NCM 0118: LECTURE

MODULE 5: RENAL EMERGENCIES

1ST SEMESTER | S.Y. 2021-2022

PRE-TEST 7. The nurse receives a client in the emergency

department following a diagnosis of renal
1. A client who develops acute kidney injury
calculi. Which of the following nursing
due to severe vomiting and diarrhea has a
diagnoses should the nurse take as having
risk factor that is categorized under:
highest priority?
A. intrarenal.
A. Acute pain
B. postrenal.
B. Impaired urinary elimination
C. prerenal.
C. Nausea
D. renal.
D. Risk for deficient fluid volume
2. The clinical feature of acute kidney injury is
8. A client with acute kidney injury develops a
best evidenced by:
serum sodium of 110 mEq/L secondary to
A. elevated blood urea nitrogen.
fluid accumulation. The nurse anticipates
B. elevated serum creatinine.
which order?
C. low magnesium.
A. Administer calcium gluconate 10% by
D. low potassium.
slow intravenous push
3. Most cases of renal calculi are caused by:
B. Encourage high sodium diet
A. gouty arthritis.
C. Monitor for signs of cerebral dehydration
B. hypercalciuria.
D. Restrict water intake
C. struvite formation.
9. The client with acute kidney injury has the
D. urinary tract infection.
latest ABG results that show ph= 7.2, PaCO2=
4. The client with gouty arthritis develops a
45 mmHg, and HCO3= 17 mEq/L. The nurse
kidney stone. This is related to:
anticipates which order?
A. elevation of potassium ions.
A. Administer ammonium chloride
B. elevation of uric acid.
B. Breathe through a paper bag
C. metabolic acidosis.
C. Normal saline at rapid infusion rate
D. metabolic alkalosis.
D. Sodium bicarbonate infusion
5. The nurse reviews the client’s latest serum
10. The client has been started on NSAIDs on a
potassium level and notes it to be 6.7 mEq/L.
client with renal stone. The nurse should
Which of the following orders should the
inform the physician if the client has:
nurse anticipate as an emergency order?
A. A prescription of antacid
A. Administer 10 units HR in 50 ml 40% in
B. Aspirin hypersensitivity
water
C. Flank pain
B. Check pulse and respiratory rates
D. Taken this medication with meals
C. Obtain an electrocardiogram to
evaluate flattening of the T waves ACUTE KIDNEY INJURY (AKI)
D. Provide oral calcium gluconate
To introduce AKI, the following are the
6. Which of the following electrolyte
related concepts with the said condition:
imbalances will be expected on a client in
acute kidney injury? 1. This refers to a sudden decline in kidney
A. Hypercalcemia function causing disturbances in fluid,
B. Hyperkalemia electrolyte, and acid base balance
C. Hypomagnesemia because of a loss of in small solute
D. Hypophosphatemia

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 clearance and decreased glomerular
filtration rate
2. The cardinal features are azotemia and
oliguria.
3. Staging identifies five stages of kidney
disease namely (a) risk, (b) injury, (c) failure,
(d) loss, and (e) ESKD based on elevation of
serum creatinine levels or decline in
Glomerular Filtration Rate (GFR)
KIDNEY FUNCTION 1
Primary regulators of fluid and electrolyte acid-
base balance.
It said that kidneys act as primary
regulators of fluid and electrolyte acid-base
balance. Specifically, whatever is in excess will
be eliminated by the kidneys. Whatever is in
deficient in the body, will try to be absorbed this
time by the kidneys.
Fluid Balance
 If the person has been found to be
dehydrated, somehow the body will be able
to understand specifically by the kidneys,
that water in terms of status is very deficient
in the body. And so, since the kidneys act to
regulate fluid balance, the kidneys will be
able to somehow absorb water so that
water lost will be further prevented.
 Similarly, when we talk of water
reabsorption, we have to understand that
kidneys function under the hormonal effects
of antidiuretic hormone and another
hormone in the form of aldosterone
because aldosterone tries to reabsorb
sodium. Since sodium attracts water, we can
say from that perspective that both ADH
and aldosterone act on the kidneys so
somehow there will be reabsorption of water
in the event if the client is found to be
dehydrated.
 Same thing with the concept of over
hydration or excessive fluid intake. It is said
that if there are excessive water molecules
in the body, the kidneys will be able to
detect them and through decreased
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reabsorption of water molecules, we can
expect therefore that there will be increased
production of urine as evidenced by a
diluted urine brought about by
overhydration or overhydration caused by
excessive drinking water.
 Similarly, from this point, we can just simply
say that if we drink a lot of water, we will be
expecting that afterwards, minutes or few
hours later, there will be excessive urine
output because the kidneys are able to
detect anything that is excess and will try to
be eliminated and anything that is deficient
will try to be reabsorbed somehow by the
body. This is in line with the concept related
to fluid balance.
Electrolyte Balance
 It is said that if the client has excessive intake
of bananas, oranges, apple, fruits, raisins or
foods which are considered high potassium
rich food items, we can say from this point
that excessive potassium somehow is not
helpful for the body. In this case, the kidneys
will try to excrete whatever is in excess so in
this case, potassium ions will be excreted by
the way of the urine. This is how the kidneys
balance excessive potassium ions. We know
very well that potassium will be excreted
under the hormonal effect of aldosterone.
 Aldosterone retains sodium, sodium attracts
water and aldosterone excretes potassium
so somehow the kidneys are able to
regulate now the that we have.
 Similarly, if for instance the client has
excessive phosphorus or intake or excessive
phosphorus absorption brought about by
antacids or brought about by enemas or
laxatives that contain magnesium (due to
excessive magnesium hydroxide or milk of
magnesia), somehow the kidneys will be
able to detect that. And so, the kidneys will
try to eliminate whatever is in excess in this
case magnesium ions.
 So, there will now be excretion of
magnesium. The main route of excretion of
magnesium is by way of urine.
 Similarly, if the client is deficient in calcium
ions or if the client has hypocalcemia
brought about by a decreased dietary
intake of calcium, the body will try to correct
such deficiency. The kidneys will try to
reabsorb calcium in the body in the
gastrointestinal tract, or maybe prevent
resorption of calcium from the bone going
towards the blood.
 Through that, somehow calcium will be
reabsorbed by the body, preventing
hypocalcemia or correcting even
hypocalcemia.
 In this case, the kidneys will try to reabsorb
more calcium ions, because we don’t want
further hypocalcemia to occur. So, in this
case, there will be calcium reabsorption in
the body, increasing calcium level in the
blood under the influence of the hormone
called, parathyroid hormone.
 The kidneys will try to balance everything.
Whatever is in excess will be eliminated, and
whatever is deficient will be conserved or
saved in order to prevent further deficiency.
 The kidneys will try to function everything,
depending also on the effects of the
hormones available in the body. Hormones
can act on the organs. Take for instance, in
the kidneys, in order to reabsorb water under
the hormonal effect of ADH or aldosterone,
or in order to somehow absorb calcium
under the influence of parathyroid
hormone.
Acid-Base Imbalance
 It is said that the kidneys also try to regulate
acid-base balance.
 In the presence of excessive alkalosis, the
body will try to absorb more hydrogen ions,
specifically in the kidneys. We know very well
that hydrogen ions contribute to acidity: the
more hydrogen ions that we have, the more
acidic our blood becomes.
 In this case, if the client has metabolic
alkalosis or respiratory alkalosis, the kidneys
will try to absorb more hydrogen ions
because hydrogen contribute to increasing
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acidity thereby correcting alkalosis that we
have.
 Another thing is in the form of acidosis. if the
client has acidosis in the blood, the kidneys
will try to correct this problem this time by
reabsorbing more bicarbonate ions and by
excreting more hydrogen ions because if
there are increased hydrogen ions being
excreted, there’ll now be correction of
acidosis.
 If in case bicarbonate ions are reabsorbed
by the body, it can also somehow correct
acidosis that we have.
KIDNEY FUNCTION 2
Excretion of potentially harmful waste products
 We have these waste products that are
somehow present in our body. The kidneys
will try to excrete them in such a way that
the level for a particular waste product in
the blood is still conducive for optimal
cellular functioning.
 So, in this case, what we have to remember
is that, there are nitrogenous waste products
that are considered to be potentially
harmful, especially on the cerebral
circulation, such as urea, uric acid, and
even creatinine.
 There are three (3) waste products that must
be excreted by the body. So in this case, the
kidneys will be able to excrete creatinine,
urea, and uric acid.
 But what if there is a significant impairment
in kidney function? We may be very much
familiar that there will be, for sure, elevation
of urea in the form of blood urea nitrogen
(BUN), elevation of creatinine, and elevation
of uric acid. If this would be the case, the
body will try to find a way in order to excrete
these waste products.
Which of these three (creatinine, urea and
uric acid) would best reflect an alteration in
kidney function?
Serum creatinine, because creatinine is a by-
product of muscle metabolism and that, it is
solely excreted by the kidneys.

