Group Assignment

NURSING CARE IN ACUTE RENAL FAILURE

By group 7
Agustinus E Koyari
Hilan Sasewa
Sudiman Hataul
Anuggrawati S

PROGRA STUDI ILMU KEPERAWATAN

FAKULTAS KEDOKTERAN
UNIVERSITAS CENDERAWASIH
JAYAPURA
2023
p

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Translated from Indonesian to English - www.onlinedoctranslator.com

PIG
INTRODUCTION
1.1 Background
In developed countries, chronic non-communicable diseases, especially
cardiovascular disease, hypertension, diabetes mellitus and chronic kidney disease,
have replaced communicable diseases as the main public health problem.
Impaired kidney function can describe the condition of the vascular system so
that it can help efforts to prevent disease early before patients experience more severe
complications such as stroke, coronary heart disease, kidney failure and peripheral
vascular disease.
Kidney failure or acute kidney injury (AKI), which was previously called
acute renal failure (ARF), can be defined as a rapid/sudden or severe decrease in
kidney filtration function. This condition is usually characterized by an increase in
serum creatinine concentration or azotemia (increased BUN (blood Urea Nitrogen)
concentration). After kidney injury occurs, the BUN concentration level returns to
normal, so that the benchmark for kidney damage is a decrease in urine production.
The death rate in the US due to acute kidney failure ranges from 20-90%.
Deaths in hospitals are 40-50% and in the ICU are 70-89%. An increase of 0.3 mg/dL
in serum creatinine is of significant prognostic significance. Increased creatinine
levels can also be caused by drugs (eg cimetidine and trimehoprim) that inhibit renal
tubular secretion. Increased BUN values can also occur without kidney damage, such
as mucosal or digestive tract bleeding, steroid use, protein intake. Therefore, careful
assessment is needed to determine whether someone has kidney damage or not.

1.2 Formulation of the problem

1. What is the definition of acute renal failure?
2. What is the epidemiology of acute renal failure?
3. What is the etiology of acute renal failure?
4. What are the clinical manifestations of acute renal failure?
5. What is the pathophysiology of acute renal failure?
6. What is the pathway to acute renal failure?
7. How is Acute Kidney Failure Tested?

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 8. What are the complications of acute kidney failure?
9. How is Acute Kidney Failure Treated?

1.3 Problem Objectives

1. To Know the Definition of Acute Renal Failure
2. To Understand the Epidemiology of Acute Renal Failure
3. To Know the Etiology of Acute Kidney Failure
4. To Know the Clinical Manifestations of Acute Renal Failure
5. To Understand the Pathophysiology of Acute Renal Failure
6. To Know the Pathway of Acute Renal Failure
7. To find out the examination of acute renal failure
8. To Know Complications of Acute Kidney Failure
9. To Know the Management of Acute Kidney Failure

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 CHAPTER II
THEORETICAL BASIS
2.1 Definition

Physiologically, the kidneys have multifunctions to regulate balance in the

body. As the main organ of filtration, the kidneys have an extraordinary effect, so
they maintain body circulation and remove all forms of toxins. Therefore,
disturbances in the filtration process will trigger systemic and local disturbances.
Acute renal failure is a disruption in kidney function that occurs suddenly with typical
symptoms in the form of oliguria / anuria with an increase in BUN (Blood Ureum
Nitrogen) or serum creatinine. In general, acute kidney failure is also referred to as
Acute Renal Faiure (ARF) or Acute Kidney Injury (AKI) (Graber, 2006; Wilcox,
2009).
Epidemiologically, acute renal failure (Acute Renal Faiure) is a kidney
disorder that is often caused by changes in age. An increase in the number of
traumatic injuries to the kidney also influences the incidence of acute renal failure. If
we examine kidney failure more deeply, it is actually a disease that occurs due to
primary comorbidities. Healthy living behavior in maintaining fluid and electrolyte
balance will improve kidney function. Failure of kidney function will result in

