Acute tubular necrosis (also called acute tubulointerstitial

nephritis) causes 75% of all cases of AKI. This disorder destroys

the tubular segment of the nephron, causing renal failure and
uremia (excess by-products of protein metabolism in the blood).
Because acute tubular necrosis is fatal in 40% to 70% of cases, prevention,
prompt recognition, and intervention by the critical care
nurse are vital.
What causes it
Acute tubular necrosis may follow two types of kidney injury:
Ischemic injury, the most common cause, interrupts blood
flow to the kidneys. The longer the blood flow is interrupted, the
worse the kidney damage.
Nephrotoxic injury usually affects debilitated patients, such as
the critically ill and those who have undergone extensive surgery.
Blood disruption
In ischemic injury, blood flow to the kidneys may be disrupted by:
circulatory collapse
severe hypotension
meet the team
Because acute kidney injury affects multiple body systems, a multidisciplinary
approach to care is needed, with the critical care nurse coordinating care. Heres
how
other members of the multidisciplinary team contribute to your patients care:
A nephrologist can evaluate and manage the patients kidney function.
A respiratory or cardiology specialist may be involved to deal with
complications.
A nutritional therapist may recommend restrictions or supplements.
A physical or occupational therapist may help the patient with energy
conservation
and rehabilitation.
A pharmacist can assist with medication dosing.
If a prolonged hospital stay is expected and the patient requires long-term care
or home care, social services should be consulted early in the patients care.
The patient and his family may benefit from spiritual counseling.
Go team!
You need to
coordinate care for
a patient with acute
kidney injury
trauma
hemorrhage
dehydration
cardiogenic or septic shock
surgery
anesthetics
transfusion reactions.
Toxic talk
Nephrotoxic injury can result from:
ingesting or inhaling toxic chemicals, such as carbon tetrachloride,
heavy metals, and methoxyflurane anesthetics
a hypersensitivity reaction of the kidneys to such substances as
antibiotics and radiographic contrast agents.
Cause and effect
Some specific causes of acute tubular necrosis and their effects
include:
a diseased tubular epithelium that allows glomerular filtrate to
leak through the membranes and be resorbed into the
blood
obstructed urine flow from the collection of
damaged cells, casts, RBCs, and other cellular
debris in the tubules
ischemic injury to glomerular epithelial cells,
causing cellular collapse and poor glomerular
capillary permeability
ischemic injury to the vascular endothelium,
eventually causing cellular swelling and tubular
obstruction.
how it happens
Deep or shallow lesions may occur in acute tubular necrosis.
Lesion lesson
With ischemic injury, necrosis creates deep lesions, destroying the
tubular epithelium and basement membrane (the delicate layer
underlying the epithelium). Ischemic injury causes patches of
necrosis in the tubules. Ischemia can also cause lesions in the connective
tissue of the kidney.
With nephrotoxic injury, necrosis occurs only in the epithelium
of the tubules, leaving the basement membrane of the nephrons
intact. This type of damage may be reversible. (See A close look at
acute tubular necrosis, page 546.)
Nephrotoxic injury
can result from
ingesting or inhaling
toxic
Toll-taking
Toxicity takes a toll on renal structures. Nephrotoxic agents can
injure tubular cells by:
direct cellular toxic effects
coagulation and destruction (lysis) of RBCs
oxygen deprivation (hypoxia)
crystal formation of solutes.
Getting complicated
There are several common complications of acute tubular necrosis:
Infections (frequently septicemia) complicate up to 70% of all
cases and are the leading cause of death.
GI hemorrhage, fluid and electrolyte imbalance, and cardiovascular
dysfunction may occur during the acute or recovery phase.
a close look at acute tubulaS necSosis
In acute tubular necrosis caused by ischemia, patches
of necrosis occur, usually in the straight portions of the
proximal tubules.
In areas without lesions, tubules are usually dilated. In
acute tubular necrosis caused by nephrotoxicity, the
tubules have a more uniform appearance.
Neurologic complications are common in elderly patients and
occur occasionally in younger patients.
Excess blood calcium (hypercalcemia) may occur during the
recovery phase.
What to look foS
Early-stage acute tubular necrosis may be hard to spot because
the patients primary disease may obscure the signs and symptoms.
The first recognizable sign may be decreased urine output,
usually less than 400 mL/24 hours.