However, with the other results though, we
have to understand that urea and uric acid
can easily be affected by diet.
And so in this perspective, we have to
understand that creatinine, which is solely
excreted by the kidneys, can become
elevated in the presence of kidney problem.
KIDNEY FUNCTION 3
Production of Erythropoietin
 Remember: erythropoietin, being produced
by the kidneys, is responsible in stimulating
the bone marrow. The bone marrow this time
will be able to produce red blood cells.
 In this perspective, we need to understand
that if there is a kidney problem, there is now
an inadequate production of erythropoietin
which now decreases stimulation on the
bone marrow to produce red blood cells.
 Therefore, we can expect that for clients
with kidney problems, especially those with
chronic renal failure, they may suffer from
signs and symptoms of anemia, and that
they may receive synthetic form of
erythropoietin to stimulate the bone marrow
to produce red blood cells, thereby
somehow correcting the signs and
symptoms of anemia that the client has
experienced.
KIDNEY FUNCTION 4
Production of Urine
 Whatever is in excess will be eliminated by
the kidneys, and that is what we call as urine.
Whatever that we consider as waste
products will be eliminated and terminally,
we can call that as urine.
 So, therefore, we can say that the kidneys
are responsible in production of urine, and
that urine reflects the body’s ability to filter
blood or to reabsorb whatever is in need
and to excrete whatever is in excess.
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What if there is a problem in the kidney
function?
There will now be a problem in urine
production. There will be a decrease in urine
production called as oliguria. There is also an
elevation of urea, creatinine, and even uric
acid for which are reflective of what we call
as azotemia. Azotemia and oliguria will be
considered as cardinal features of acute
kidney injury.
 When we talk of kidney injury, it may be
progressive, and that it may start off with
increased risk for renal injury.
o Eventually, if that risk is not controlled or is
not eliminated, there will now be injury of
the kidney tissues. If there is now injury of
the kidney tissues, there will be a
significant disruption in the function of the
kidneys.
 After injury of the kidney tissues and if the
precipitating event has not been corrected,
there will be somehow failure on the part of
the body to maintain kidney functions.
o Eventually, there will be significant loss of
nephrons although we can say that
nephrons are very much capable of
compensation, but eventually, if in case
the precipitating events have not been
eliminated, there will be now significant
loss of kidney function.
o The nephrons will be lost, and that
optimally, the cells may not be able to
survive.
 The late stage of this kidney injury may be in
the form of end-stage kidney disease for
which the patient will now be dependent
highly on the so called artificial kidney, and
that is what we call as dialysis in the form of
hemodialysis or may be in the form of
peritoneal dialysis.
The kidneys are responsible in the production
of urine. But the question is, how does urine
form?
 Remember that the amount of blood that
enters the kidneys will actually determine
the amount of urine that can be
produced by the kidneys.
 From this perspective, we can say that the
kidneys filter blood, and whatever is
filtered will become as urine, and that this
urine will be able to pass this renal pelvis,
and eventually, the ureter connected to
the bladder and finally to the urethra for
expulsion or for excretion.
 Oxygenated blood goes into the renal
artery, and then will pass through the
afferent arterioles, efferent arterioles, and
finally to the renal vein.
 The point in here is that, the kidneys are
able to clean or filter blood, and the
filtered blood will pass through the renal
vein.
 We can say now that the urine that we
produce is basically dependent on the
blood that has flown in the kidneys.
 The functional unit of the kidney is the
nephron. There are around one million
nephrons in every kidney.
 The nephron consists of 2 parts: the
Bowman’s capsule and the glomerulus
(that we call as the ball of capillaries).
 The capillaries hold the blood, and that
whatever is filtered in this blood will go
now to the tubules, and whatever is
present in the tubule will eventually be at
risk to becoming the urine. It will undergo
certain processes called glomerular
filtration, tubular reabsorption, secretion,
and finally water conservation.
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 The oxygenated blood will travel in the
afferent arteriole and eventually will go in
this ball of capillaries called, glomerulus.
 In here you have to remember is that, the
blood can be pushed eventually in the
Bowman’s capsule and in the tubule.
 There is a membrane that has pores large
enough to allow for passage of excessive
water and electrolytes that must be
eliminated, but it also has spores small
enough to prevent passage of large
molecules.
 In this case, albumin and red blood cells
cannot pass through the membrane,
because whatever has passed in the
membrane will eventually go and will
become as filtrate and that whatever
filtrate is available there, can be at risk to
becoming urine. We don’t want ourselves
having red blood cells in the urine.
 We also don’t want ourselves to have
albumin or proteins in our urine which can
eventually deplete our red blood cells and
albumin, causing now anemia and
hypoalbuminemia, respectively
increasing the risk for anemia, increasing
the risk for edema formation.

 The filtrate is the one that enters the
tubule, and that normally, we have 150 or
180 liters per day.
 We have the glomerular filtration rate. This
is the amount of filtrate that enters the
tubule per minute. Normally, we have
around 125 ml of filtrate being produced
per minute.
 Remember: this 125 ml will not become
the urine that is produced by the body. In
fact, out of that 125 ml per minute
becoming the filtrate, only 1% of that
becomes the urine.
 That is why, normally speaking, we only
produce around 1 ml of urine per minute,
and we have 60 minutes per hour. That is
why, we have 160 ml per hour. But at a
minimum, we can consider that the
acceptable amount of urine per hour will
still be at least 30 ml.
 What happens to this remaining 124 ml of
filtrate? Not all that has been part of the
filtrate will become the urine. Majority of
the filtrate will be reabsorbed by the body.
 Whatever is in deficient will try to be
reabsorbed by the body.
 If in this case the client has hyponatremia,
there will be reabsorption of sodium and
these sodium ions will now go from the
tubule going back into the blood vessel or
the peritubular capillary. So, there will be
reabsorption of whatever is deficient.
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 There will also be reabsorption of water if
in case the patient has been found to be
dehydrated.
 There will be reabsorption of potassium if
the patient is hypokalemic.
 There will be reabsorption of bicarbonate
if the patient is acidotic.
 There will be the reabsorption of hydrogen
ions if in case the patient has been found
to be alkalotic
 Anything that is deficient will be
reabsorbed by the body.
 If the client is hypoglycemic, there will be
reabsorption of glucose.
 If the client is dehydrated, there will be
reabsorption of water.
 If there is hypovolemia and hypotension,
there will be reabsorption of water,
making the urine very minimal in amount
and making the urine very concentrated
because from this 125 ml of filtrate, we only
have now 1 ml of urine being produced
per minute.
 We will reabsorb whatever is deficient and
we will try this to secrete or excrete
whatever is no longer needed by the
body
 REABSORPTION: Whatever is really needed
will be reabsorbed.
 EXCRETION/SECRETION OF IONS,
ELECTROLYTES, & WATER MOLECULES: They
will be excreted if in case the body does
not need them anymore.
Urine is a reflection of the body’s ability
to filter blood, of the body’s ability to reabsorb
anything that is deficient, and of the body’s
ability to secrete or excrete substances which
the body considers to be no longer needed.
If in case, there is a significant loss in
kidney function, there will now be a problem
with the production of urine, which is anuria and
oliguria.
The fact that there is a decrease in urine
output may also mean that there is an excessive
amount of electrolytes or acids or nitrogenous
waste products out there that have not been
eliminated.
In this case, they have accumulated in
the blood, too, causing several problems in the
form of hypervolemia, hyperkalemia,
hypermagnesemia, and even
hyperaccumulation of these acids, causing
metabolic acidosis.
ACUTE KIDNEY INJURY (AKI) AND ITS CAUSES
The etiologies associated in the
development of AKI can be grouped into
prerenal, intrarenal, and postrenal causes:
1. Prerenal Causes
 These involve conditions that affect kidney
perfusion. Limited blood flow reduces the
glomerular filtration rate. If adequate blood
flow is restored to the kidney, normal renal
function resumes. If, however, the prerenal
cause is prolonged or severe, it can progress
to intrarenal damage and cause acute
tubular necrosis (ATN) or acute cortical
necrosis. Examples under this category of
causes are intravascular fluid depletion,
(hemorrhage, trauma, surgery, diuretics,
fluid volume shifts, burns).
 Anything that related to blood blow in the
kidneys are considered to be pre-renal
causes.
 Oxygenated blood goes into the kidneys.
The kidneys need oxygen for them to survive.
Significant obstruction in blood flow can
impair kidney function. Any condition that
relates to a problem with blood flow to the
kidneys can be considered to be pre-renal
cause.
 If in case the client develops AKI caused by
excessive nausea, vomiting, or excessive
intake of laxative or there is peripheral
vasoconstriction, the client has been
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dehydrated, or the client has received high-
dose dopamine hydrochloride for which
have resulted into peripheral
vasoconstriction and vasoconstriction of the
renal artery, this can actually decrease
blood flow to the kidneys, which can cause
injury to the kidney tissues. Hence, we can
consider them as pre-renal causes
2. Intrarenal Causes
 The intrarenal causes of kidney injury result
from conditions that cause direct renal tissue
injury. The most common intrarenal cause of
injury is Acute Tubular Necrosis (ATN). It is a
condition that may occur because of
prolonged ischemia, exposure to
nephrotoxic substances or a combination of
these. ATN usually occurs when the perfusion
to the kidneys is significantly reduced. The
renal ischemia overwhelms the normal
autoregulatory defenses of the kidneys and
initiates cell injury that may result to cell
death. Nephrotoxic substances damage
the tubular epithelium as a result of drug
toxicity, intrarenal vasoconstriction and
intratubular obstruction.
 Conditions that cause direct injury to the
kidney tissues are considered to be intra-
renal causes.
 Acute tubular necrosis is considered to be
the most common form of intra-renal cause.
 If the client has been taking analgesics, such
as NSAIDs or chemotherapeutic
medications for cancer which are believed
to be nephrotoxic, in this case, we can say
that such condition that the client presents is
considered to be intra-renal causes and the
client has developed AKI.
 Having knowledge or thorough
understanding of medications can help
nurses in monitoring clients’ serum creatinine
while receiving a particular antibiotic, for
instance. So, in this case, we may be able to
understand what drugs are considered to
be nephrotoxic, because they somehow do
contribute in the development of AKI.
3. Postrenal Causes
 The postrenal causes lead to acute kidney
injury through urine obstruction of flow.
Obstruction can occur at any point of the
urinary system. Postrenal conditions increase
intratubular pressure that reduce GFR and
cause abnormal renal function.
 The kidneys do produce urine, but the
problem is we do know that the urine is a
reflection of the body’s ability to secrete
whatever is not needed, and most of which
that are not needed are these nitrogenous
waste products.
 But what if these nitrogenous waste products
have been formed in the urine however
there’s a problem with urine flow? The fact
that this obstruction of urine flow can
contain nitrogenous waste products and
other harmful substances out there,
accumulation of these waste products
brought about by urine flow obstruction can
actually now cause irritation in kidney tissues,
and that is what we call as post-renal cause.
 Post-renal causes are conditions that are
related to obstruction in urine flow which
can cause hydronephrosis or significant
irritation of kidney tissues brought about by
accumulation of urine, and that this urine
has infiltrated tissues of the kidneys, causing
significant injury.
COURSE OF ACUTE KIDNEY INJURY
1. Initiation Phase
 This is the period from the occurrence of the
precipitating event to the beginning in the
change in urine output. No actual renal
damage has yet to occur. Signs and
symptoms reflect the inability of the client to
compensate for the diminished renal
function.
 The precipitating event is present on a client.
There is no actual renal damage, but the
client has an observable change in urine
output.
 We know very well that urine production is
one of the major functions of the kidneys.
2. Maintenance Phase
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 Urine volume is usually at its lowest point;
although some patients may be non-
oliguric. This phase usually lasts 8 to 14 days
but it may last up to 11 months.
 Remember: we don’t want the client
experiencing maintenance phase for a
longer period of time the longer a patient
remains in this stage, the slower the
recovery, the greater the chance of
permanent renal damage. Complications
resulting from uremia, including
hyperkalemia, and infection occur in this
stage.
 The client develops uremia: elevation of
nitrogenous waste products in the blood.
 The client may also have problems with
accumulation of some electrolytes that must
be excreted in the urine, such as
hyperkalemia. The client has excessive
potassium ions in the blood because
potassium ions at the majority are excreted
by way of the urine.
 Since there is now a significant decrease in
urine production, that may also mean that
potassium ions are not excreted normally in
the urine. Hence, we have hyperkalemia.
3. Recovery Phase
 This is the period when the renal tissue
recovers and repairs itself. There is a gradual
increase in urine output and an in
improvement in laboratory values occur.
Osmotic diuresis occurs because of the
excretion of the salt and water
accumulated during the maintenance
phase. It also occurs because of the
administration of diuretics.
 If in case the nephrons have died at a
significant number, the client’s possibility of
recovery will still be possible.
 In here, the renal tissues try to recover. There
is now gradual increase in urine output, and
that there will now be improvement in the
laboratory values.
 Remember: The longer the phase that the
client has stayed on maintenance phase,
the harder for the client to recover and be
in the recovery phase of AKI.
 APPLICATION OF THE NURSING PROCESS
Assessment
Part of the nurses’ assessment includes
history-taking of precipitating events and
expected and significant physical assessment
findings. Physical assessment includes general
appearance (signs of uremia such as malaise,
fatigue, disorientation, and drowsiness), skin
assessment (color, texture, bruising, petechiae,
edema); hydration status (body weight, intake
and output, skin turgor, mucous membranes,
breath sounds, presence of edema, neck vein
distention); and vital signs).