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systemic disorders, so that the body's hemodynamics will decrease and become life
threatening. In laboratories, a striking change in clients with kidney failure is serum
creatinine levels (Hoste, 2007)
Acute kidney injury (formerly known as acute renal failure) is a syndrome
characterized by rapid loss of renal excretory function and is usually diagnosed by the
accumulation of end products of nitrogen metabolism (urea and creatinine) or
decreased urine output, or both. It is a clinical manifestation of several disorders
affecting the acute kidney. Acute kidney injury is common in hospital patients and
very common in critically ill patients. In these patients, it most often occurs secondary
to extrarenal events. How such events lead to acute kidney injury is controversial. No
specific therapies have emerged that can reduce acute kidney injury or speed
recovery; Thus, treatment is supportive. New diagnostic techniques (e.g., renal
biomarkers) may aid early diagnosis. Patients are administered renal replacement
therapy if the acute kidney injury is severe and biochemical or volume-related, or if
complications related to uraemictoxaemia are a concern. If patients survive their
disease and do not have chronic premorbid kidney disease, they usually recover to
dialysis independence. However, evidence suggests that patients who have had acute
kidney injury are at increased risk of subsequent chronic kidney disease. ( Evidence
suggests that patients who have had acute kidney injury are at increased risk of
subsequent chronic kidney disease. ( Evidence suggests that patients who have had
acute kidney injury are at increased risk of subsequent chronic kidney disease.
(Lancet2012; 380: 756–66)
Acute kidney injury (AKI) is a global public health problem associated with
morbidity, mortality, and high healthcare costs. Apart from dialysis, there are no
therapeutic interventions that can improve survival, limit injury, or speed recovery.
Despite acknowledged shortcomings in in vivo animal models, the pathophysiology
underlying AKI and its consequence, chronic kidney disease (CKD), is rich in
biological targets. We review recent findings related to renal vascularization and the
cellular stress response, especially the intersection of the unfolded protein response,
mitochondrial dysfunction, autophagy, and the innate immune response. Maladaptive
repair mechanisms that persist after the acute phase promote inflammation and
fibrosis in the chronic phase. Here macrophages, growth-arrested tubular epithelial
cells, endothelium, and surrounding pericytes are key players in the development of

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 chronic disease. A better understanding of these complex interacting
pathophysiological mechanisms, their relative importance in humans, and the utility
of biomarkers will lead to therapeutic strategies to prevent and treat AKI or inhibit
progression to CKD or end-stage renal disease (ESRD). (Annu. Rev. Med. 2016.
67:293–307)

2.2 Epidemiology
The ideas described have led to a consensus definition of acute kidney injury
by the Acute Dialysis Quality Initiative. These RIFLE (risk, injury, failure, loss, late
stage) criteria have been widely supported with minor modifications by the Acute
Kidney Injury Network, and both definitions have now been validated in thousands of
patients3 and appear to perform similarly to each other. A new consensus definition
combining the RIFLE Criteria and the Acute Kidney Injury Network definition has
emerged from the Kidney Disease: Improving Global Outcomes (K-DIGO) group.
Acute kidney injury is a common and important diagnostic and therapeutic
challenge for physicians. Incidence varies between definitions and populations, from
more than 5000 cases per million person-years for acute kidney injury without
dialysis, to 295 cases per million person-years for dialysis-requiring disease. This
disorder has a frequency of 1·9% in hospital inpatients4 and is very common in
critically ill patients, among whom the prevalence of acute kidney injury is greater
than 40% on admission to the intensive care unit in the presence of sepsis. Occurs in
greater than 36% on the day after admission to the intensive care unit, and prevalence
is greater than 60% during intensive care unit stay.
Some causes of acute kidney injury are highly prevalent in some geographic
settings. For example, cases associated with secondary hypovolemia Diarrhea are
common in developing countries, whereas open heart surgery is a common cause in
developed countries. Furthermore, in certain countries, certain disorders are common
in society, whereas others only appear in hospitals. Thus, any diagnostic approach to
the causes or triggers of acute kidney injury must consider the local context and
epidemiology.
(Lancet2012; 380: 756–66).

2.3 Etiology

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 1. Prerenal causes (kidney hypoperfunction occur) due to conditions that cause
reduced renal blood flow and decreased glomerular filtration. Volume
depletion states (hypovolemia such as burns and bleeding or fluid loss through
the digestive tract), vasodilation (sepsis and anaphylaxis), cardiac dysfunction
(myocardial infarction, CHF, or cardiogenic shock), and diuretic therapy. This
is usually characterized by decreased skin turgor, dry mucous membranes,
weight loss, hypertension, oliguria, or anuria.
2. Intrarenal causes actual damage to kidney tissue due to trauma to the
glomerular tissue or renal tubules. Conditions related to intrarenal ischemia,
toxins, immunological, systemic and vesicular processes. Use of non-steroidal
anti-inflammatory drugs (NSAIDs), especially in elderly patients because they
interfere with prostaglandins which protect renal flow. NSAIDs cause renal
ischemia. Injuries due to burns and impacts cause the release of hemoglobin
and myoglobin (proteins released from muscles when injured, resulting in
renal toxicity, ischemia, or both). Injuries due to impact and infection as well
as nephrotoxic agents cause acute tubular necrosis (ATN). In addition, the
transfusion reaction causes intrarenal failure where hemoglobin is released
through a hemolysis mechanism across the glomerular membrane and
concentrates in the renal tubules.
3. Post renal causes occur due to blockage or disruption of the flow of urine
through the urinary tract (blockage of the distal part of the kidney). The
pressure in the tubules increases so that the glomerular filtration rate increases.
This is usually characterized by difficulty emptying the bladder and changes in
urinary flow.

