Acute Kidney

Injury
B4
Definition

…is a rapid loss of renal function due to damage to the

kidneys. Depending on the duration and severity of AKI,
a wide range of potentially life-threat metabolic
complications can occur, including metabolic acidosis
as well as fluid electrolyte imbalances.
Types of Acute Kidney Injury

● AKI occurs in three types—

1. Prerenal
2. Intrinsic
3. Postrenal
 COMPARING TYPES OF AKI

TYPES OF KIDNEY INJURY CAUSES

● PRERENAL INJURY : decreased renal ● Prolonged low-volume states, such as

blood flow resulting from sepsis, trauma, sepsis, decreased blood pressure, and
bleeding, or poor cardiac output. hemorrhage
● Such drugs as nonsteroidal anti-
inflammatory agents or cyclooxygenase
inhibitors, which inhibit prostaglandin
synthesis; In turn, inhibition triggers action
of vasoconstrictors on renal arterioles,
which decreases glomerular filtration rate.
● INTRINSIC INJURY: acute tubular ● Nephropathy caused b contrast agents
necrosis from sepsis and renal ischemia ● Aminoglycoside drug therapy without
and ultimately, from poor organ careful dosage monitoring.
perfusion and multisystemic failure.

● Renal calculi
● POSTRENAL: obstructive nephropathy ● Tumors
resulting from mechanical obstruction of ● Prostatic hypertrophy
urine flow. ● Strictures
● Congenital defects
Pathophysiolog
y
AKI commonly results from extracellular volume depletion, decreased
renal blood flow, or toxic/inflammatory injury to kidney cells that result in
alterations in renal function that may be minimal or severe. Even small
changes in renal function may be associated with significant morbidity and
mortality. The etiologies of AKI can be described considering three
categories of injury: (1) renal hypoperfusion (prerenal AKI); (2) disorders
involving the renal parenchymal or interstitial tissue (intrarenal or intrinsic
AKI); and (3) disorders associated with acute urinary tract obstruction
(postrenal AKI). Most types of AKI are reversible if diagnosed and treated
early.
 Prerenal Acute Kidney
Injury
• Poor perfusion can be caused by
hypotension, hypovolemia associated with
hemorrhage or fluid loss (e.g., burns),
sepsis, inadequate cardiac output (e.g.,
myocardial infarct), multiple organ
dysfunction, renal vasoconstriction (e.g.,
caused by nonsteroidal antiinflammatory
drugs [NSAIDs] or radiocontrast agents),
renal artery stenosis, or kidney edema that
restricts arterial blood flow.
 Prerenal Acute Kidney
Injury
• During the early phases of
hypoperfusion, protective
autoregulatory mechanisms
maintain GFR at a relatively constant
level through afferent arteriolar
dilation and efferent arteriolar
vasoconstriction (mediated by
angiotensin II).
 Prerenal Acute Kidney
Injury
• Tubuloglomerular feedback mechanisms
also maintain GFR and distal tubular
nephron flow The GFR ultimately declines
because of the decrease in filtration
pressure. Sepsis/septic shock and
cardiogenic shock following cardiac surgery
are the most common causes of AKI in the
critical care unit.
 Intrarenal (intrinsic) acute kidney
injury (AKI)
• can result from ischemic acute tubular necrosis (ATN),
nephrotoxic ATN (i.e., exposure to radiocontrast media or
antibiotics), acute glomerulonephritis, vascular disease
(malignant hypertension, disseminated intravascular
coagulation, and renal vasculitis), allograft rejection, or
interstitial disease (drug allergy, infection, tumor
growth).
• ATN is generally described as postischemic or
nephrotoxic, or it can be a combination of both
 Intrarenal (intrinsic) acute kidney
injury (AKI)
• Creatinine level usually increases with decreased
renal blood flow and decreased GFR. However, in
sepsis-induced AKI, creatinine values can remain
within normal ranges and may be related to
alterations in intrarenal microcirculatory blood flow
that are different from the kidney ischemia that
develops related to systemic hypotension and
hypoperfusion of nonseptic AKI.
Postrenal
Postrenal acute
acute kidney
kidney
injury
injury
• is rare and usually occurs with urinary tract obstruction that
affects the kidneys bilaterally (e.g., bilateral ureteral
obstruction, bladder outlet obstruction-prostatic hypertrophy,
tumors or neurogenic bladder, and urethral obstruction).
• obstruction causes an increase in intraluminal pressure
upstream from the site of obstruction with a gradual decrease
in GFR
 Clinical
Manifestation
• decreased urine output
• chest pain or pressure
• jugular vein distention
• fluid retention, causing edematous
legs, ankles, or feet
• shortness of breath
• confusion
• nausea
• seizures or coma in severe cases.
Nursing Management

