radiopaque dye administered in radiologic diagnostic studies).
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Phases of ATN
• Initiation phase: This phase is the period from the initial insult
until cell injury occurs. It is characterized by acute decrease in
GFR (90 - 120 mL/min/1.73 m2) to very low levels, with a sudden
increase in serum creatinine and BUN concentrations. This phase
lasts hours to days depending on the cause. Prompt treatment can
alleviate irreversible damage.
• Oliguric or anuric phase: This phase lasts 5-8 days in the nonoliguric patient and 10-16 days in the oliguric (< 500 CC of
urine/24 hours) one. The GFR is greatly reduced resulting in high
BUN, elevated serum creatinine, hyperkalemia, and metabolic
acidosis (rapid breathing, confusion, shock or death in severe
cases).
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Phases of ATN (Continued….)
• Diuretic phase: This phase lasts 7-14 days and is characterised by
an increase in GFR and sometimes by polyuria (urine output 2-4
L/day).
• Recovery phase: In this phase, kidney tubular cells that have
survived prior injury contribute to the healing process through
proliferation and migration to the damaged areas. Oliguric or
nonoliguric patients may have increased urine output, and kidney
function slowly returns to normal or near normal.
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Assessment and Diagnosis
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Acidosis: pH of <7.35 indicates severe acute kidney insult.
BUN: Increased (normal range 5-25 mg/dL).
Creatinine: Increased (normal range 0.5-1.5).
Creatinine clearance: Decreased (normal range 110-120 mL/min);
values <50 mL/min indicates significant kidney dysfunction.
• BUN: Creatinine ratio. 20:1 (Ischemia); 10:1 (Toxic).
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Disease States That Increase the Risk of ATN
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Underlying chronic kidney disease.
Older age, diabetes, and hypertension.
Heart failure.
Respiratory failure.
Sepsis.
Trauma.
Contrast-induced nephrotoxic injury.
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Hemodynamic Monitoring and Fluid Balance
• Hemodynamic monitoring: This involves surveillance of the
central venous pressure (2-5 mm Hg), pulmonary artery occlusion
pressure (5-12 mm Hg), cardiac output (SV*HR = 4-8 L/min),
and cardiac index (CO/BSA) . Body surface area (BSA) ranges
from 2.5 to 4.5 L/min/m2). Stroke volume (SV) is the amount of
blood in mL ejected from the ventricles with each beat.
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Hemodynamic Monitoring and Fluid Balance (Continued…)
• Daily weight and accurate intake and output monitoring. These
are powerful indicators of fluid gains or losses over 24 hours. A 1kg weight gain/ day represents 1 liter of additional fluid retention.
• Physical assessment: Signs that suggest extracellular fluid
depletion include thirst and decreased skin turgor. Signs that
imply intravascular fluid volume overload include pulmonary
congestion, increasing heart failure, and high BP.
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Medical Management of ATN.
Medical treatment of ATN focuses on prevention, fluid balance,
medications, and electrolyte balance.
• Prevention: This is the only truly effective remedy for acute
kidney insult (AKI). Nephrotoxic drugs are avoided in patients
with AKI or chronic kidney disease (CKD). Nonsteroidal
antiinflammatory (NSAID) drugs are avoided in patients with
high creatinine levels. Intravascular contrast dye is delayed, if
possible, until the patient is fully rehydrated.
• Fluid resuscitation: These include crystalloids (normal saline
0.9%, 0.45% saline, and lactated ringer) and colloids (albumin
5% & 25%). Fluid restriction (1 L/day) aims to prevent
circulatory overload and the development of interstitial edema
when the kidneys cannot remove excess fluid. Fluid removal is
achieved by diuretics. However, hemodialysis is the treatment of
choice.
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Medical Management of ATN.
• Medications: These include diuretics, dopamine (2-3 mcg/kg/min)
to increase blood flow to the kidneys.
• Nutrition: The recommended energy intake is between 20 and 30
kcal/kg/day with 1.2 to 1.5 g/kg of protein/day to control high
BUN. Oral or enteral nutrition is indicated.
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Nursing Management of ATN.
• Nurses are responsible for recognising potential risk factors for
AKI and acts as an advocate for the patient. Such patients include
the elderly, dehydrated patients, patients with high creatinine level
before admission, and patients for radiologic tests using a dye.
• Nurses need to monitor patients for signs of infection (high WBC,
redness at wound or intravenous line site, and fever).
• Nurses should perform hemodynamic monitoring (HR, BP, CVP,
PAOP, CO, and CI), measure weight daily, and record intake and
output. Nurses should also recognise early signs and symptoms of
fluid overload.
• Nurses should monitor the patient for hyperkalemia and
hypocalcemia as these increase the risk for cardiac dysrhythmias.
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Nursing Management of ATN.
• Hyperphosphatemia causes severe itching. Nurses can help by
applying emollients for skin care, discouraging scratching, and
administering phosphate-binding agents (calcium carbonate &
calcium acetate) with food.
• Finally, anemia in AKI results from kidney failure to produce the
hormone erythropoietin which stimulates bone marrow to produce
RBCs. Nurses are in position to minimise blood withdrawal as
much as possible, administer of human erythropoietin as
prescribed, and transfuse blood.
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