2.4 Clinical Manifestations

1. The patient appeared extremely miserable and lethargic with persistent nausea,
vomiting, and diarrhea.
2. The mouth and mucous membranes are dry due to dehydration, and the breath
may smell like urine (fetouremic).
3. Nervous system manifestations (weakness, headache, muscle twitching, and
seizures).

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 4. Changes in urine output (slight, may contain blood, BJ slightly low, namely
1,010) (Brunner and Suddarth, 2001).
5. The increase in BUN (fixed), creatinine levels and erythrocyte sedimentation
rate (ESR) depends on catabolism (protein breakdown), renal perfusion and
protein intake. Serum creatinine increases in glomerular damage.
6. Hyperkalemia due to decreased glomerular filtration rate as well as protein
catabolism results in the release of cellular potassium into body fluids.
Hyperkalemia causes cardiac dysrhythmias. Sources of potassium include
normal tissue catabolism, such as dietary intake, blood in the gastrointestinal
tract, or blood transfusions and other sources (intravenous infusion, penicillin
potassium, and extracellular exchange in response to metabolic acidosis).
7. Metabolic acidosis, due to acute oliguria, the patient is unable to eliminate
metabolic loads such as acid-type substances formed by normal metabolic
processes. A decrease in the kidney buffer mechanism is characterized by a
decrease in carbon dioxide and blood pH. Metabolic acidosis accompanies
renal failure.
8. Abnormalities in Ca++ and PO4- increases in serum phosphate concentrations
may occur. Serum calcium may decrease in response to decreased intestinal
absorption of potassium and as a compensatory mechanism for increased
serum phosphate levels.
9. Anemia occurs due to decreased erythropoietin production, digestive tract
lesions, decreased red blood cell life, and blood loss (usually from the
digestive tract).

2.5 Pathophysiology
The condition of acute kidney failure is caused by 3 trigger factors, namely
pre-renal, renal and post-renal. These three factors have different relationships. Pre-
renal is related to conditions where blood flow to the kidneys decreases (hyperfusion).
This condition is triggered by hypovolemia, hypotension, vasoconstriction and
decreased cardiac output. With this condition, the GFR (Glomerular Filtration Rate)
will decrease and tubular reabsorption will increase. Renal factors are related to
damage to the renal parenchymal tissue. This damage is triggered by trauma or
diseases of the kidney itself, the tissue which is the main physiological location of the

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kidney, if damaged it will affect the function of the kidney. Meanwhile, post renal
factors are related to the presence of obstruction in the urinary tract, So there will be
stagnation and even reflux of urine flow in the kidneys. In this way, the burden of
kidney resistance will increase and eventually fail (Judith, 2005).
The pathogenesis of inflammatory renal parenchymal diseases (e.g.
glomerulonephritis and vasculitis) is complex and involves nearly all aspects of the
innate inflammatory system and antibody-mediated and immune-mediated ammatory
cell mechanisms. 11-11 In this Seminar, we focus on acute kidney injury secondary to
prerenal factors. as this form is the most common in developed countries, hospitalized
inpatients, and especially in critically ill patients. Most of our understanding of the
pathophysiology of acute prerenal acute kidney injury comes from work in animals.
18,19 Study models of acute ischemia induced by acute occlusion of renal arteries
many possible pathways involved and mechanisms of organ injury. 20,21 The
coagination system is activated locally, 22 leukocytes infiltrate the kidney, 23 the
endothelium is wound24 and adhesion molecules state, 25 cytokines were released, 26
toll receptors were induced, 27 intrarenal vasoconstrictor pathways were activated, 28
and apoptosis was induced. 29 Associated changes also occur in tubular cells with
loss or reversal of polarity30 and loss of adhesion to the basement membrane.20
Renal injury appears to trigger organ injury elsewhere (so-called cross-organ talk) 31
through unclear pathways, further emphasizing the complexity of the response
biologics for acute kidney injury. Unfortunately, this ischemic model has little clinical
relevance to diseases such as sepsis. 32.33 Sepsis is the most common trigger of acute
kidney injury in hospitals 29 Associated changes also occur in tubular cells with loss
or reversal of polarity30 and loss of adhesion to the basement membrane.20 Renal
injury appears to trigger organ injury elsewhere (so-called cross-organ talk) 31
through unclear pathways, further emphasizing the complexity of the response
biologics for acute kidney injury. Unfortunately, this ischemic model has little clinical
relevance to diseases such as sepsis. 32.33 Sepsis is the most common trigger of acute
kidney injury in hospitals 29 Associated changes also occur in tubular cells with loss
or reversal of polarity30 and loss of adhesion to the basement membrane.20 Renal
injury appears to trigger organ injury elsewhere (so-called cross-organ talk) 31
through unclear pathways, further emphasizing the complexity of the response
biologics for acute kidney injury. Unfortunately, this ischemic model has little clinical