1. Monitor fluid & Electrolyte

Imbalance
2. Reducing metabolic rate
3. Promoting pulmonary function
4. Preventing infection
5. Provided skin-care
6. Providing psychosocial support
Monitor Fluid & Electrolyte
Imbalance
Because acute kidney injury can produce major fluid and electrolyte
imbalances, the nurse checks the patients' serum electrolyte levels and
physical signs of these complications throughout the condition. IV
solutions must be carefully chosen based on the fluid and electrolyte status
of the patient. The heart function and musculoskeletal state of the patients
are continuously examined for symptoms of hyperkalemia.
Monitor Fluixd & Electrolyte
Imbalance
Closely monitor the patients’ fluid status by paying attention to fluid

intake, might as well accurately weight I&O. Indicators of

deteriorating fluid and electrolyte status should be reported

immediately to the primary provider. Severe fluid and electrolyte

disturbances may be treated with hemodialysis, PD, or CRRT.

Reducing metabolic
rate
The nurse works to lower the patient's metabolic rate.
During the most intense stage of the disease, bed
rest may be recommended to minimize exertion
and metabolic rate. Fever and infection, which both
increase metabolic rate and catabolism, are
avoided or treated as soon as possible.
Promoting Pulmonary
Function
In order to avoid atelectasis and respiratory
tract infection, the patient is encouraged to
turn, cough, and take deep breaths
regularly. Drowsiness and lethargy might
make it difficult for the patient to move or
turn without help.
Preventing
Infection
With invasive lines and catheters, asepsis is required
to reduce the danger of infection and enhance
metabolism. Because of the significant risk of UTI
associated with its usage, an indwelling urinary
catheter is avoided whenever feasible, although it
may be necessary to provide continuous data
required to correctly monitor fluid I&O.
Providing Skin
Care
As a result of the edema, the skin may be dry or prone to
breakdown; thus, thorough skin care is essential.
Furthermore, excoriation and itching of the skin may
occur as a result of irritating toxins being deposited in
the patient's tissues. Bathing the patient in cool water,
rotating him frequently, and keeping the skin clean and
moisturized, as well as keeping the fingernails clipped
to minimize excoriation, are all helpful in preventing
skin breakdown.
Providing Psychosocial
Support
Hemodialysis, PD, or CRRT may be required for a patient with Acute
Kidney Injury. The length of time these therapies are required
varies depending on the cause and amount of kidney impairment.
During this time, the patient and family require aid, explanation,
and support. The primary provider explains the treatment's
purpose to the patient and family. High degrees of worry and
dread, on the other hand, may need the nurse's frequent
explanation and clarification. Family members may be hesitant to
touch and talk to the patient during these operations at first, but
they should be encouraged to do so.
Providing Psychosocial
Support
Many of the nurse's responsibilities in an intensive care
unit are focused on the technical elements of patient
care; nevertheless, it is critical that the patient's
psychological needs and other issues be addressed.
Continued monitoring of the patient for Acute Kidney
Injury consequences and precipitating factors, also
known as ESKD.
Collaborative
Care
Medical Management
● Objectives of treatment for AKI are restore normal chemical balance and prevent
complications until repair of renal tissue and restoration of renal function can occur
● Management includes eliminating the underlying cause
● Maintaining fluid balance
● Avoiding fluid excess
● When indicated, providing renal replacement therapy
● Prerenal azotemia is treated by optimizing renal perfusion
● Postrenal failure is treated by relieving the obstruction
● Intrarenal azotemia is treated with supportive therapy with removal of causative
agent, aggressive management of prerenal and postrenal failure, and avoidance
of risk factors
● Myoglobinuria is treated for rhabdomyolysis
● Mannitol (Osmitrol), furosemide (Lasix), or erthacrynic acid (Edecrin) may be
prescribe to initiate diuresis especially when there is enema
● Hemodialysis a procedure that circulates the patient’s blood through an artificial
kidney [ dialyzer] to remove waste products and excess fluid