ASSESSMENT
Cardiovascular Heart Failure Fluid overload and hypertension

Pulmonary edema Increased pulmonary capillary permeability

Fluid overload
Left ventricular dysfunction

Dysrhythmias Electrolyte imbalances (hyperkalemia, hypocalcemia)

Peripheral edema Fluid overload

Right ventricular dysfunction

Hypertension Fluid overload

Increased sodium retention
Hematological Anemia Decreased erythropoietin secretion
Loss of RBCs through GI tract, mucous membranes, or dialysis
Decreased RBC survival time
Uremic toxins interference with folic acid secretion

Alterations in Platelet dysfunction

coagulation

Increased Altered leukocyte function

susceptibility to
infection
Respiratory Pneumonia Thick tenacious sputum form decreased oral intake
Depressed cough reflex
Decreased pulmonary macrophage activity
Fluid overload

Pulmonary edema Left Ventricular Dysfunction

Increased pulmonary capillary permeability
Gastrointestinal Anorexia, nausea, Uremic toxins
vomiting Decomposition of urea releasing ammonia that irritates mucosa,
Stomatitis causing ulcerations and increased capillary fragility
Uremic halitosis
Gastritis and bleeding
Neuromuscular Drowsiness, confusion, Uremic toxins produce encephalopathy
irritability, coma Metabolic acidosis

Tremors, twitching, Altered nerve conduction from uremic toxins

and

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 convulsions

Psychosocial Decreased mentation, Uremic toxins produce encephalopathy

decreased Electrolyte imbalances
concentration, and Metabolic acidosis
altered perceptions Tendency to develop cerebral edema
Integumentary Pallor Anemia
Yellowish skin Retained urochrome pigment
Dryness Decreased secretions from oil and sweat glands

Pruritus Dry skin

Calcium and/or phosphate deposits in skin
Uremic toxins’ effect on nerve endings

Purpura Increased capillary fragility

Platelet dysfunction

Uremic frost (rarely Urea or urate crystal excretion

seen)
Endocrine Glucose intolerance Peripheral insensitivity to insulin
Prolonged insulin half-life from decreased renal metabolism

Skeletal Hypocalcemia Hyperphosphatemia from decreased excretion of phosphates

Decreased GI absorption of vitamin D
Deposition of calcium phosphate crystals in soft tissues

Metabolic acidosis Decreased hydrogen ion excretion

Decreased bicarbonate ion reabsorption and generation
Decreased excretion of phosphate salts or titratable acids
Decreased ammonia synthesis and ammonium excretion
Diagnostic Procedures:
1. Kidney-Ureter-Bladder (KUB) x-ray: size, shape, position of the kidneys; calculi, hydronephrosis, cysts, tumors
2. Renal ultrasound: size of the kidneys, and obstruction
3. Magnetic Resonance Imaging (MRI): renal structures

CARDIOVASCULAR accumulated in the blood, causing

hypervolemia
Heart Failure
 The client may have fluid overload. Increase
 The client may have some signs related to in blood volume may also increase the
heart failure because the kidneys are no blood pressure, and so, the client may
longer producing enough urine. Therefore, develop heart failure because the client will
the excessive water molecules have have severe difficulty in pumping this