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relevance to diseases such as sepsis. 32.33 Sepsis is the most common trigger of acute
kidney injury in hospitals This ischemic model has little clinical relevance to diseases
such as sepsis. 32.33 Sepsis is the most common trigger of acute kidney injury in
hospitals This ischemic model has little clinical relevance to diseases such as sepsis.
32.33 Sepsis is the most common trigger of acute kidney injury in hospitals

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 2.6 GGA pathway

Pre Renal Renal Post Renal

ACUTE KIDNEY FAILURE

Filtration Disorders Reabsorption disorders Ammonia excretion

Decreased
dysfunction
bicarbonate
secretion
Hypofiltration Hypernatremia Ammonia retention

Decreased urine excretion H2O levels increase Capillary permeability

pH drops
is impaired

Oliguria, Anuria
Edema Metabolic acidosis

MK: DISORDERS OF Decreased circulating

URINE oxygenation
Compensation
ELIMINATION MK: EXCESS FLUID
mechanism
VOLUME
hypoxemia

Accumulation of residual urine hyperventilation

Cell hypoxia

Accumulation of metabolic waste MK:

substances MK: INEFECTIVITY OF PERFUSION INEFFECTIVENE
OF PERIPHERAL TISSUE SS OF BREATH

Intoxication PATTERN

Muscle work increases O2 and CO2

Circulation
balance

Lactic acid deposits increase

Dry, itchy, pale, purpura skin
MK : GG. GAS
EXCHANGE
MK: DAMAGE TO SKIN fatigue
INTEGRITY

Energy balance
MK: INTOLERANCE
OF ACTIVITIES
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2.7 Inspection
The clinical examination required to establish a diagnosis of acute renal failure is
(Anymous, 2008; Judith, 2002):
1. Blood chemistry levels
Includes sodium, potassium, ureum, cretinin and bicarbonate. Usually sodium
decreases (< 20 mmol / I). while urea will increase (> 8) which will affect the
RAA (Renin Angiotension Aldosterone) system.
2. Urinalist
Chemical analysis examination of urine to see kidney function
3. Ultrasonography (USG)
This is to obtain supporting data regarding kidney size, obstruction of the
urinary tract, hydronephoris, and diseases of the lower urinary tract.
Ultrasound is also used for complications of kidney failure, for example
cardiomegaly and pulmonary edema
4. Whole blood
The specific results from the results of a complete blood test in clients with
acute renal failure are:
a. Increased BUN (Blood Urea Nitrogen) levels
b. Increased serum creatinine levels
c. Increased potassium levels
d. Decreased blood PH
e. Decreased bicarbonate levels
f. Decreased hematocrit levels and hemoglobin levels
In acute renal failure, normochrome anemia rarely occurs. However,
chronic kidney failure often occurs. Usually there is thrombocytopenia, red
blood cell fragmentation and hemolytic uremic syndrome.
5. ECG (electrocardiography)
Usually indicates cardiac ischemia with symptoms of bradycardia and
widening of the QRS complex.

