Acute Kidney Failure

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INTRODUCTION:

 Acute kidney failure happens when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and
waste materials from the blood. This elimination is the core of your kidneys’ main function.

 Body fluids can rise to dangerous levels when kidneys lose their filtering ability. The condition will also cause
electrolytes and waste material to accumulate in your body, which can also be life-threatening.

 Acute kidney failure is also called acute kidney injury or acute renal failure. It’s common in people who are
already in the hospital. It may develop rapidly over a few hours.

 It can also develop over a few days to weeks. People who are critically ill and need intensive care have the
highest risk of developing acute kidney failure.

 Acute kidney failure can be life-threatening and requires intensive treatment. However, it may be reversible. If
you’re in good health otherwise, recovery is possible.

EPIDEMIOLOGY:

 In the United States, approximately 1% of patients admitted to hospitals have AKI at the time of admission. The
estimated incidence rate of AKI during hospitalization is 2-5%.

 AKI develops within 30 days postoperatively in approximately 1% of general surgery cases and arises in more
than 50% of intensive care unit (ICU) patients. In recipients of solitary kidney transplants, 21% developed AKI
within the first 6 months after transplantation.

 Harding et al calculated that in the US from 2000 to 2015, hospitalization rates for dialysis-requiring AKI in
adults increased considerably while mortality decreased.

 It occurs in – 5%of all hospitalized patients and – 35% of those in intensive care units • Mortality is high: • up to
75–90% in patients with sepsis • 35–45% in those without

 Median hospital length of stay (LOS) stratified by single acute organ system dysfunction (AOSD), including
acute renal failure (ARF).

PATHOPHYSIOLOGY:

In view of the different clinical presentations, ARF in the NS is not a single, uniform pathophysiological entity.
Factors that can be singled out to contribute to the decrease in glomerular filtration rate (GFR) are a low renal
perfusion pressure, a decreased filtration coefficient, high intratubular pressure, ATN, interstitial nephritis and
interstitial oedema.

In the case of overt hypotension, a pre‐renal cause can be suspected. This is encountered particularly in children with
persistent proteinuria that is so severe that blood volume cannot be maintained, such as in congenital NS. In children
with relapsing minimal lesion NS, hypovolemic ARF may be encountered early during a relapse. The acute start of
heavy proteinuria probably causes a disequilibrium between plasma and interstitial albumin concentrations. However,
when plasma protein drops, proteinuria diminishes, and is often insufficient to remain a threat for hypovolemia as in
congenital NS. We have tried to amend this in children presenting with early relapse of minimal lesion NS . Half of
them had ‘hypovolemic symptoms’. Compared with non‐symptomatic children, they had stimulated neurohumoral
factors and strong tubular sodium reabsorption, and a suppressed urinary dilution capacity, compatible with the
presence of a pre‐renal factor. However, even in these children renal plasma flow was high, and the decreased GFR
thus reflected a decreased filtration fraction.
In adults, proteinuria is generally not marked enough to endanger the circulation. Relapses of minimal lesion NS
develop more slowly, but may occasionally be acute, as occurs in children. It cannot be excluded, however, that adults
with established NS are more liable to develop ARF if they suffer from some other complications such as septicaemia
or blood loss. Indeed, blood volume that is normal while recumbent may drop below normal when standing. On the
other hand, mobilization of excess tissue fluid in hypoproteinemic conditions is highly efficient. Excess fluid can
mostly be removed without inducing hypotension or renal failure. However, complete removal of excess fluid may
create an unsteady condition were changes in blood volume cannot be compensated.

Approximately 30% of children and adults with idiopatic NS have a significant decrease in GFR. This is due to an
intrinsic filtration impairment, since filtration fraction is low. Conceivably, ARF may reflect worsening of this
intrinsic problem. However, glomerular changes, i.e. obliteration of epithelial slit pores as visible with electron
microscopy, are not correlated with the reduction in GFR in humans. Filtration can also be impaired by a high
intratubular pressure caused by protein casts, but this possibility has received little attention. The following case
history illustrates the possible importance of this factor.