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 excessive fluid volume that is present in the
body
Pulmonary Edema
 The client may also have pulmonary edema.
Why? Because of hypervolemia, these
pulmonary capillaries are exposed to an
increased amount of pressure brought
about by increasing fluid volume. This
increase in fluid volume can actually
increase capillary permeability, increasing
now hydrostatic pressure, allowing the fluid
from the intravascular space going into the
interstitial space. Hence, the client develops
edema.
 In this case, the client develops pulmonary
edema and it is because of fluid overload
and even left ventricular function.
 We know very well that the left ventricle is in
line with ejection of blood into the systemic
circulation after the blood has been
oxygenated by the lungs.
 However, because of excessive fluid in the
left ventricle, the fluid will go back into the
left atrium.
 The left atrium is connected to the
pulmonary circulation vita the pulmonary
veins.
 After the blood has been oxygenated, the
blood from the lungs will go into the
pulmonary veins, and finally in the left
atrium.
 Since there is left ventricular failure, the
blood will go back from the left ventricle,
finally to the left atrium, finally to the
pulmonary veins, and then finally into the
lungs, causing now pulmonary congestion.
 That is why the client with AKI may present in
the emergency department complaining of
severe difficulty of breathing.
 The client may even have rales or crackles
upon auscultation. And so, the client is in
real need of oxygenation. And so, the client
may be receiving diuretics in order to ensure
that what excessive fluid is available or that
is impairing oxygen exchange can
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somehow be eliminated by the body
through urine.
Dysrhythmias
 The client may also have excessive
accumulation of electrolytes that can
impair cardiac function in such a way that
the client may develop hyperkalemia and
hypocalcemia. In this case, the client may
develop altered cardiac rate and rhythm.
 In hyperkalemia, the client may show
elevation or peak T wave, prolonged PR
interval, and widened QRS complex.
 Why hypocalcemia? It is said that the
kidneys somehow activate Vitamin D (a
vitamin that enhances absorption of
calcium in the GI tract).
 What if there is not enough synthesis of
Vitamin D? Even if the client has been taking
adequate amount of calcium-rich food
items or even calcium medications or oral
supplements for calcium, if there isn’t
enough Vitamin D available that will
enhance absorption of calcium in the body,
calcium ions will not be adequately
absorbed in the bloodstream.
 Hence, if there is a kidney problem, there is
a decreased Vitamin D synthesis by the
kidneys, and that there will be a decrease in
calcium absorption in the intestines, causing
significant hypocalcemia.
 Since calcium is related to myocardial
contraction, there will now be
hypocalcemia. And so, the client can have
an alteration in ECG finding which can be
evidenced by shortened QT interval or
shortened ST segment for instance.
Peripheral Edema
 Since there is excessive water in the body,
not only will the client develop pulmonary
edema. The client may also develop edema
in the peripheries. Hence, we have this co
called peripheral edema.
 This is associated with fluid overload and
even right ventricular dysfunction. How?
Since there is excessive fluid volume in the
 body, the heart can somehow have a
difficulty pumping blood because of the
excessive fluid volume presence. In this
case, the right ventricle will find it difficult for
it to pump the blood that is present in that
chamber.
 Since there is now failure in the right
ventricle, there will be now backflow of
blood from the right ventricle, finally to the
right atrium.
 Since the right atrium is connected in the
systemic circulation via the superior and
inferior vena cava or the blood that has
been coming from the systemic circulation,
there will be now signs and symptoms of
peripheral edema or even peripheral
congestion of fluid.
 So, in this case, the client may develop
(because of right-sided heart failure or right
ventricular dysfunction) not only peripheral
edema, but also hepatomegaly,
splenomegaly, distention of jugular veins,
and even cerebral edema. It is because of
an increase in fluid volume in the peripheries
in the systemic circulation.
Hypertension
 We know very well that blood volume is
almost directly proportional with blood
pressure. The higher the volume of fluid
present in the body, the higher will be the
required pressure on the heart to pump to
ensure that oxygenation will be maintained.
 In this case, the client may develop
hypertension because of fluid overload.
 Because of the possibility of decreased
sodium excretion by the kidneys, sodium
can accumulate.
 Although sometimes, the client with AKI may
also develop hyponatremia, because
sodium ions can easily be diluted by the
excessive water molecules that are not
excreted by the kidneys. Hence, the client
may develop maybe hyponatremia or
hypernatremia, depending on the client’s
presentation of condition. Whatever the
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case is, the client will develop hypertension
because of fluid overload.
 If in case hypernatremia develops, sodium
ions can easily attract more water. Hence,
sodium retention can be considered a
culprit in the development of hypertension.
HEMATOLOGICAL
Anemia
 Clients with AKI may also develop
impairment in erythropoietin production.
Since erythropoietin has been reduced, the
client may develop anemia.
 Signs and symptoms of anemia may include
pallor, easy fatigability, weakness, increased
heart rate, and increased respiratory rate as
compensation for a lack of oxygenation in
the cells.
 Some clients with AKI may develop loss of
red blood cells in the GI tract. Why? It is
because when we talk of AKI or end stage
renal disease, urea will not be excreted by
the body because excretion of urea is
actually the function of the kidneys in the
disease process of kidney failure.
 Remember: Urea, if it has accumulated
abnormally in the blood, will try to convert
itself to ammonia by the salivary glands or by
the GI tract.
o Urea will be converted to ammonia and
that ammonia is irritating to body tissues.
In this case, the GI tract may cause
irritation because of the ammonia that
has been generated from urea. This can
be evidenced by the presence of GI
bleeding because of the irritation or
injury of the GI tract.
 The client may even have halitosis or may
even have problems with regard to odor. It’
s because of the body’s attempt to excrete
whatever is considered to be harmful. In this
case, the nitrogenous waste called urea,
which will be converted back to ammonia
that can irritate the GI tract.
 Some clients with ESRD may depend on
hemodialysis. Since the hemodialysis makes
 use of a filtration membrane by which the
blood passes through, there is a possibility of
residual blood loss because some portion of
blood will have to stay in the dialyzer even
after the procedure. So, the client may
develop significant anemia.
Alterations in Coagulation
 Platelets are very much sensitive of all the
formed elements inclusive of red blood cells,
or white blood cells. It is said that platelets
are very much sensitive especially if there is
an accumulation of waste products such as
ammonia, urea. These waste products are
able to destroy the very fragile platelets and
that the client may develop platelet
dysfunction evidenced by
thrombocytopenia, increasing the risk for
bleeding.
Increased Susceptibility to infection
 There will also be an impairment in white
blood cell function because of
accumulation of these waste products.
Hence, the client may have a decreased
resistance to infection, increasing the risk for
the client to easily develop infection.
 If the client develops chronic kidney
problem, the thing that we’ll have to monitor
as one of the most important areas for client
monitoring is the client’s susceptibility to
develop infection because mortality would
most likely be high in the event that a client
with end-stage renal disease develops
immunosuppression.
 What is the difference between ammonia
and urea? If the client has ingested protein-
rich food, there will now be digestion and
part of the waste product of digestion will
initially be ammonia.
o The liver is able to convert ammonia to
urea, because no matter how we want
it to be, ammonia cannot be excreted
by the body if it is not in the excretable
form in the urine.
o After ingestion of protein, there will be
now production of ammonia. The
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ammonia will have to be converted by
the liver to become urea because
ammonia cannot be excreted by the
kidneys, but urea can be excreted by
the kidneys.
o In this case, there’s no problem with the
liver. The client only has a problem in the
kidneys. And so, urea would most likely
be elevated in AKI but not ammonia.
 With the disease process, urea will be
converted back to ammonia because of
the body’s attempt to eliminate these
nitrogenous waste products.
RESPIRATORY
Pneumonia
 The client may develop pneumonia
because of fluid overload and that this can
be evidenced by thick sputum.
 The client may also have an increased risk to
develop respiratory infection because of an
altered leukocyte function.
Pulmonary Edema
 This can be associated with left ventricular
dysfunction, fluid overload, and increase in
pulmonary capillary permeability.
GASTROINTESTINAL
Anorexia, nausea, vomiting, stomatitis, uremic
halitosis, gastritis, and GI bleeding (uremic
toxins)
 All of which are related to accumulation of
urea which can be considered as a toxin.
 Urea will be converted back to ammonia,
and that ammonia is very much irritating in
the GI tract, causing these manifestations.
NEUROMUSCULAR
Drowsiness, confusion, irritability, coma
 Neuromuscular manifestations are related to
uremic encephalopathy: What does it mean
by that? Uremia can actually alter cerebral
function, as evidenced by drowsiness,
confusion, irritability, and even coma.
 In the event that the client develops uremic
encephalopathy, it is but important that
safety will be our priority. Most likely, the
physician will be ordering for a hemodialysis
that will be served as an emergency
measure to ensure that these toxins can be
eliminated by the body through an artificial
mean, called hemodialysis.
Tremors, twitching and convulsions
 These are also related to alteration in
cerebral function.
 Remember: these are also reflective of the
development of hypocalcemia.
ELECTROLYTE IMBALANCES BROUGHT ABOUT
BY AKI OR END STAGE RENAL DISEASE
 Potassium and magnesium’s main route
of excretion will be by way of urine.
 If there is a decrease in production of
urine, that may also mean that there is
accumulation now of potassium ions and
magnesium ions because they are not
excreted in the urine by the body. Hence,
the client will develop hyperkalemia and
hypermagnesemia.
 Since kidneys produce or synthesize
Vitamin D necessary for calcium
absorption, the client may develop
hypocalcemia.
 Since there is a lowering of calcium, we
can also indicate now that there is an
increasing phosphorus level in the blood.
Hence, the client will develop
hyperphosphatemia.
 Since excessive water molecules can
dilute remaining sodium ions in the blood,
the client may develop hyponatremia in
the form of dilutional hyponatremia.
 Some clients with renal problem may also
develop hypernatremia brought about by
impairment in excretion of sodium ions in
the urine.
 5 electrolyte imbalances that are
commonly implicated in the client’s
experience of Kidney Injury:
Hyperkalemia, hypermagnesemia,
hypocalcemia, hyperphosphatemia and
dilutional hyponatremia. We may also
expect hypernatremia to develop.
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INTEGUMENTARY
Pallor
 This is brought about by anemia.
Yellowish Skin
 Retained urochome pigment
 This indicates that there is an excessive
presence of urobilinogen, a by-product that
must be excreted, bilirubin, which is yellow in
color.
 Since there’s impairment in its excretion
brought about by kidney failure, the client
may also develop jaundice or yellowing of
the skin.
Dryness
 Dryness of the skin is brought about by a
decrease in the function of oil and sweat
glands.
Pruritus
 The client may have itchiness or itching
sensation on the skin which can be
associated with the body’s attempt in order
to excrete these waste products by way of
the skin.
 Hence, these waste products, when
accumulated in the skin, can produce an
itching sensation.
 So, the presence of dry skin, calcium
phosphate deposits, and uremic toxins can
irritate too the nerve endings, causing the