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2.8 Complications
As a vital organ that maintains body homeostasis, the kidneys regulate several
regulatory processes. Therefore, disruption of the function/failure of physiological
function in the kidneys will have an impact on an imbalance in the body's circulation
and metabolism. The following are several potential complications that can occur in
patients with acute renal failure (Leppert, 2004):
1. Body electrolyte balance
a. Hyperkalemia
b. Hyponatremia
c. Metabolic acidosis
d. Hypocalcemia
e. Hyperphosphatemia
f. Hypermagnesia
2. Heart and lung function
a. Pulmonary edema
b. Pericarditis
c. Hypertension
3. Gastrointestinal
a. Nausea
b. Vomiting
c. Anorexia
d. Bleeding
4. Hematology
a. Anemia
b. Platelet dysfunction
5. Neurological
a. Dizzy
b. Obtundation
c. Asterixis
d. Myoclonus
e. Seizures
f. Dialytc

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 6. Infections of the urinary tract, lungs, surgical wounds, and sepsis
7. Drug intoxication

2.9 Management
Management of clients with acute kidney failure is carried out comprehensively
from medical disciplines, nurse practitioners, nutritionists and so on. The following is
management management for clients with acute kidney failure (Judith, 2002):
1. General management
In general, what must be done for clients with acute kidney failure is to strictly
implement and monitor a diet high in calories and low in protein, sodium,
potassium, with additional vitamin supplements. And the most important thing is
to limit fluid intake. To control imbalanced electrolyte levels in the body, dialysis
(hemodilysis / peritoneal dialysis) is required.
2. Medical management
The use of medical therapy in acute renal failure is primarily intended to
maintain fluid volume in the body in accordance with renal compensation and
maintain the acid-base condition of the blood.
a. Furosemide, administration of 20 to 100 mg IV every 6 (six) hours will
maintain fluid volume stability in the body
b. Calcium guconate, giving 10 ml / 10% in solute infusion (IV) fluid will
help potassium levels
c. Sodium polystyrene, 15 gr in a dose 4 times a day mixed in 100 ml of 20%
sorbitol, 30 to 50 gr in 50 ml of 70% sorbitol and 150 ml in water will
maintain potassium levels.
d. Sodium bicarbonate, this administration will overcome the condition of
metabolic acidosis
3. Close observation
Laboratory examination results (BUN, creatinine and potassium levels) must
be monitored closely. This is very meaningful in maintaining the client's life.

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 CHAPTER III
NURSING CARE THEORY
3.1 Assessment
A. Assessment
In the study of determining nursing problems in kidney failure patients,
there are several basic studies that must be carried out to produce focused data,
both subjective and objective. The following are several anamnesis and
physical studies on clients with kidney failure (Kahan, 2009).
1. Assess vital signs to detect hypo/hypertension, hypo/hyperthermia,
tachycardia or respiratory distress caused by decreased cardiac output:
In clients with kidney failure where systemic circulation is
impaired/decreased, this will have an impact on blood flow in the
circulation which will also decrease (cardiac output decrease).
However, it should be noted that clients who are hospitalized in the
acute phase often experience increased metabolism and increased fluid
requirements due to the impact of secondary conditions of the disease,
for example sepsis and post-operative complications.
2. Analyze and calculate urine output accurately:
It is recommended to objectively calculate urine output in
clients with kidney failure by making a draft on a sheet of urine output
observation paper. This will be useful for knowing kidney function in
terms of excretion and how much fluid is retained in the body.
3. Assess fluid intake (food, drinks, parenteral fluid therapy and other
sources of input):
Urine output is influenced by the amount of fluid input.
Therefore, calculating the balance between input and output will
provide accurate information in determining kidney function.
4. Assess history of disorders in urine elimination:
Assess for hesistance, urgency, dissatisfaction after urination,
dysuria, hematuria, difficulty in urinating, history of prostate disease
(BPH).
5. Assess the history of other diseases that affect kidney function:

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 This is to explore whether impaired kidney function is caused
by prenatal, renal or post-renal factors. Several diseases that can cause
complications of kidney failure include hypertension, diabetes
mellitus, congestive heart failure (chronic heart failure), and SLE
(System Lupus Erythematous).
6. Review your history of drug use:
Drugs that have nephrotoxic side effects will impact kidney
function disorders if consumed in the long term and especially if they
are not controlled by medicine, for example NSAIDs, ACE inhibitors,
anminoglycosides.
7. Assess the history of differences in the pelvic area:
Kidney infections can be caused by surgery in the pelvic area,
which will affect kidney function.
8. If a catheter is installed, then assess the characteristics of the urine:
Assess the color, presence/absence of blood, presence/absence
of sediment, and density, and amount. Clients with kidney failure
experience oliguria and even urinary retention. If this condition
continues for a long time (chronic), then hydrophrosis is likely to
occur.
9. Check kidney function through laboratory tests:
This is to find out how clear the kidneys are to carry out
filtration through analysis of creatinine, urea and nitrogen.