CLINICAL MANIFESTATION:

You may not have any symptoms of acute kidney failure. Your doctor may discover you have this condition while
doing lab tests for another reason.If you do have symptoms, they’ll depend on how bad your loss of kidney function is,
how quickly you lose kidney function, and the reasons for your kidney failure. Symptoms may include:

 Peeing less than normal

 Swelling in your legs, ankles, and feet (caused by your body holding on to fluid)

 Feeling drowsy or very tired

 Shortness of breath

 Itching

 Joint pain, swelling

 Loss of appetite

 Confusion

 Throwing up or feeling like you’re going to

 Chest pain or pressure

 Muscle twitching

 Seizures or coma (in severe cases)

 Stomach and back pain

 Fever

 Rash

 Nosebleed
TYPES:

AKI occurs in three types—prerenal, intrinsic, and postrenal.


AKI has four phases.

1. Onset phase: Kidney injury occurs.


2. Oliguric (anuric) phase: Urine output decreases from renal tubule damage.
3. Diuretic phase: The kidneys try to heal and urine output increases, but tubule scarring and damage occur.
4. Recovery phase: Tubular edema resolves and renal function improves.

CAUSES:

There are three main reasons your kidneys fail all of a sudden. Something is stopping blood flow to your kidneys. It
could be because of:

 An infection

 Liver failure

 Medications (aspirin, ibuprofen, naproxen, or COX-2 inhibitors like Celebrex)

 Blood pressure medications

 Heart failure

 Serious burns or dehydration

 Blood or fluid loss

 You have a condition that’s blocking urine from leaving your kidneys. This could mean:

 Bladder, cervical, colon, or prostate cancer

 Blood clots in your urinary tract

 An enlarged prostate

 Kidney stones

 Nerve damage in your bladder

 Something has directly damaged your kidneys, like:

 Blood clots

 Cholesterol deposits

 Medications that can directly damage kidneys, including NSAIDs like ibuprofen and naproxen, chemotherapy,
and antibiotics

 Glomerulonephritis (inflamed kidney filters; can be caused by an infection, autoimmune


disease (like lupus), multiple myeloma, scleroderma, chemotherapy drugs, antibiotics, or other toxins)
RISK FACTORS:

Most of the time, kidney failure happens along with another medical condition or event. If you fall into any of the
following categories, you may have a greater chance of acute kidney failure:

 You’ve been hospitalized for a long time, especially in intensive care.

 You have diabetes.

 You’re elderly.

 You have coronary artery disease.

 You have heart failure or high blood pressure.

 You have chronic kidney or liver disease.

DIAGNOSTIC ASSESSMENT:

 Creatinine is a waste product in your blood that’s made by muscle activity. Normally, it’s removed from your
blood by your kidneys. But if your kidneys stop working, your creatinine level rises.

 Urea nitrogen is another waste product in your blood. It’s created when protein from the foods is broken down.
Like creatinine, your kidneys remove this from your blood. When your kidneys stop working, your urea nitrogen
levels rise.

 Serum potassium is a substance found in your blood that balances water levels in your bloodstream. Kidney
disease can cause either high or low potassium levels.

 Serum sodium is another substance in your blood that helps with fluid balance in your body. High sodium levels
can mean that your kidneys aren’t working properly because your body can’t get rid of the right amount of
sodium.

 Urine tests. Your doctor will check your pee for blood and protein. They’ll also look for certain electrolytes. The
results help your doctor understand what’s causing your kidney failure.

 Urine output measurement. This measures how much urine you pass in 24 hours. You will get a container to take
home, pee into, and then return to the lab after a full 24 hours. It can help your doctor determine why you’re
having kidney failure.

 Kidney biopsy (renal biopsy) is a procedure where the doctor pushes a thin needle through your skin and takes a
small piece of your kidney to look at under a microscope. It can show if there is any damage or disease in your
kidney.

 Imaging tests. Some tests, like ultrasonography or a CT scan, can show whether your kidneys are enlarged or
there’s a blockage in your urine flow. An angiogram can tell your doctor if the arteries or veins that lead to your
kidneys are blocked. An MRI can show this, too.