sensation of itchiness.
Purpura
 Increased capillary fragility, platelet
dysfunction
 This is suggestive of bleeding tendencies
brought about by platelet dysfunction.
Uremic Frost (rarely seen)
 Urea, urate crystal excretion in skin
 Uremic frost is a condition by which the
uremic toxins find their way to be excreted
not by way of urine because the client
 already has a kidney failure, but this time by
way of the skin.
ENDOCRINE
Glucose Intolerance
 Peripheral insensitivity to insulin, prolonged
insulin’s half-life.
 In the presence of a kidney problem, there
will be a decrease in insulin sensitivity.
Hence, the client may develop
hyperglycemia, because insulin is not
producing its intended effects.
 Although some books would say that there
will be an increase in the half-life of insulin,
increasing now the effect of insulin in the
body, therefore, increasing the risk for
hypoglycemia.
 Basically, if the client has kidney injury, the
client may show erratic blood glucose levels.
SKELETAL
Hypocalcemia
 Hyperphosphatemia, decreased calcium
absorption in GI tract
 The client may develop hypocalcemia and
hyperphosphatemia which can increase
the fragility of the bones, increasing the risk
for pathologic fractures.
 The client may also have a decrease in
calcium absorption in the GI tract, therefore,
decreasing the availability of calcium ions in
the bones which are supposed to strengthen
them, therefore increasing the weakening of
the bones.
ACID-BASE IMBALANCES
Metabolic Acidosis
 There will be an increased accumulation of
hydrogen ions, decreased ability of the
kidneys to conserve bicarbonate, therefore,
the client may be at risk to develop acidosis,
and it is metabolic in nature, because we
did not mention anything about the
breathing here, so we can say from this
perspective that is it is metabolic in nature
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plus the fact that kidneys are highly
metabolic in nature.
 Clients can develop metabolic acidosis
which can be evidenced by lowering of the
pH, and lowering of the bicarbonate level.
 The management for this acid-base
imbalance will be in the way of sodium
bicarbonate in order to increase the sodium
bicarbonate, therefore increasing the pH,
correcting the pH between 7.35 and 7.45.
 As a compensation though because of the
increased acidity present in the blood, the
body will try to find a way in order to excrete
this excessive acid, and that is by way of
increasing the rate and depth of respiration,
known as hyperventilation, characterized by
rapid and deep breathing in the form of
Kussmaul’s breathing.
o We more oftenly used the term
Kussmaul’s breathing in the case of
diabetic ketoacidosis, for which a client
also presents metabolic acidosis as a
common acid-base imbalance.
 In this case, the client may develop
respiratory alkalosis because of increased
rate and depth of respiration, increasing
CO2 loss, causing now a decrease in PaCO2
level.
 The normal of which should be between 35
and 45 mmHg.
Diagnostic Procedures
1. Kidney-Ureter-Bladder (KUB) x-ray: size,
shape, position of the kidneys; calculi,
hydronephrosis, cysts, tumors
 X-ray of the kidney, urethra, and bladder
to determine possibility of obstruction
caused by stones. Stones can impair
urine flow or tumors that can significantly
obstruct the blood flow through the
kidneys.
2. Renal ultrasound: size of the kidneys, and
obstruction
 This may also provide a more detailed
picture of the kidneys and associated
structures.
3. Magnetic Resonance Imaging (MRI): renal
structures
 This may also provide a more detailed
picture of the kidneys.
Nursing Diagnosis
Depending on the client’s presentation
of emergent symptoms resulting from AKI, the
nursing diagnoses may include (but not limit)
the following:
Ineffective Airway Clearance - If the client
shows manifestations of pulmonary congestion,
therefore this will be our top priority. Ineffective
breathing pattern will be the second, and finally
an impairment in gas exchange if in case the
client develops pulmonary congestion and
pulmonary edema).
1. Ineffective tissue perfusion - This can be
related to a pre-renal cause of AKI.
2. Fluid volume excess (deficit) - If the client
develops peripheral edema or congestion
of the peripheries, the client most likely will
have this as a priority nursing diagnosis.
 Because of the vomiting episodes, more
so, the client may develop fluid volume
deficit, which is considered to be a
priority nursing diagnosis, too.
 Excess, in the form of interstitial space;
because the fluid has accumulated in
the interstitial space, only less fluid is now
available in the intravascular space,
causing now deficiency (so, depending
on the compartment plus depending on
the presentation of fluid excess or
deficit).
Risk for aspiration - if the client presents in the
emergency department with severe nausea
and vomiting because of the vomiting
episodes.
3. Risk for injury (electrolyte excess/ deficit)
 The client may develop increasing
muscle weakness brought about by
hyperkalemia or the client may easily
suffer from seizure, increasing threshold
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for seizure brought about by
hypocalcemia.
 The client may have a reduction in
respiratory effort.
 The client may have a decrease in
deep tendon reflex or maybe an
increasing muscle weakness brought
about by hypermagnesemia.
Planning
Consistent with the identified nursing
diagnoses, the plan of care is geared towards:
1. Achieving adequate renal tissue perfusion
- adequacy of blood flow to the kidneys
2. Establishing fluid balance
3. Prevention of injury - maintenance of
safety through normalization of these
electrolyte values.
We may be able to address these problems
depending on the presentation of symptoms of
the client that would require emergency
measures.
In this case, if the client suggests that
there’s a need for emergency hemodialysis or
emergency cleaning of the blood in order to
improve the symptoms of the client, the
physician may actually order for emergency
dialysis.
Implementation
To address the plan of care,
implementation strategies include the
following:
1. Treatment of underlying cause
a. Prerenal causes. We look into improving
perfusion to the kidneys by way of hydration
and prevention of shock.
 If the client suggests pulmonary
congestion or pulmonary edema or
hypervolemia, in this effort, no matter
how we would like to consider hydration,
it will not be possible because hydration
can increase or even aggravate the
presence of congestion of the client.
  But if in case the client did not show any
signs of congestion and that the client
has elevated serum creatinine and
through hydration, the urine output
actually increases, that may mean that
hydration is the most important priority
intervention.
Management involves the following:
 Prompt replacement of extracellular fluids
and aggressive treatment of shock help
prevent AKI.
 Replacement of fluids (may depend on the
specific prerenal cause)
o Blood transfusion. It is important that the
blood pressure may be considered
because through blood transfusion, we
can correct hypervolemia, we can
correct severe blood loss, and that
through this, we can increase blood flow
through the kidneys.
o Isotonic fluids for clients with pancreatitis
and peritonitis. In the presence of
hypovolemia, we do prefer isotonic
fluids.
o Hypotonic fluids from large urine or
gastrointestinal losses. If the client
develops hyper-osmolarity, hypotonic
fluids may be considered, and this can
be evidenced through its effectiveness,
there is a decrease in sodium level
because we would like to reduce the
osmolarity, reduce the sodium level until
such time that sodium will be within the
normal value.
o Positive inotropic agents,
antidysrhythmic agents. Inotropic agents
can improve the blood pressure just if in
case the client develops hypovolemia,
hypotension, decreasing perfusion to the
kidney tissues. Inotropic agents or
vasopressors can actually increase the
blood pressure, improve blood flow to
the kidneys, thereby increasing urine
output, eventually.
o Vasopressors, isotonic fluids
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b. Intrarenal causes. We would like to avoid
these nephrotoxic substances that
continually impaire/destroy kidney tissues.
Management involves the following:
 Drug therapy
 Dietary management of protein and
electrolyte restrictions. We would like to
reduce the effort of the kidneys in trying to
get rid of these waste products
o Urea, creatinine, and uric acid are
related with protein intake. That is why it
is expected that if the client develops AKI
or End-Stage Renal Disease (ESRD) or any
part of the disease process of kidney
injury, we have to take note that protein
intake should be minimal or restricted
because of all the macronutrients (fats,
proteins, and carbohydrates), it is
actually protein that makes it hard for the
kidneys to excrete the metabolic waste
products brought about by protein
digestion.
o We may also consider a restriction of
elevation of electrolytes. We may restrict
potassium, magnesium, and phosphorus-
rich food items because these can lead
to further hyperkalemia,
hyperphosphatemia, and
hypermagnesemia.
 Management of fluid and electrolyte
imbalances and renal replacement
therapies
 Preventive measures are as follows:
o Avoid nephrotoxins. We should
familiarize ourselves with the medications
that if ordered for a patient, can increase
the risk for kidney tissue injury.
Nephrotoxic Drugs
ANTIMICROBIAL
Aminoglycosides
May be ordered for clients with heart failure,
but we’ll have to carefully monitor serum
creatinine because this is considered to be
the most sensitive indicator of kidney function.
In this case, if the client is taking this for heart may not be considering administration of ACE
failure and we have observed for rising or ARB because they are considered to be
creatinine level, it is important that the nephrotoxic. Because for a client with
physician must be notified right away. hypertension, even if he or she is entitled for
these medications for blood pressure control,
Either an aminoglycoside may be shifted to may not be able to take them because of a
another medication for heart failure or its problem with kidney involvement.
dosage may be reduced in such a way that
the kidneys will not be going towards injury, Continuation for Preventive measures:
eventually failure or loss of function. o Optimize fluid volume status before
surgery or invasive procedures
Antiviral agents, Amphotericin B, Colistin o Reduce incidence of nosocomial
Polymixin B, SulfadiazIne, Quinolones, infections such as using indwelling
Vancomycin are also considered to be catheters judiciously, removing
nephrotoxic. indwelling catheters when no longer
Analgesics
needed, use aseptic technique with all IV
Nonsteroidal anti-inflammatory drugs
lines. If in case there is a need for foley
(NSAIDs), Selective Cyclo-oxygenase-2
inhibitors, Phenacetin, Analgesic catheterization, it should be decided
combinations judiciously because foley catheterization
Immunosuppressives increases the risk for infection. Infection
Calcineurin inhibitors, Sirolimus, everolimus can also cause destruction of kidney
Chemotherapeutic agents tissues.
 Are believed to be nephrotoxic based on o Implement tight glycemic control in the
randomized controlled trials. critically ill. Blood sugar control is a part
Platins (cisplatin), Ifosfamide (can cause of the management because
hemorrhagic cystitis), Mitomycin, hyperglycemia, observing diabetes
Gemcitabine, Methotrexate, Pentostatin, mellitus can actually lead to diabetic
Interleukin-2 (high dose), Antiangiogenesis nephropathy, which is a potential
agents, immunotherapies (immune complication brought about by chronic
checkpoint inhibitors, chimeric antigen
elevation of blood glucose level
receptor T cells)
o Aggressively treating sepsis
Other Medications that can be considered to
be nephrotoxic c. Postrenal causes. Management strategies
 Antgiotensin-converting enzyme inhibitors are usually resolved with relief of urine flow
(ACE inhibitors) / angiotensin-receptor obstruction.
blockers (ARBs) / renin inhibitors 2. Fluid balance
 Sodium glucose transporter-2 (SGLT-2)
An impairment in fluid balance in AKI can be
inhibitors (canagloflozin, dapagliflozin)
 Methoxyflurane evidenced by excessive fluid accumulation in
 Sucrose (IVIg excipient), hydroxyethyl the intravascular space secondary to limited
starch, mannitol, dextran) excretion of excessive water molecules. Due to
 Pamidronate, Zolendrat hypervolemia, hydrostatic pressure increases
 Topiramate, Zonisamide which causes pulmonary congestion and signs
 Orlistat of third spacing.
 Statins
 Mesalamine Related interventions include the following:

a. Obtain daily weights. Daily weights validate

ACE inhibitors are given for clients with
intake and output measurements.
hypertension. If a client has hypertension, and
at the same time renal injury, the physician
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  Weight is the most sensitive indicator of
fluid balance.
 If we are going to measure the client’s
weight, it should be performed at the
same time each day, with the same
clothes, and with the same weighing
scale.
 Only then can we accurately monitor
the client’s weight.
b. Maintain accurate intake and output
records. Fluids are usually restricted to the
amount of urine output in a 24-hour period
plus insensible losses.
 I&O monitoring is helpful in order to
estimate the recommended fluid
allowance that the client will be taking
the next day.
 We are going to monitor and calculate
the urine output or the total output of the
client on the previous day and we’re just
going to add around 400 or 1,000 ml
based on the output of the client
yesterday plus 400 or 1,000 ml for the
insensible fluid loss. That would be the
recommended fluid allowance of the
client the next day.
 If the client with AKI has around 400 ml of
output from yesterday inclusive of
vomitus and diarrhea, 400 or 1,000 is to
be added, depending on the institution
or unit policy.
 The recommended fluid allowance of
the client the next day will be around
1,400, but that would be in line with fluid
allowance and that it is going to be the
physician who’s going to be deciding on
that
c. Monitor respiratory status, including
respiratory rate and crackles. Respiratory
status in terms of rate, rhythm, and depth,
congestion.
d. Assess the heart rate, blood pressure, and
respiratory rate.
e. Administer all fluids and medications in the
least amount of fluid possible. If the client
shows signs and symptoms of hypervolemia,
distention of jugular veins, peripheral
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edema, and pulmonary congestion, fluid
restriction will be necessary.
 Hydration will be considered if in case it
is related to pre-renal cause, a decrease
in perfusion to the kidneys, showing a
decreased amount of urine output
without signs of congestion and that
through hydration, the client’s urine
output has improved, the client is
actually in need of hydration measures.
The client is indeed dehydrated.
f. Monitor blood and urine laboratory tests.
 We do not only monitor osmolarity,
electrolytes, acid-base, and ABGs. We
also have to monitor CBC count: platelet
count (because clients may develop
thrombocytopenia), Hemoglobin,
hematocrit, and RBC. Secondary to
decreased erythropoietin production.
g. Avoid invasive equipment whenever
possible.
h. Use good handwashing techniques.
i. Use aseptic technique in all procedures.
j. Perform pulmonary preventive techniques
such as turning, coughing, deep breathing.
Exercises can improve maximal lung
expansion, improving oxygenation and
ventilation.
k. Assess potential sites of infection (urinary,
pulmonary, wound, intravenous catheters).
l. Provide diet with essential nutrients but
within restrictions.
3. Electrolyte balance
Since the kidneys are the major regulators of
electrolyte balance, such imbalances may
occur in AKI. Concepts and related
interventions related with electrolytes
imbalances include the following:
Hyperkalemia occurs due to
hypercatabolism, and reduction of potassium
excretion due to the decreased GFR. Sudden
changes can cause dysrhythmias such as heart
blocks, asystole, ventricular fibrillation, may
induce muscle weakness, diarrhea, and
abdominal cramps
a. Regular insulin 10 units IV with D50% 50mL
can be given intravenously as an
emergency management.
 10 units of Humulin R, which will have to
be incorporated to any dextrose-
containing fluid, preferably hypertonic
glucose in the form of 50 dextrose,
around 50 ml of which will have to be
given intravenously for over 30 minutes or
depending on unit policy.
b. Sodium polystyrene sulfonate (Kayexalate)
increases fecal excretion of potassium by
exchanging sodium ions for potassium ions.
Mix the powder with full glass of liquid,
preferably chilled to increase palatability.
 Administration of SPS orally or rectally.
 We prefer rectal administration because
this is considered to be a more effective
route for SPS in treatment for emergency
hyperkalemia.
c. Calcium gluconate 10 mL in 10% solution
given by SIVP (slow intravenous push).
 The client may receive calcium not to
reduce potassium level but to prevent
cardiac arrest in order to reverse the
effect of potassium on the heart’s
conduction system.
d. Albuterol 10 to 20 mg via nebulization over
15 minutes increases plasma insulin
concentration, shifts potassium to
intracellular spaces.
 Albuterol can cause sympathetic
response: bronchodilation. It can
promote movement of potassium ions
from the blood into the cell, thereby
correcting hyperkalemia.
e. Loop diuretic in the form of a potassium-
wasting diuretic such as furosemide. We
have to remember that furosemide can be
considered nephrotoxic, same with that of
mannitol, which is another diuretic.
 In this case, we have to be judicious and
cautious enough in line with the
administration of these diuretics,
because even if they do correct
hyperkalemia, they can contribute to
development of renal injury.
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Hyponatremia occurs from water overload.
However, as nephrons are progressively
damaged, the ability to conserve sodium is lost
causing hyponatremia. Hyponatremia is
treated with fluid excretion through diuretics,
and fluid restriction.
 The main reason as to why hyponatremia
occurs is because of the excessive water
molecules. Therefore, restrict fluid.
 Diuretics can promote movement of
water molecules in the urine, thereby
correcting sodium level.
Hypocalcemia / hyperphosphatemia
 Calcium gluconate 10% SIVP
 The client may receive calcium
gluconate, and at the same time, the
client may receive a phosphate binder
which is indicated for
hyperphosphatemia.
 This phosphate binder, in the form of
aluminum hydroxide, can actually bind
phosphate in the GI tract, making it
possible for phosphates to be excreted in
the stool.
 However, aluminum hydroxide or most
phosphate binders can actually cause
constipation as the most common side
effect.
 Therefore, if in case hydration is
recommended by the physician, it is
important that we emphasize increased
oral fluid intake to prevent constipation,
but if the client with ESRD is on fluid
restriction, it is never allowed for the
client to increase oral fluid intake just to
prevent constipation.
 In that event, most likely, the physician is
going to order for a stool softener.
Hypermagnesimia
 Calcium gluconate 10% SIVP, diuretics
 In the event that a client develops
hypermagnesemia, the antidote for
magnesium toxicity is calcium gluconate
  So, calcium gluconate can be given plus
the fact that magnesium’s main route of
excretion is by way of urine. Therefore, a
diuretic may be ordered and may be
administered, depending on the
physician’s order.
4. Acid-base balance
Metabolic Acidosis occurs with the inability
of the kidney to excrete hydrogen ions,
decreased production of ammonia by the
kidney which normally assist with ion excretion
and retention of acid end products of
metabolism, which use available buffers in the
body and the inability of the body to synthesize
bicarbonate. Clients with serum bicarbonate
levels less than 15 mEq/L and ph less than 7.20
are treated with sodium bicarbonate. Watch
out for hypocalcemia, hypokalemia, and
metabolic alkalosis as adverse effects of sodium
bicarbonate.
 The client may develop metabolic acidosis,
therefore, the drug of choice will always be
sodium bicarbonate.
 If we are to give sodium bicarbonate, it’s
going to be by way of infusion.
 Rapid administration though of sodium
bicarbonate can lead to metabolic
alkalosis, lowering the H evidenced by
alkalosis. Lowering of the hydrogen ion
concentration can lower potassium ions,
too, which can cause hypokalemia.
 Since alkalosis increases protein-binding with
ionized calcium, the client may also
develop hypocalcemia.
 Therefore, if the client is receiving sodium
bicarbonate infusion, it is but important that
we monitor for adverse effects, inclusive of
hypokalemia, hypocalcemia, and even
metabolic alkalosis.
5. Pharmacological Agents
a. Diuretics (fluid overload, electrolyte excess
of K and Mg) may be used to manage fluid
overload but puts the patient at risk for
excessive diuresis and renal hypoperfusion
compromising an already insulted renal
system.
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b. Low dose dopamine HCl causes a transient
increase in renal blood flow and GFR by
stimulating dopaminergic receptors in the
kidney.
 High-dose dopamine hydrochloride can
cause vasoconstriction.
 Low-dose, on the other hand, can cause
renal artery vasodilation, improving the
perfusion in the kidneys.
c. N Acetylcysteine may be given as a
prophylactic agent against contrast
induced AKI.
 This is considered to be a
nephroprotectant, meaning, it protects
the kidneys.
 It can be given on clients who are to take
oral contrast or contrast-based
procedures, such as CT with oral
contrast.
 Acetylcysteine can be ordered before
and after the contrast procedure,
because this oral contrast can cause
injury to the kidneys and in order to
promote protection of the kidneys,
acetylcysteine can actually be
administered before and after the
procedure.
d. Fenoldapam is also administered as
prophylaxis against contrast induced AKI as
it acts as a vasodilator of peripheral arteries
which reduces blood pressure and as a
renal vasodilator which increases blood
flow.
 This is considered to be a renal artery
vasodilator, increasing perfusion to the
kidneys, preventing further injury of the
kidney tissues or of the nephrons.
6. Nutritional Recommendations
a. Caloric intake of 25 to 35 kcal/kg of ideal
body weight per day.
 Carbohydrates must be increased. Why
high carbohydrate? Because we would
like to avoid this protein being used by
the body.
b. Protein intake of no less than 0.8g/kg 75-80%
of which should come from essential amino
acids.
  Protein intake must be reduced in order
to prevent usage of protein-based
sources in the body, because there will
be by-products of protein which are
considered to be nitrogenous, which
can strain the failing kidney in that
situation.
c. Sodium, potassium, and calcium are also
carefully measured.
 Low dietary intake of potassium,
magnesium, and phosphorus will be
expected.
d. Fluid intake is equal to the volume of urine
output plus insensible losses.
e. Nutritional support must supply the patient
with sufficient non protein glucose calories,
essential amino acids, fluids, electrolytes,
and essential vitamins.
 There must be essential amino acids
because the body needs to obtain these
essential amino acids through diet,
because the body can utilize amino
acids, but there are some amino acids
called essential that must be derived
from the diet, and that meat and poultry
products are considered to be rich
sources of essential amino acids.
 It is important to somehow follow the
regulation provided by the physician or
the dietician in the allowable grams of
proteins to be taken on a daily basis.
f. Adequate nutrition prevents further
catabolism, muscle wasting and other
uremic complications, but also enhances
the tubular regenerating capacity,
resistance to infection, and ability to
combat multisystem dysfunctions.
 Adequate nutrition prevents further
catabolism, muscle wasting and other
uremic complications, but also
enhances the tubular regenerating
capacity, resistance to infection, and
ability to combat multisystem
dysfunctions.
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Evaluation
Consistent with the plans of care towards
nursing problems, the evaluation is focused on:
1. Renal tissue perfusion (urine output, serum
creatinine, GFR, blood urea nitrogen). The
best sensitive indicator of renal function is
serum creatinine.
 Creatinine. Creatinine should be within
the normal range, and that is between
0.6 and 1.2 mg/dL.
 Depending also on the presentation of
the client. If the client has ESRD, we’ll
have to take note that creatinine will be
higher than usual, and that dialysis will be
going to be the main method of
management for this client.
 Creatinine may be higher than usual
when compared to usual clients without
kidney problem.
 We are to monitor too urine output
because urine output is the most
sensitive indicator for tissue perfusion.
 Tissue perfusion will have to be related
with the kidneys, because among all the
body organs, it’s actually the kidneys are
very much sensitive towards changes in
perfusion status.
 Another thing is, we may look into the
Glomerular filtration rate. The normal is
around 125 ml per minute, which is the
amount of filtrate that is produced by the
body every minute, and that the urine
from that 125 would only be 1 ml per
minute. Therefore, we have the normal
urine output around 60 ml per hour. At an
average, this is around 62.5 ml per hour,
and the cut-off range when you talk of
urine output is at least 30 ml per hour.
Urine output may change, depending
on environmental conditions, dietary
status, and the like.
 Blood urea nitrogen. The normal level for
BUN is between 8 and 25 mg/dL. Some
would say around 10 to 20 mg/dL.
2. Fluid balance (weight, vital signs)
  Weight is the most sensitive indicator of
fluid balance.
 Hemodynamic status in the form of
blood pressure, blood volume, central
venous pressure, and presence or
absence of distended jugular veins.
 We may also look into compensatory
tachypnea and tachycardia brought
about by decreasing perfusion or maybe
brought about by pulmonary
congestion.
3. Maintenance of safety (electrolyte, and
acid-base balance). Normalization of
electrolytes that can increase safety if the
client has presentation of AKI.
QUESTIONS
1. A client with acute kidney injury develops
peaked T wave, widened QRS complex,
and prolonged PR interval (hyperkalemia).
The nurse anticipates which emergency
order?
A. 40% dextrose and 10 units regular insulin
B. Calcium carbonate PO 1 tab
C. 20 mEqs KCl in 200 mL NS over 2 hours
D. Spironolactone 1 tab PO STAT
Rationale: Dextrose and insulin are emergency
measures because insulin promotes movement
of potassium from the blood into the cell, but we
would like to avoid hypoglycemia because of
giving intravenous insulin, therefore, dextrose
will have to be added to prevent
hypoglycemia.
2. A client with a pulmonary congestion is
brought to the emergency department
following acute kidney injury. The nurse
places the client in which position?
A. Dorsal recumbent
B. Prone
C. Semi-Fowler’s
D. Left lateral
Rationale: In order to achieve maximal lung
expansion, semi-Fowler’s positioning must be
placed on a client with such difficulty of
breathing.
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3. To determine the allowable fluid intake of
the patient with ESKD for the day, the nurse
should evaluate the patient’s:
A. Serum osmolarity
B. Weight
C. Previous day’s urine output
D. Central venous pressure
Rationale: We’ll just have to add around 400
and 1,000 ml depending on unit policy, to
compute for the output that is considered to be
insensible by way of breathing, perspiration,
and the like.
4. The nurse understands that which of the
following laboratory findings should be
considered an emergency presentation
A. Magnesium: 1.8 mEq/L (normal: 1.5 to 2.5
mEq/L)
B. Potassium: 6.6 mEq/L
C. Creatinine: 1.4 mg/dL (normal: 0.6 to 1.2
mg/dL)
D. pH: 7.35 (normal: 7.35 to 7.45)
Rationale: Potassium is elevated, increasing the
risk for cardiac arrest, thereby presenting in itself
an emergency condition.
5. The nurse understands that a client on
chemotherapy may develop acute kidney
injury. Which of these is not part of the
client’s history of medication intake related
to AKI?
A. Ifosfamide
B. Methotrexate
C. Cisplatin
D. Streptomycin
Rationale: Streptomycin is an antibiotic, not a
chemotherapeutic drug. Although it is
nephrotoxic, it is not part of the answers.
6. The nurse takes care of a client with a
pseudomonas infection who has been on
pharmacologic treatment. Latest serum
creatinine shows 4.4 mg/dL. The nurse
informs the physician on call about the latest
medication regimen related to the client’s
laboratory finding which is:
A. Colistin
 B. Ifosfamide.
C. Cisplatin.
D. Paracetamol.
Rationale: Colistin: an antibiotic that can be
ordered for a client with pseudomonas
infection. Maybe after determining the culture
and sensitivity, colistin has been ordered for the
client, however, it has resulted to an increase in
creatinine, therefore, the nurse should inform
the physician of the current medication
regimen for such client with presentation of
possible AKI.
Ifosfamide and Cisplatin. Chemotherapeutic
agent not related to the development of
pseudomonas infection and treatment strategy
for a bacterial infection.
Paracetamol. It is somehow related to
antipyretic effect brought about by bacterial
infection, but it is not considered to be a
nephrotoxic drug.
RENAL CALCULI
Stone formation in the kidneys
commonly presents with pain among clients in
the emergency department. Related concepts
to introduce this topic include the following:
1. Stone formation requires supersaturation of
dissolved salts in the urine, which condense
into a solid phase. Increasing the amount of
solvent (urine) and decreasing the amount
of solute presented to the kidney (calcium,
oxalate, uric acid) can aid in prevention.
 There are stones that have formed in the
kidneys.
 When we talk of the urinary tract, the
kidney is actually one of the organs
present.
 Other than the kidneys, we also have
other structures, inclusive of the ureter,
bladder, and urethra.
 KIDNEYS can form at any part of the
urinary tract. It is said that kidneys are
often considered to be the common
structure for stone formation because
that is where urine forms.
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 STONES have to be produced if the urine
is so much concentrated that it allows
supersaturation of this solution,
precipitating now stone to form.
Basically, stone formation will occur if
there is supersaturation of dissolved
substances that are present in the urinary
tract.
2. About 80% of calculi are composed of
calcium oxalate, calcium phosphate, or a
combination of both. Calcium excretion is
elevated in conditions that include
hyperparathyroidism, absorptive and renal
hypercalciuria, and immobilization
syndrome. Complex interactions between
the gut, kidney, and bones contribute to
calcium oxalate stone formation.
 At the majority, it is said that kidney
stones are mostly composed of calcium:
calcium oxalate or calcium phosphate,
or may be in combination.
 Other forms of stones can also be present
in the form of other conditions. Basically,
other forms may be in the form of urinary
tract infection or maybe a genetic
defect in the metabolism of certain
amino acids, or may be in line with
precipitation of uric acid crystals that are
in line with formation of stones.
 So mostly, calcium phosphate or calcium
oxalate are the ones responsible in the
formation of kidney stones.
3. About 10% of stones are struvite
(magnesium-ammonium phosphate), which
are found most in women with recurrent
urinary tract infections. These stones are
associated with infection by urea-splitting
bacteria (Proteus, Klebsiella,
Staphylococcus species, Providencia, and
Corynebacterium) and are the most
common cause of staghorn calculi, which
are large stones that form a cast of the renal
pelvis. Antibiotic penetration into staghorn
calculi is poor, and the potential for urosepsis
exists if the stones remain.
 Struvite Stones are stones that are
produced based from the interaction of
 magnesium, ammonium phosphate we call as cystine stone at a very minor
caused by urinary tract infection. representation or formation of kidney
 So, if the client has repeated or recurrent stone.
urinary tract infection and the client
Remember
complains of flank pain, and a diagnosis
For a stone to develop, there must be
of stones has been made specifically
supersaturation of that solution; of these
produced in the kidneys, we know very
dissolved salts; only then will there be stone
well that most likely, the stone type is formation.
most likely going to be struvite.
4. Uric acid causes about 10% of urolithiasis,
occurs more commonly in men, and is RENAL CALCULI AND ITS CAUSES
associated with gout or chemotherapy.
Presented in table are the causes
Urate stones are radiolucent, and the urine
commonly implicated in the development of
is typically acidic.
kidney stones. Alongside each risk factor is the
 Another form of kidney stone is uric acid
reason for stone formation.
stone brought about by conditions such
as gout or chemotherapy. RISK FACTORS OF RENAL CALCULI
 Why chemotherapy? It is said that Obesity Promotes
through chemotherapy, there will be hypercalciuria
destruction of cancer cells, and that as a Low urine volume Allows solute to
by-product of destruction of cancer supersaturate
cells, there will be rupture of these Excess dietary meat Creates acidic
cancer cells, allowing for uric acid (purine) urinary milieu,
depletes available
present inside the cell to go in the blood
citrate, promotes
and will be filtered eventually by the
hyperuricosuria
kidneys. And so, uric acid elevation can Excess dietary Promotes
actually cause precipitation of uric acid sodium hypercalciuria
stones. Insulin resistance, Causes ammonia
 Gout is a metabolic condition by which metabolic syndrome mishandling, alters
the body is unable to metabolize uric urine pH
acid, which is a by-product of purine Family history Genetic
metabolism or from proteins that we are predisposition to
ingesting, and eventually absorbing in renal calculi
the bloodstream. Gout Promotes
5. Cystine stones account for approximately hyperuricosuria
1% of all stones and occur in patients with Bowel surgery, Promotes low urine
cystinuria, an autosomal recessive genetic inflammatory bowel volume, acidic urine
disorder affecting amino acid transport disease depletes available
citrate, hyperoxaluria
(COLA: cysteine, ornithine, lysine, arginine).
Primary Creates persistent
 Cystine stones are a result of a genetic
hyperparathyroidism hypercalciuria
defect in the metabolism of certain
Prolonged Bone turnover
amino acids in the form of COLA: immobilization creates
cysteine, ornithine, lysine, and arginine. hypercalciuria
 If there is a defect in the metabolism of Medications Indinavir, ephedrine,
these amino acids, this will actually favor loop diuretics,
crystallization in the kidneys, allowing for topiramate,
precipitation of kidney stones; this is what