B. Kidney Examination
During a kidney examination, several things need to be observed when
carrying out:
1. Inspections include the presence of enlargement in the waist area or
upper abdomen. Enlargement is a result of hydronephrosis or tumors in
the retroperitoneal area. Meanwhile, palpation is a must
2. Meanwhile, for palpation, this examination method is intended to
determine if there is enlargement of the kidney due to stretching of the
kidney capsule.
Important conditions to pay attention to during the inspection are:

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 a. The room light is quite good
b. The patient continues to relax
c. Clothing should be open from the xyphoid process to the
symphysis pubis.
To get relaxation from the patient is:
1) The urinary bladder must be emptied first
2) The patient is in a sleeping position with a pillow under the
head and knees in a flexed position (if necessary)
3) Both hands beside or folded above the chest. If the hands are
above the head, it will pull and tense the abdominal muscles
4) The examiner's palms should be warm enough, and the nails
should be short. By rubbing your hands, your palms will
become warm
5) Carry out the examination slowly, avoiding fast and unwanted
movements
6) If necessary, invite the patient to talk so that the patient will be
more willing
7) If the patient is very sensitive, begin palpation with the
patient's hand under the examiner's hand, replacing the
patient's hand
8) Pay attention to the results of the examination by paying
attention to the patient's facial expressions and emotions.
Kidney Palpation:
1. Right kidney
Place your right hand below and parallel to rib 12 with your
fingertips touching the costovetebral angle. Lift and push the
right kidney anteriorly. Place your right hand gently in the right
upper quadrant laterally and parallel to the right rectus muscle.
Tell the patient to breathe deeply when the patient is at the peak
of inspiration, press the hand quickly and deeply in the right
upper quadrant below the edge of the archus costarum and the
right kidney will be felt between the hands

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 Have the patient hold his breath. Slowly release the
pressure on your right hand and feel how the right kidney
returns to its original position during expiration. If the right
kidney is palpable, determine the size, contour and presence of
tenderness.
2. Left kidney
To feel the left kidney, move to the patient's left. Use your right
hand to push and lift from the bottom, then use your left hand to
press the upper left quadrant, do as before. In normal conditions
the left kidney is rarely palpable.
3. Kidney examination by percussion; Kidney tenderness may be
encountered on abdominal palpation, but can also be noted at
the costovertebral angle. Sometimes pressing the fingertips in
this place is quite painful, and you can also punch the ulnar
surface of the head of the right hand with the volar base of the
left hand (fish percussion).

3.2 Nursing diagnoses

Nursing diagnoses that can appear in clients with acute renal failure (ARF) are
(NANDA I 2012-2014):
1. Excess fluid volume (00026)
Definition: increased isotonic fluid retention
Characteristic limitations:
 Electrolyte disturbances
 Anxiety
 Azotemia
 Changes in blood pressure, mental status, breathing patterns
 Decreased hematocrit, hemoglobin
 Dyspnea
 Edema
 Increased central venous pressure
 Intake exceeds output
 Jugular vein distention
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  Oliguria, orthopnea
Related factors:
Disruption of regulatory mechanisms
2. Ineffective peripheral tissue perfusion (00204)
Definition: decreased blood circulation to the periphery which can disrupt health
Characteristic limitations:
 No pulse / decreased pulse
 Changes in motor function
 Changes in skin characteristics (color, elasticity, hair, moisture, nails,
sensation, temperature)
 Changes in blood pressure in the extremities
 Ankle brachial index < 0.90
 Capillary refill time > 3 seconds
 Color does not return to the leg when the leg is lowered
 Edema
 Extremity pain
 Pale skin color
Related factors:
 Lack of knowledge about the disease process
 Hypertension
3. Activity intolerance
Definition: insufficient psychological or physiological energy to continue or
complete daily life activities that must or want to be carried out.
Characteristic limitations:
 Abnormal blood pressure response to activity
 Abnormal heart frequency response to activity
 ECG changes reflecting arrhythmia/ischemia
 Discomfort after activity
 Dyspnea after activity
 Expresses feeling tired or weak
Related factors:
 General weakness