Difficult to detect
Acute tubular necrosis is difficult to detect in its early stages, so
look closely at members of high-risk populations, such as elderly
patients or those with diabetes, and be alert for subtle signs and
symptoms during your nursing assessments.
Other signs and symptoms depend on the severity of systemic
involvement and may include:
bleeding abnormalities
vomiting of blood
dry skin and mucous membranes
lethargy
confusion
agitation
edema
fluid and electrolyte imbalances
muscle weakness with hyperkalemia
cardiac arrhythmias.
Mortality can be as high as 70%, depending
on complications from underlying
diseases. The patient with a nonoliguric
form of acute tubular necrosis has a better
prognosis.
What tests tell you
Acute tubular necrosis is difficult to diagnose except in advanced
stages. The following tests are commonly performed:
Urinalysis shows dilute urine, low osmolality, high sodium levels,
and urine sediment containing RBCs and casts.
Blood studies reveal high BUN and serum creatinine levels, low
serum protein levels, anemia, platelet adherence defects, metabolic
acidosis, and hyperkalemia.
ECG may show arrhythmias from electrolyte imbalances and,
with hyperkalemia, a widening QRS complex, disappearing P waves,
and tall, peaked T waves.
Acute tubular
necrosis is difficult
to detect in its
early stages, so look
closely at patients
who are members of
high-risk groups, such
as elderly
how its tSeated
The patient with acute tubular necrosis requires vigorous supportive
measures during the acute phase until normal kidney function
is restored. Therapy may include:
diuretics and fluids to flush tubules of cellular casts
and debris and to replace lost fluids (initially)
emergency I.V. infusion of 50% glucose, regular insulin,
and sodium bicarbonate in case of hyperkalemia
sodium polystyrene sulfonates given by mouth or by
enema to reduce potassium levels
calcium channel blockers and prostaglandins, which
may aid in treating nephrotoxic acute tubular necrosis.
Furthermore
Treatment for the patient with acute tubular necrosis
may also include:
daily replacement of projected and calculated fluid
losses
transfusion of packed RBCs for anemia
non-nephrotoxic antibiotics for infection
hemodialysis or peritoneal dialysis to prevent severe fluid and
electrolyte imbalance and uremia.
What to do
Take steps to maintain the patients fluid balance. Accurately
record intake and output, including wound drainage, NG tube output,
and hemodialysis or peritoneal dialysis balances. Weigh the
patient daily.
Assist with insertion of a central venous or PA catheter to monitor
fluid status. Monitor hemodynamic parameters as indicated.
Watch the patient for fluid overload, a common complication
when infusing large fluid volumes.
Monitor Hb levels and HCT, and administer blood products, as
needed. Use fresh packed cells instead of whole blood to prevent
fluid overload and heart failure.
Maintain electrolyte balance. Monitor laboratory results and
report imbalances.
Monitor the patients vital signs, oxygen saturation, cardiac
rhythm, and cardiopulmonary status. Treat hypotension immediately
to avoid renal ischemia. Monitor vital signs closely. Fever
and chills may signal the onset of an infection, which is the leading
cause of death in acute tubular necrosis. (See Temperature
regulation in elderly patients.)
Check for potassium content in prescribed drugs (for example,
potassium penicillin). Provide dietary restriction of foods
All this talk about
vigorous treatment
has tired me out!
Watch out for fluid
overload! Its a
common complication
when infusing large
fluid
containing sodium and potassium, such as bananas, orange juice,
and baked potatoes.
Provide adequate calories and essential amino acids while
restricting protein intake to maintain an anabolic state. Total parenteral
nutrition may be indicated for a critically ill and debilitated
or catabolic patient.
Use sterile technique, especially when handling catheters,
because the critically ill or debilitated patient is vulnerable to
infection.
Administer sodium bicarbonate, as ordered, for acidosis or
assist with dialysis in severe cases.
Provide the patient with reassurance and emotional support.
Encourage him and his family to verbalize their concerns. Fully
explain each procedure.
To prevent acute tubular necrosis, make sure the patient is well
hydrated before surgery or after X-rays requiring use of a contrast
medium. Administer mannitol, as ordered, to the high-risk critically
ill patient before and during these procedures. Administer
nephrotoxic drugs cautiously and avoid using contrast dyes in the
high-risk patient.