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 acyclovir,
triamterene
Obesity
 Obesity can promote hypercalciuria,
increasing the amount of uric acid that is
present in the urine, allowing also for
hypercalcemia to develop.
 And so, hypercalciuria is also a suggested or
associated link with obesity as to why renal
calculi commonly develops
Low Urine Volume
 Why low urine volume? In the presence of
dehydration, the kidneys try to absorb more
water, causing now an increase in the
concentration of urine.
 Since urine becomes super concentrated,
this can actually allow for stones to develop.
Excess Dietary meat (purine)
 Protein will have a by-product called purine,
and part of purine metabolism will cause a
by-product called uric acid, which then
again cause uric acid deposits in the urine,
causing uric acid stone.
Excess Dietary Sodium
 It can cause super concentration of the
urine, therefore, causing stone formation.
Insulin Resistance, Metabolic Syndrome
 If there is a problem with glucose
metabolism, it can actually increase the
possibility of dehydration. Why? It is because
glucose can exert osmotic diuresis, therefore
causing polyuria, eventually dehydration,
and that, this can also favor stone formation.
Family History
 There is a genetic predisposition associated
with stone formation, and that it runs in
family.
 Not only in line with genetic defect, but it
may also be associated with a shared
environment, therefore, increasing the risk
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for obesity, increasing the risk for dietary
intake of protein-rich foods, purine-rich food
items, increased sodium in the diet.
Gout
 Gout is considered to be a metabolic
disorder in purine metabolism, increasing
uric acid deposition in the urine, causing uric
acid stones.
Bowel Surgery, Inflammatory Bowel Disease
 These can cause dehydration secondary to
increased amount of fluid loss in the body.
 If there is increased fluid loss, the kidneys will
try to compensate for this by increasing
more water reabsorption, causing now
supersaturation of the urine, favoring stone
formation.
Primary Hyperparathyroidism
 In this condition, there is an increase in
parathyroid hormone that increases
calcium absorption in the GI tract.
 Parathyroid hormone will act on the kidney
in order to decrease calcium excretion in
the urine.
 Parathyroid hormone also stimulates
increased bone resorption, meaning,
calcium from the bones goes into the blood,
thereby causing hypercalcemia, and that
hypercalcemia will trigger the kidneys in
trying to eliminate extra calcium ions in the
blood, but calcium will be very much
available in the urine, causing now
hypercalciuria, therefore causing the
possibility of stone formation.
Prolonged Immobilization
 Immobilization, if prolonged, can increase
bone resorption, and so in this case, calcium
from the bone leaves the bone and goes
into the blood, causing hypercalcemia,
thereby causing now kidneys’ excretion of
calcium through the urine.
 Now, calcium is present in the urine, thereby
causing hypercalciuria, causing now stone
formation.
 Medications
 Indinavir, ephedrine, loop diuretics,
topiramate, acyclovir, triamterene.
o Are medications that allow
crystallization of dissolved salts, favoring
stone formation.
APPLICATION OF THE NURSING PROCESS
Assessment
Assessment of a client with renal calculi
commonly includes determination of classic
symptom complex which is the acute onset of a
crampy intermittent flank pain that radiates
toward the groin. As pain originates from a
hollow viscus (ureter), the pain is visceral in
nature without associated peritoneal irritation.
Clients writhe in pain, unable to find a position
of comfort.
The classic manifestation of clients with
kidney stone is in line with the fact that this
kidney stone that has been present in the
kidneys can dislodge itself and can go into the
ureter.
Now, the problem is that, the ureter is
very much sensitive in the presence of these
kidney stones, plus the fact that these kidney
stones may have irregular edges, and the very
sensitive tissues that line the ureter can trigger
an increasing amount of pain experience.
Therefore, the client will complain of
flank pain, because that is where the stone is
located. That is where the kidneys are located
(in the flank region). Therefore, the classic
manifestation of renal calculi may be
associated with crampy, intermittent flank pain
radiating towards the groin.
Other expected assessment findings
may include the following:
1. Rebound abdominal tenderness, guarding,
and rigidity. These are associated with pain
experience.
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2. Nausea and vomiting. Due to abdominal
pain, stimulation of the medulla oblongata
causes nausea and vomiting.
 Because of the increasing abdominal
pain experienced, there will be
stimulation of the medulla oblongata,
triggering nausea and vomiting,
increasing the risk for dehydration or
increased risk for fluid volume deficit
3. Tachycardia, hypertension, and diaphoresis.
In response to adrenergic system, these
manifestations occur because of existing
pain experience.
 Due to an adrenergic system response of
the pain experience, the client may
develop tachycardia, tachypnea, and
hypertension because of an increased
pain experience.
4. Hematuria. It is present in 85% of patients
with renal colic, and 30% of them present
with gross hematuria.
 85% of clients with kidney stones tend to
develop hematuria due to the damage
of these kidney stones with irregular
edges on the lining of the tissues of the
very sensitive urinary tract. Hence, the
client may develop hematuria.
 Because of the disruption also in the
membrane in the glomerulus or in the
tubules, this would actually now impair
the filtration membrane, allowing
passage of red blood cells across that
filtration membrane, causing now
hematuria.
5. Pain. The location of the pain correlates
somewhat with the location of the stone.
Stones in the upper ureter refer pain to the
flank, whereas those in the mid-ureter
radiate to the lower anterior quadrant of the
abdomen. A distal ureter stone, which is
where 75% of stones are diagnosed, refers
pain to the groin. Stones positioned at the
ureterovesical junction can mimic a urinary
tract infection by causing frequency,
urgency, and dysuria in 3% to 24% of clients.
 The pain may be associated with the
location of the stones.
  For instance, if the stone has dislodged
itself from the kidneys and has been
present now in the upper ureter region,
the client may have a pain referred to
the flank.
 If in case it is around the mid-ureter
region, their pain may be present in the
lower anterior quadrant of
abdomen.
 Finally, if it’s distal to the ureter region, the
client may have pain referred in the
groin.
 UPPER URETER STONE: Pain referred to the
flank
 MID-URETER STONE: Lower anterior
quadrant of the abdomen
 DISTAL URETER STONE: Pain referred to the
groin
6. Urinalysis report. This result may help
evaluate the presence of any urinary tract
infection. A culture and sensitivity report
may be needed to guide in antibiotic
therapy.
 Urinalysis report may be reviewed by the
nurses and nurses may look into the
presence of red blood cells in the urine,
or maybe the presence of an existing
infection.
 This is because we have noted that
infection, if recurrent, can trigger the
formation of struvite stones or if in case
the stones have been present in there, it
can favor bacterial growth, increasing
the risk for infection as well.
 A culture and sensitivity report may be
needed to guide in antibiotic therapy
7. Imaging studies. These may confirm the
presence of stones.
Nursing Diagnosis
The clients who present in the
emergency department may report of flank
pain and other related symptoms. Common
nursing diagnoses include the following:
1. Acute pain - in line with the pain experience
associated with renal stones or renal calculi,
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our priority nursing diagnosis especially if the
clients present in the emergency
department will always be geared towards
pain control, pain relief.
2. Impaired urinary elimination
3. Risk for fluid volume deficit
Planning
the
Consistent with the identified problems,
the plan of care is focused on:
1. Relief from pain
2. Adequate urinary elimination
3. Maintenance of fluid volume
Implementation
Treatment for renal calculi in the
emergency department includes pain and
nausea/ vomiting control as needed.
Antibiotics for those with evidence of infection
may be provided.
1. Forced intravenous hydration
 Fluids should be given to correct any fluid
deficit due to vomiting or limited oral fluid
intake caused by pain.
 Since the client has been considered to be
nauseous, has been experiencing vomiting
episodes, it is very important that hydration
be considered as one of our priority
interventions in order to ensure that the
client may have prevented development of
dehydration, plus the fact that the client
who is vomiting may not be advised to take
in orally as of the moment, especially in the
emergency department.
 So, if that will be the case, intravenous
infusion of ordered intravenous solutions
may be an expected order for the clients.
2. Pain control
 Non-steroidal anti-inflammatory drugs
(NSAIDs) have a direct action on the ureter
by inhibiting prostaglandin synthesis. IV
administration achieves more rapid relief
than IM or PO dosing (e.g., ketorolac). In line
with NSAIDs, these medications cannot be
given to those with aspirin or NSAID
hypersensitivity, high risk for bleeding, and
 with renal impairment. Opioids (e.g.,
hydromorphone) are also routinely
administered for pain control. Because pain
and opioids both cause vomiting, anti-
emetics may be frequently required.
Intravenous lidocaine can reduce smooth
muscle tone and reduce transmission by
afferent sensory pathways. It is administered
slowly to avoid numbness or dizziness. It
provides pain relief sooner than IV morphine.
 Pain control will always be our priority
nursing intervention in the form of
administration of NSAIDs or non-steroidal
anti-inflammatory drugs.
o Intravenous administration of
medications is preferred more than IM or
per orem dosing considering that we
would like to achieve the therapeutic
effect of analgesia the quickest onset
possible.
o Contraindication though for NSAIDs will
be those clients with aspirin or NSAID
hypersensitivity because we don’t want
the client developing into anaphylactic
shock brought about by hypersensitivity
towards these medications.
 Other medications that can be ordered in
the form of opioid analgesics can be in the
form of morphine, hydromorphone, and
lidocaine.
o Lidocaine may be administered, but it
should be administered slowly.
 Other consideration that we can look into
will be the control of nausea and vomiting.
The pain causes nausea and vomiting.
o Not only that, analgesics when
administered, can actually trigger
nausea and vomiting. That is why
lidocaine must be administered slowly.
 Pain and analgesics can trigger nausea
and vomiting. Therefore, antiemetics will be
ordered for the client, in the form of
metoclopramide.
3. Antibiotic therapy
 The clients with kidney stones, renal
insufficiency and/ or systemic signs of
infection are treated with intravenous
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antibiotics (e.g., piperacillin-tazobactam,
cefipime, ciprofloxacin, ticarcillin-clavulanic
acid).
 Antibiotic therapy may also be ordered for
the client especially if the client presents
signs and symptoms of systemic infection.
 Antibiotics may be ordered especially if the
triggering event for stone formation is in
relation to recurrent urinary tract infection.
 Antibiotics may be ordered especially if
there are renal stones, this may actually
increase the risk for the development of
infection. Why? Because these stones can
trigger tissue injury, triggering an
inflammatory response, causing systemic
signs and symptoms of infection.
 Therefore, antibiotics may be ordered in the
form of: terazosin or piperacillintazobactam,
cefepime, ciprofloxacin, or
ticarcillinclavulanic acid.
 Antibiotics will be specifically ordered after
the result of urine culture and sensitivity, but
broad-spectrum antibiotics can be ordered
while waiting for the urine culture and
sensitivity report.
 Only after the result of CNS for urine can the
physician be targeting that specific
microorganism with the use of a specific
antibiotic to kill that pathogenic
microorganism.
Evaluation
Evaluation should investigate the
following parameters reflected from prioritized
concerns:
1. Absent/ tolerable pain – relief of pain
2. Urine output (color, amount)
 We may also look at the amount of urine
because if kidneys have been present for
a long time and without any intervention,
it can actually cause an impairment in
nephron function, increasing the risk for
acute kidney injury, which is considered
to be a post-renal cause for acute
kidney injury.
  Therefore, we would like to look the B. increased predisposition to urinary tract
amount of urine being produced. infection
 If the client develops azotemia or C. increased bone resorption releasing
oliguria, we might consider that the calcium from blood
client’s case is no longer renal calculi, D. low urine production.
but also AKI-induced renal calculi in that
Rationale: Calcium leaves the bone, goes into
particular situation.
the blood, causing hypercalcemia,
3. Hemodynamic status (blood pressure, heart
hypercalciuria, causing calcium stone
rate, weight) – normalization of vital signs.
development in the kidneys.
QUESTIONS
4. The priority management on a client with
1. A client with hyperparathyroidism develops renal calculi who presents in the
flank pain and has kidney stone presence emergency department would most likely
confirmed by ultrasound. Upon be:
examination, the kidney stones would most A. Anxiety (Maybe because of pain)
likely be: B. Acute pain.
A. calcium oxalate C. Ineffective tissue perfusion (Because of
B. struvite difficulty breathing because of the pain)
C. cystine D. Nausea (Because of the severe
D. uric acid abdominal pain)