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  Imbalance between supply and oxygen demand
 Immobility
4. Gas exchange disorders (00030)
Definition: excess or deficit in oxygen and/or elimination of carbon dioxide in the
alveolar-capillary membrane
Characteristic limitations:
 Abnormal arterial blood pH
 abnormal breathing (rate, rhythm, depth)
 Abnormal skin color (pale, black)
 confusion
 diaphoresis
 dyspnea
 headache when waking up
 hypercapnea, hypoxemia, hypoxia
 nostril breathing
 restless, restless
 tachycardia
Related factors:
 Alveolar-capillary membrane changes
 Ventilation-perfusion

3.3 Nursing Intervention

The following are interventions formulated to address nursing problems in
clients with acute renal failure (NANDA-I, NIC NOC)

1. Excess fluid volume can cause disruption of regulatory mechanisms

NOC :
After nursing actions are carried out...x 24 hours, the client will:
 Fluid balance
 Kidney function as evidenced by indicators (1: very severe, 2: severe,
3: Moderate, 4: Light, 5: No disturbance)

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Result criteria:
 Blood pressure, radial pulse, MAP, CVP, peripheral pulse are within
normal limits
 Balance intake and output in 24 hours
 Good skin turgor
 Moist mucous membranes
 Serum electrolyte levels, hematocrit, and urine specific gravity were
normal
 8 hour urine output is normal
 Urine color, urine pH and electrolyte levels are within the normal
range
 There was no increase in BUN, serum creatinine, serum sodium, urine
glucose, urine protein, leukocytes
 There is no increase in body weight, hypertension, nausea, fatigue,
malaise, anemia and edema

NIC :
 Fluid monitoring
Nursing activities:
 Assess history of amount and type of fluid intake and elimination
habits
 Check capillary refill time and skin turgor
 Monitoring body weight, intake and output, serum and urine
electrolytes, serum albumin and total protein, urine and serum
osmolality, vital signs, orthostatic blood pressure
 Maintain a balance of intake and output
 Monitor for signs of ascites
 Plan dialysis procedures
 Hypervolemia management
Nursing activities:
 Weigh yourself every day

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  Monitoring laboratory results for potential increases in plasma
oncotic pressure (increased protein and abumin)
 Monitor laboratory results that cause hypervolemia
 Monitoring intake and output
 Limit fluid intake
 Avoid administration of hypotonic parenteral fluids
 Prepare the patient for dialysis
2. Ineffectiveness of peripheral tissue perfusion related to lack of knowledge
about the disease process, hypertension.
NOC :
After nursing actions are carried out...x 24 hours, the client will:
 Circulation status
 Tissue perfusion: peripheral as evidenced by indicators (1: very severe,
2: severe, 3: Moderate, 4: Mild, 5: No disturbance)

Result criteria:
 Systolic blood pressure, diastolic, pulse, MAP, CVP, pulmonary
pressure, carotid pulsation, brachial pulsation, radial pulsation, femoral
pulsation, within normal range
 PaO2 and PaCO2 are within normal range
 Normal oxygen saturation
 Capirally refill time < 2 seconds
 There is no sudden weight gain
 Extremity skin temperature is normal
 There is no localized pain in the extremities, necrosis, tingling, muscle
weakness, paleness, muscle cramps.

NIC :
 Fluid/electrolyte management
Nursing activities:
 Monitor abnormalities in serum electrolyte values

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  Perform laboratory tests (hematocrit, BUN, protein, sodium and
potassium)
 Give fluids as needed and increase oral intake
 Limit/avoid fluids that are dieretic/lactative in nature
 Correct preoperative conditions of dehydration
 Peripheral sensation management
Nursing activities:
 Monitor the level of sensitivity to hot and cold sensations
 Monitor for decreased sensation (numbness, tingling and pain)
 Advise clients to be careful when in contact with hot and cold
objects
 Protect the body against extreme environmental temperature
changes
 Plan to administer analgesics, corticosteroids, anticonvulsants,
antidepressants
 Monitor for thrombophlebitis and venous thromboembolism
3. Activity intolerance related to general weakness, imbalance between
oxygen supply and demand, immobility
NOC :
After nursing actions are carried out...x 24 hours, the client will:
 Activity tolerance
 Self-Care: activities of daily living (ADL) as evidenced by indicators
(1: very severe, 2: severe, 3: Moderate, 4: Light, 5: No disturbance)

Result criteria:
 Oxygen saturation, pulse rate, respiratory rate after normal activity
 No shortness of breath
 Systolic and diastolic blood pressure after normal activity
 There is no cyanosis after activity
 Ability to perform daily activities

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  Able to carry out daily activities, including: eating, putting on clothes,
toileting, dressing up, personal hygiene, walking, mobility in a
wheelchair and moving independently.