MEDICAL MANAGEMENT:

The treatment will depend on the cause of acute kidney failure. The goal is to restore normal kidney function.
Preventing fluids and wastes from building up in body while kidneys recover is important. In the majority of cases, a
kidney specialist called a “nephrologist” makes an evaluation.

Diet:

The doctor will restrict diet and the amount of liquids eat and drink. This will reduce the buildup of toxins that the
kidneys would normally eliminate. A diet high in carbohydrates and low in protein, salt, and potassium is usually
recommended.
Medications:

The doctor may prescribe antibiotics to treat or prevent any infections that occur at the same time. Diuretics may help
kidneys eliminate fluid. Calcium and insulin can help avoid dangerous increases in blood potassium levels.

Dialysis

It may need dialysis, but it’s not always necessary, and it will likely only be temporary. Dialysis involves diverting
blood out of body into a machine that filters out waste. The clean blood then returns to body. If your potassium levels
are dangerously high, dialysis can save life. Dialysis is necessary if there are changes in mental status or if you stop
urinating.it may also need dialysis if develops pericarditis or inflammation of the heart. Dialysis can help eliminate
nitrogen waste products from body.

COMPLICATION:

Acute kidney failure can sometimes cause complications. These include:

 Fluid buildup. Acute kidney failure can sometimes cause a buildup of fluid in your body. If fluid builds up in
your lungs, this can cause shortness of breath.

 Chest pain. If the lining that covers your heart becomes inflamed, you may have chest pain.

 Acidic blood (metabolic acidosis). If your blood has too much acid due to acute kidney failure, you can end up
with nausea, vomiting, drowsiness, and breathlessness.

 Muscle weakness. When your body's fluids and electrolytes are out of balance, you can get muscle
weakness. In serious cases, this can lead to paralysis and heart rhythm problems.

 Permanent kidney damage. Acute kidney failure can become chronic and your kidneys will stop working
almost entirely or completely. This is called end-stage renal disease. If this happens, you will need to go on
permanent dialysis (to filter your blood and remove toxins) or get a kidney transplant.

 Death. Acute kidney failure can lead to loss of kidney function that is so bad, it can cause death.

PREVENTION:

 Be careful when taking over-the-counter (OTC) pain medications. Whether you are taking NSAID medications
like aspirin, ibuprofen, and naproxen or other types of OTC pain medications like acetaminophen, it’s important
to read and follow the recommended dosing instructions on the package. If you take too much of these meds, you
could increase your chances of getting acute kidney failure.

 Follow your doctor’s advice. If you have a higher risk of getting acute kidney failure because of pre-existing
kidney disease or other conditions, make sure to follow your doctor's advice for treating and managing your
condition.

 Keep a healthy lifestyle. Exercise, eating right, and drinking little or no alcohol can go a long way to preventing
acute kidney failure.
NURSING MANAGEMENT:
The nurse has an important role in caring for the patient with ARF.

Nursing Assessment

Assessment usually focuses on the characteristics of the urine.

 Assess urine output. Urine output varies from scanty to a normal volume.

 Assess blood in the urine. Hematuria may be present in patients with ARF.

 Assess laboratory results. Laboratory results may increase, decrease, or stabilize and these may indicate each
phase of ARF.

Nursing Diagnosis
Based on the assessment data, appropriate nursing diagnoses for a patient with ARF include:

 Electrolyte imbalance related to increased potassium levels.


 Risk for deficient volume related to increased in urine output.
The goals for a patient with ARF are:

 Improve nutritional intake.


 Restore fluid balance.
 Reduce metabolic rate.
 Promote pulmonary function.
 Prevent infection.

Nursing Interventions
Nursing interventions are aimed at restoring renal function and reducing potential causes of increased renal injury.