● Peritoneal dialysis (PD; a procedure that uses the patient’s peritoneal membrane
[the lining of the peritoneal cavity] as the semipermeable membrane to exchange
fluid and solutes) or a variety of continuous renal replacement therapies (CRRTs)
methods used to replace normal kidney function by circulating the patient’s
blood through a hemofilter) may be performed
Pharmacological Therapy
● Monitor hyperkalaemia through serial serum electrolyte levels (potassium value greater
than 5.0 mEq/L)
● ECG changes (tall, tented, or peaked T waves)
● Changes in clinical status
● Elevated potassium levels may be reduced by administering cation-exchange resins
(sodium polystyrene sulfonate [Kayexalate] orally or by retention enema
● Sarbitol may be given with Kayelexate to induce diarrhea-type effect
● Kayexalate retention enema, rectal cathether with a balloon may be used to
facilitate retention if necessary
● Patient should retain the Kayexalate for at least 30-60 minutes (preferable 6-10
hours) to promote potassium removal (Comerford, 2015)
● Cleansing enema may be prescribed to remove remaining medication as a
precaution against fecal impaction
● Hemodynamially unstable patient (low blood pressure, changes mental status,
dysrhythmia) IV dextrose 50% insukin, and calcium replacement may be given to
shift potassium back into the cells
● Arrangement for dialysis need to be made on an emergent basis
● Dosages must be reduced, example antibiotic medications (especially
aminoglycosides) digoxin (Lanoxin), phenytoin (Dilantin), ACE inhibitors and
magnesium-containing agents
● Diuretic agents are often used to control fluid volume, but they have shown to
improve recovery from AKI
● In patients with severe Acidosis, arterial blood gases and serum bicarbonate
levels (CO2) must be monitored; sodium bicarbonate therapy or dialysis
● In respiratory problems, appropriate ventilator measures must be instituted
● Elevated serum phosphate level may be controlled with phosphate-binding
agents (e.g., calcium or lanthanum carbonate) help prevent a continuing rise in
serum phosphate levels by decreasing the absorption of phosphate from the
intestinal tract
Assessment and Diagnostic Findings
● Assessment of the patient with AKI includes evaluation for changes in the urine,
diagnostic test that evaluate kidney contour and a variety of laboratory values for
information about the normal characteristics of urine, diagnostic findings, and
laboratory values in the renal system.
● In AKI, urine output varies from scanty to a normal volume, hematuria may be present,
and the urine has a low specific gravity.
● One of the earliest manifestations of tubular damage is the inability to concentrate the
urine. Patients with prerenal azotaemia usually have urinary sodium levels greater than
40 mEq/L with urinary casts and other cellular debris.
● Ultrasonography is a critical component of the evaluation of the patients with kidney
disease. A renal sonogram or a CT or MRI scan may show evidence of anatomic
changes.
● Serum creatinine levels are useful in monitoring kidney function and disease
progression and increase in glomerular damage.
● Anemia is another common laboratory finding in AKI, as a result of reduce
erythropoietin production, uremic GI lesions, reduced RBC lifespan and blood loss from
the GI tract.
Nutritional Therapy
● In patient with AKI on renal replacement therapy, a caloric intake of 25 to 30 kcal/kg
and a minimum amount of 1.5 g/kg day of protein is recommended to minimize protein
catabolism and prevent metabolic complications.
● Nutritional support is based on the underlying cause of AKI, the catabolic response, the
type and frequency of renal replacement therapy, comorbidities and nutritional status.
● Caloric requirements are met with high-carbohydrate meals because carbohydrates
have a protein- sparing effect.
● Foods and fluids containing potassium or phosphorus.
● The oliguric phase of AKI may last 10 to 14 days and is followed by the diuretic phase
at which time urine output begins to increase, signalling the patient is in the recovery
phase.
● Results of blood chemistry tests are used to determine the amounts of sodium,
potassium and water needed for replacement, along with assessment for over or
underhydration.
● Following the diuretic phase, the patient is placed on a high protein, high calorie diet
and is encouraged to resume activities gradually.