Care Plan Template

This care plan template provides a step-by-step guide for nurses to address priority problems in patient care. It includes nursing actions and rationales based on evidence and references.

CARE PLAN TEMPLATE
Name of patient: Scenario
situation
number
List the cluster of cues related to one priority problem in the identified scenario situation.
Clearly indicate which cues are abnormal and provide the normal ranges (with referencing) for
comparison where appropriate.
An analysis of the presenting complaints suggest that there was an increase in blood pressure to
160/90 mmHg, thus suggesting presence of hypertension (normal levels are 120/80 mmHG). Reduced
urine output also occurs under circumstances that are marked by a reduction in blood supply to the
kidneys. His urine output was abnormal (300ml/day), compared to normal levels of 800-2000ml/day.
Puffy ankles show signs of retaining water and salt. In addition, renal tissue hypoxia can be cited as
the reason behind low oxygenation (89%), compared to normal 95-100%. Compared to normal levels
of 136-145 mmol/L of sodium, those in the patient was considerably low (130 mmol/L) (O'donnell et
al., 2014). Abnormalities were also observed in levels of chloride and urea, which were lesser and
greater than the normal levels of 98-106 mmol/L and 2.5 to 7.1 mmol/L, respectively (Grant et al.,
2014; Marttinen et al., 2016). The patient also demonstrated abnormalities in the pulse rate (110 vs.
60-100 normal), body temperature (38.4 vs. 37 normal) and respiratory rate (28 vs. 12-18 normal),
thus suggesting presence of tachypnea and tachycardia ( Forbes & Watt, 2015). Purulent drainage
from the wound also suggests the presence of a localised excavation or defect of the skin, and the soft
tissues that underline it, thereby leading to the release of fluid from the one side. Furthermore,
metabolic acidosis due to renal failure was the major reason for the onset of tachypnea, and fatigue in
the patient.
Process information - Pathophysiology: Discuss abnormalities in relation to the associated risk
factors and pathophysiological processing occurring
The patient is suffering from acute kidney injury (AKI), which can be defined as a sudden episode of
renal failure that occurs within a few days for few hours, and results in a buildup of waste products in
bloodstream, thereby making it difficult for the kidneys to maintain appropriate fluid balance in the
body (Schrezenmeier et al., 2017). Some of the major risk factors that are involved in this condition
include bleeding, low blood pressure, overuse of pain medications, injury, allergic reactions, blockage
of the urinary tract, and conditions that result in damage to the kidney tubule (Chawla et al., 2014). An
analysis of the case study suggests that the patient reports presence of an abdominal wound due to
abdominal surgery that has been conducted on him. There is mounting evidence for the impact that
renal impairment creates on wound healing (Huen & Cantley, 2015). In addition, failure of the kidneys

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in removing waste products and excess water, results in the accumulation of waste product and
shortage of red blood cell. These lead to fatigue and weakness in the patient. Moreover, AKI is also
associated with buildup of fluid in the lungs that results in shortness of breath, manifested in the form
of tachypnea. Intrinsic renal failure creates an impact on the glomerular filtration rate that is associated
with afferent vasoconstrictor release. Thus, obstruction in urinary tract leads to an increasing tubular
pressure that reduces the filtration driving force and causes AKI. Depression of renal blood flow is
also responsible for cell death and ischemia that generally occurs prior to systemic hypertension and
activate the cascade the cellular events that includes production of cytokinin, enzymes, and oxygen
free radical (Malek & Nematbakhsh, 2015). Leukocyte adhesion, endothelial activation, coagulation,
activation, and apoptosis initiation, result in cell injury, even after restoring the blood flow, thus
decreasing the glomerular filtration rate and causing oliguria, as observed in the patient.

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Actual
nursing
diagnosis with
related to and
evidenced by
statements
Goal of care
including SMART
outcome criteria
Priority Nursing actions (4)
including specific detail
Rationales for actions
clearly explained with in
text reference
The priority
problem is the
deterioration in
kidney
function in the
patient. The
nursing
diagnosis used
to detect this
priority
problem is the
RIFLE criteria
that helps in
defining
progressive
kidney injury
spectrum as
observed in the
patient based
on five stages
namely, risk,
injury, failure,
loss, and end
stage kidney
disease (Luo et
al., 2014).
The SMART goal for
addressing this priority
problem is given
below:
 Specific-
Improve renal
function in the
patient by
increasing his
urine output
and decreasing
the level of
serum
creatinine in
blood
 Measurable-
The glomerular
filtration rate
should increase
by at least 50%
and the urine
output should
be at least
greater than
<0.5 mL/kg per
hour, for a
1. Administering or
restricting fluids in order
to prevent fluid
overload. This will limit
the quantity of
beverages and fluids that
the patient would have
each day, and will
primarily be
administered under
circumstances when the
body contains excess of
water.
2. Administration of
diuretics such as,
torsemide, bumetanide,
mannitol, and
furosemide. Diuretics
encompass substances
that promote increased
urine production,
commonly referred to as
diuresis. These diuretics
will increase water
excretion from the body,
thereby preventing fluid
1. Fluid management is
typically calculated
for replacing output
from different
sources, in addition
to estimated loss by
the process and
metabolism. Pre-
renal failure also
referred to as
azotemia will be
treated by volume
replacement and
administration of
vasopressin (Prowle,
Kirwan & Bellomo,
2014). The oliguric
patient will be
subjected to
restriction of fluid
intake, in order to
prevent fluid
overload and
maintain an
appropriate balance
of salt and water in