 Monitor fluid and electrolyte balance. The nurse monitors the patient’s fluid and electrolyte levels and
physical indicators of potential complications during all phases pf the disorder.
 Reducing metabolic rate. Bed rest is encouraged and fever and infection are prevented or treated promptly.
 Promoting pulmonary function. The patient is assisted to turn, cough, and take deep breaths frequently to
prevent atelectasis and respiratory tract infection.
 Preventing infection. Asepsis is essential with invasive lines and catheters to minimize the risk of infection
and increased metabolism.
 Providing skin care. Bathing the patient with cool water, frequent turning, and keeping the skin clean and well
moisturized and keeping the fingernails trimmed to avoid excoriation are often comforting and prevent skin
breakdown.
 Provide safety measures. Patient with CNS involvement may be dizzy or confused.

Evaluation
A successful nursing care plan has achieved the following:

 Improved nutritional intake.


 Restored fluid balance.
 Reduced metabolic rate.
 Promoted pulmonary function.
 Prevented infection.
Discharge and Home Care Guidelines
The nurse plays an important role in teaching the patient and family with ARF.

 Nutrition. A referral to the nutritionist is made because of the dietary changes required.
 Problems to report. The patient and family must know what problems to report to the healthcare provider.
 Follow-up examinations. The importance of follow-up examinations and treatment is stressed to the patient
and family because of changing physical status and renal functions.

Documentation Guidelines
The focus of documentation in a patient with ARF include:

 Vital signs.
 Muscle strength and reflexes.
 Results of laboratory tests and diagnostic studies.
 Degree of deficit and current sources of fluid intake.
 I&O and fluid balance.
 Plan of care.
 Teaching plan.
 Client’s responses to treatment, teaching, and actions performed.
 Attainment or progress towards the desired outcomes.
 Modifications to plan of care.
 Long term needs.

SUMMARY:

Acute renal failure is caused by damage to the kidneys, which can occur as a result of blood loss, toxins, or physical
damage to the kidneys. Acute renal failure occurs rapidly, causing generalized symptoms, such as nausea and
confusion.1 It is a serious condition, but it can be treated. With proper treatment, most people can survive an episode
without long-term consequences.

CONCLUSION:

Acute renal failure is a serious medical condition that could complicate the course of many of your patients. The
mortality rate from acute tubular necrosis is around 50% and hasn't changed much over the past 3 decades, despite
significant advances in supportive care. Mortality rates differ, however, depending on the cause of renal failure; rates
around 15% in obstetric patients, around 30% in toxin-related acute renal failure, and around 60% after trauma or
major surgery. Oliguria (<400 mL per day) at presentation, a rise in serum creatinine of greater than 3 mg/dL, old age,
and multiorgan failure portend a grave prognosis.[8] Patients with acute renal failure are also at high risk for infections;
in fact, infection is the leading cause of death among these patients. So limit invasive procedures and try not to use
indwelling urinary catheters.
BIBLIOGRAPHY:

 Kuruvilla, Jaya. Essentials of Critical Care Nursing. 1st edition, Jaypee Brothers,Medical Publishers
Pvt.Limited, 2007, pp. 632–45.

 Chintamani, Mani M. Lewis’s Medical-Surgical Nursing, Third South Asia Edition - E-Book. 3rd edition.
Elsevier Health Sciences; 2018, pp.1525-1530.

 Brunner suddarth. Brunner and Suddarth’s Textbook of Medical surgical Nursing. 13th edition. washington:
wolters kluwer; 2014, pp.504-520.

 Meducationdotnet. Acute renal failure [Internet]. Share and Discover Knowledge on SlideShare. 2016 [cited
2021 Apr 27]. Available from:https://www.slideshare.net/meducationdotnet/airway management-57321289.

 Reza Aminnejad. Acute renal failure [Internet]. Share and Discover Knowledge on SlideShare. 2017 [cited
2021 Apr 27]. Available from: https://www.slideshare.net/rezaaminnejad/airway-management-79135709.

 Contributors to Wikimedia projects. Acute renal failure - Wikipedia [Internet]. Wikipedia, the free
encyclopedia. Wikimedia Foundation, Inc.; 2004 [cited 2021 Apr 27]. Available
from:https://en.wikipedia.org/wiki/Airway_management.

 Reynolds SF, Heffner J. Acute renal failure of the critically ill patient. Chest. 2005 Apr 1;127(4):1397-412.

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