Rationale: The client has hyperparathyroidism, POST-TEST

causing hypercalcemia, causing hypercalciuria
1. A client who develops acute kidney injury
brought about by the kidneys’ attempt to
due to ureteral stone has a risk factor that is
excrete the excessive amount of calcium
categorized under:
present in the blood. Therefore, calcium has
A. intrarenal.
been present in the urine which favors calcium
B. postrenal.
stone formation.
C. prerenal.
2. Which of the following is not associated D. renal.
with kidney stone development? 2. The clinical feature of acute kidney injury is
A. high urine volume best evidenced by:
B. high calcium diet (favors calcium A. decreased creatinine clearance.
development in the form of kidney stone, B. low blood urea nitrogen.
favoring kidney stone formation) C. low calcium.
C. urinary tract infection (favors struvite D. low phosphorus.
stone formation) 3. Most cases of renal calculi are caused by:
D. hyperuricemia (favors uric acid stone) A. high serum calcium.
B. struvite formation.
Rationale: Low urine volume can trigger
C. uric acid deposits.
supersaturation of dissolved salts, but not higher
D. urinary tract infection.
in volume.
4. The client with urinary tract infection
3. A client who has been on prolonged develops a kidney stone. This is related to:
immobility caused by cerebrovascular A. Calcium oxalate stones
accident develops flank pain. The nurse B. Cystine stones
recognized that kidney stones may have C. Struvite stones
formed due to: D. Uric acid stones
A. elevation of uric acid level
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5. The client with acute kidney injury develops
pallor. This is due to:
A. Genetic impairment in hemoglobin
synthesis
B. Low erythropoietin synthesis
C. Platelet destruction
D. Severe gastrointestinal losses
6. The nurse administers sodium bicarbonate
on a client with acute kidney injury. The
nurse monitors drug’s effectiveness by
checking on:
A. blood pH.
B. serum sodium.
C. urine output.
D. weight.
7. The nurse administers hydromorphone on a
client with renal calculi and monitors the
drug if it has taken effectiveness by
checking on:
A. Absence of nausea
B. Clarity of urine output
C. Relief from pain
D. Strength of urine flow
8. A client with acute kidney injury has his fluid
balance regularly monitored. The nurse
understands that the most sensitive indicator
of fluid balance is:
A. capillary refill.
B. level of consciousness.
C. urine output.
D. weight.
9. The client with acute kidney injury has been
started on sodium polystyrene sulfonate
(Kayexalate). The nurse monitors the
effectiveness of the drug by regular
checking of:
A. Calcium
B. Magnesium
C. Potassium
D. Sodium
10. The classic symptom of renal calculi
includes:
A. Flank pain
B. Hematuria
C. Nausea and vomiting
D. Rebound abdominal tenderness

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