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duration of 12
hours. Serum
creatinine level
should also be
near 0.6 to 1.2
milligrams/deci
liter.
 Achievable-
This goal can
be easily
attained by
implementing
adequate
nursing
interventions
that are based
on evidences of
clinical
research
 Relevant-
Increasing the
urine output
and decreasing
serum
creatinine
levels will help
in preventing
further
deterioration of
the kidney
injury and will
also prevent the
onset of other
co-morbid
conditions.
buildup.
3. A central venous
catheter will be placed
in the large vein, in
order to avoid under-
replacement or over-
replacement of fluid in
the body.
4. Administration of
prostaglandins that
would exert a
vasodilatory effect.
Prostaglandins are
primarily produced by
nucleated cells and are
paracrine or autocrine
mediators, which act on
endothelium, uterine,
platelet, and mast cells.
the body, with the
aim of stimulating
kidney function.
2. Diuretics will
increase urine
production by
reducing the blood
pressure. They are
primarily secreted
from proximal
convoluted tubule
through anion
transporter-1, and
bind to the Na(+)-
K(+)-2Cl(-) co-
transporter type 2,
and Na(+)-Cl(-) co-
transporter that are
located in the
ascending limb, and
the distal convoluted
tubule, respectively
(Dreischulte et al.,
2015). This binding
will promote free
water excretion,
thereby increasing
urine production
3. Insertion of a central
venous catheter will
help in taking out
blood from the body
that will be cleaned
by dialysis machine,
and returned through

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 Time bound-
this goal will be
accomplished
within 5 days.
another port, thus
helping in
purification of blood
and preventing
accumulation of
waste products
inside the body
(Cullis et al., 2014).
However, risks of
bloodstream
associated infections
are associated with
this particular
intervention at the
site of catheter
placement.
4. Administration of
vasodilatory
prostaglandins will
increase kidney
blood flow, along
with the rate of
glomerular filtration,
under circumstances
that are associated
with a decrease in
effective or actual
circulating volume
(Jia et al., 2015).
This will eventually
result in more
secretion of
potassium and
increased tubular
flow, thereby

CARE PLAN TEMPLATE restoring normal
kidney function.

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References:
Chawla, L. S., Eggers, P. W., Star, R. A., & Kimmel, P. L. (2014). Acute kidney injury and chronic kidney
disease as interconnected syndromes. New England Journal of Medicine, 371(1), 58-66.
Cullis, B., Abdelraheem, M., Abrahams, G., Balbi, A., Cruz, D. N., Frishberg, Y., ... & Pecoits-Filho, R.
(2014). Peritoneal dialysis for acute kidney injury. Peritoneal dialysis international, 34(5), 494-517.
Dreischulte, T., Morales, D. R., Bell, S., & Guthrie, B. (2015). Combined use of nonsteroidal anti-
inflammatory drugs with diuretics and/or renin–angiotensin system inhibitors in the community increases
the risk of acute kidney injury. Kidney international, 88(2), 396-403.
Forbes, H., & Watt, E. (2015). Jarvis's physical examination and health assessment. Elsevier Health
Sciences.
Grant, S. W., Hickey, G. L., Wisely, N. A., Carlson, E. D., Hartley, R. A., Pichel, A. C., ... & McCollum, C.
N. (2014). Cardiopulmonary exercise testing and survival after elective abdominal aortic aneurysm
repair. British journal of anaesthesia, 114(3), 430-436.
Huen, S. C., & Cantley, L. G. (2015). Macrophage-mediated injury and repair after ischemic kidney
injury. Pediatric nephrology, 30(2), 199-209.
Jia, Z., Zhang, Y., Ding, G., Heiney, K. M., Huang, S., & Zhang, A. (2015). Role of
COX-2/mPGES-1/prostaglandin E2 cascade in kidney injury. Mediators of inflammation, 2015.
Luo, X., Jiang, L., Du, B., Wen, Y., Wang, M., & Xi, X. (2014). A comparison of different diagnostic
criteria of acute kidney injury in critically ill patients. Critical care, 18(4), R144.
Malek, M., & Nematbakhsh, M. (2015). Renal ischemia/reperfusion injury; from pathophysiology to
treatment. Journal of renal injury prevention, 4(2), 20.
Marttinen, M., Wilkman, E., Petäjä, L., Suojaranta‐Ylinen, R., Pettilä, V., & Vaara, S. T. (2016).
Association of plasma chloride values with acute kidney injury in the critically ill–a prospective
observational study. Acta Anaesthesiologica Scandinavica, 60(6), 790-799.
O'donnell, M., Mente, A., Rangarajan, S., McQueen, M. J., Wang, X., Liu, L., ... & Rosengren, A. (2014).
Urinary sodium and potassium excretion, mortality, and cardiovascular events. New England Journal of
Medicine, 371(7), 612-623.
Prowle, J. R., Kirwan, C. J., & Bellomo, R. (2014). Fluid management for the prevention and attenuation of
acute kidney injury. Nature Reviews Nephrology, 10(1), 37.

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Schrezenmeier, E. V., Barasch, J., Budde, K., Westhoff, T., & Schmidt‐Ott, K. M. (2017). Biomarkers in
acute kidney injury–pathophysiological basis and clinical performance. Acta physiologica, 219(3), 556-574.