NIC :
 Energy management
Nursing activities:
 Assess the client's psychological status and fatigue condition
 Monitoring nutritional intake as a source of energy
 Consult with a nutritionist about how to increase the energy intake
of nutrients
 Assess the client's sleep patterns and sleep time
 Assess the location that causes pain/discomfort during activities
 Use active/passive ROM to train muscle strength
 Set a balance pattern of activity and rest
 Self-care assistance
Nursing activities:
 Consider the client's culture and age when increasing self-care
activities
 Monitor the client's ability to fulfill daily needs
 Help clients to fulfill their daily needs
 Encourage clients to fulfill their needs according to their level of
ability.
 Encourage the family to help the client if they experience difficulties in
meeting their needs
4. Gas exchange disorders bd Changes in alveolar-capillary membrane,
ventilation-perfusion
NOC :
After nursing actions are carried out...x 24 hours, the client will:
 Electrolyte ang acid / base balance
 Respiratory status: gas exchange as evidenced by indicators (1: very
heavy, 2: severe, 3: Moderate, 4: Light, 5: No disturbance)

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Result criteria:
 All results showed normal values (pulse and radial pulse, RR,
respiratory rhythm, serum sodium, serum potassium, serum chloride,
serum calcium, serum magnesium, serum pH, serum albumin, serum
cretinin, serum bicarbonate, serum CO2, plasma osmolarity, glucose
serum, hemtocrit, BUN, BUN and crestinine ratio, urine pH, urine
sodium, urine chloride, urine osmolarity, urine BJ)
 No function, muscle weakness/muscle cramps, abdominal cramps
 There is no nausea, dysrhythmia, or restlessness
 Arterial pH is normal
 Oxygen saturation is normal
 Perfusion-ventilation balance occurs
 There is no dyspnea at rest or on light activity
 There is no cyanosis

NIC :
 Acid-Base Management
Nursing Activities:
 Assess airway patency
 Adjust the position to optimize ventilation (open the airway and
elevate the head)
 Ensure patency of intravenous access
 Monitor BGA values (arterial pH, paCO2, and HCO3, etc.) to
determine respiratory/metabolic type, and physiological mechanism
compensation (pulmonary/renal compensation)
 Monitoring circulating tissue oxygenation (PaO2, SaO2, Hb, and
cardiac output)
 Monitor for symptoms of respiratory failure (low PaO2, increased
PaCO2, and respiratory muscle weakness)
 Monitor intake and output of electrolyte fluids

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  Monitor excessive acid loss (vomiting, nasogastric tube discharge,
diarrhea, and dieresis)
 Monitoring neurological status (consciousness and dizziness)
 Provide adequate hydration and balanced electrolytes

 Ventilation Assistance
Nursing Activities:
 Maintain airway patency
 Position the client to relieve dyspnea
 Encourage and encourage clients to take deep breaths and cough
effectively
 Assess respiratory function with a spirometer
 Auscultate breath sounds to find areas that are decreased.
 Administer additional oxygen, pain management, therapy to
improve ventilation (bronchodilators)
 Perform resuscitation if respiratory failure occurs

3.4 Nursing Implementation

3.5 Nursing Evaluation
CHAPTER IV
CLOSING

4.1 Conclusion
Acute renal failure is a disruption in kidney function that occurs suddenly with
typical symptoms in the form of oliguria / anuria with an increase in BUN (Blood
Ureum Nitrogen) or serum creatinine. In general, acute kidney failure is also referred
to as Acute Renal Faiure (ARF) or Acute Kidney Injury (AKI) (Graber, 2006;
Wilcox, 2009). The causes of acute kidney failure are divided into 3 main ones,
namely: Pre-renal, Renal, Post-renal.
The clinical symptoms of acute renal failure that appear are oliguria, anuria,
high output renal failure BUN, and increased serum creatinine. The main goals of
managing ARF are to prevent kidney damage, maintain hemostasis, carry out

26
 resuscitation, prevent metabolic complications and infections, and keep the patient
alive until his kidney function recovers spontaneously.

4.2 Suggestion
In making this paper the group is still far from perfect. Therefore, the group
asks for constructive criticism and suggestions from readers. We hope that the paper
we wrote can be useful for readers.

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Graber MA.2006. Family Doctor's Pocket Book University of OIWA. Jakarta: EGC
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Jorres A. 2010. Management of Acute Kidney problems. New York: Springer Heidelberg
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