2. 2
Table of Contents
1. Section one - Simulation Scenario 3-9
2. Section two 10
2.1. Pathophysiology of acute kidney injury (AKI) 10
2.2. Signs and Symptoms 11-12
2.3. Treatment Modalities 12
2.3.1. Treatment of AKI 12
2.3.2. Fluid management 12
2.3.3. Avoid nephrotoxic - ACEi 12
2.3.4. Nutrition therapy 13
2.4. Discharge care/plan 13
2.5. Multi-disciplinary Care 14
3. References 15-18
3. 3
1. Section one - Simulation Scenario
Curtin University School of Nursing Simulation Template
Course: Nursing Patient Name: Jack Daniels DOB: 01/01/1940
Scenario Title and Concept: An acute case of kidney injury
Level of Scenario
✓ Complex (see algorithm in Part B to develop flow of scenario )
Setting for Scenario
ü Other: Renal ward
BACKGROUND
A 75 year old male had collapsed at William Street due to severe dehydration, nausea and vomiting.
Post investigation in emergency (ED), Doctor? acute kidney injury (AKI) secondary due to severe
dehydration and angiotensin-converting enzyme inhibitor (ACEi) uses
Past medical history – Type II diabetes, hypertension (HTN), smoker for 30 years and chronic
alcoholic
Surgical history – Not known
Social history – Divorcee, living in a homeless shelter
Allergies – None
Current medications – Metformin per oral (PO) 500 mg twice per day (BD), Ramipril 5mg BD
Pre-Sim Study
Skills: Knowledge*:
1 Obtaining and recognising normal values in
vital signs
1 Under the Royal Perth hospital (RPH) policy,
nurses are required to have efficient knowledge in
performing, documenting and recognising
abnormalities in vital signs (Government of
Western Australia Department of Health, 2010b).
2 Performing physical checks (airway,
breathing, circulation, disability and exposure
[ABCDE])
2 The use of ABCDE is useful in emergencies as it
allows health professionals to perform direct
assessment of sick patients (Thim, Krarup, Grove,
Rohde & Lofgren, 2012). It also helps to recognise
4. 4
any life-threatening issues and avoid worsening of
condition (Thim et al., 2012).
3 Conducting focus assessments (cardiac and
urogenital)
3 Performing regular cardiac monitoring allow
health professionals to address any potential
abnormalities and recognise changes in heart’s
function (Baird & Bethel, 2011). It is important to
assess genitourinary system to identify kidney’s
functions amongst AKI patients (Baird & Bethel,
2011).
4 Administering fluids and medications 4 Nurses are to practice safe medication
administration and adhere towards hospital’s
protocols (Government of Western Australia
Department of Health, 2006).
5 Indwelling catheter (IDC) care, performing
bladder scan documentation of intake and
output
5 Nurses are required to be competently skilled
and knowledgeable in performing urinary
catheterisation and bladder care (Agency for
clinical innovation, 2014).
Performing bladder scan helps to assess amount
of residual urine and analyse the need for
catheterisation in patients with oliguria. The
guidelines in Royal College of Nursing (2011)
highlights the benefits, instruction and proper
documentation of a bladder scan examination.
6 Performing electrocardiogram (ECG), blood
sugar level (BSL) and interpret findings
6 The purpose of ECG is to evaluate heart
functions or detect any electrolyte imbalances,
therefore it is often used in regular health
examinations (“ECGs 1: Carrying out,” 2011).
BSL indicates individual’s glucose level in the
body, thus nurses can implement appropriate
interventions by accessing Diabetes Australia
(2012) policies to aid in proper management.
7 Maintaining optimal physical and
psychological wellbeing
7 Nurses need to encourage patient to achieve
personal hygiene at all times and ensure proper
manual handling when assisting clients with daily
activities (Government of Western Australia
Department of Health, 2010a).
8 Collaborating with other multi-disciplinary
teams
8 The use of interprofessional practice amongst
various health professionals can help to address
patient’s needs and achieve realistic goals
focusing on a patient centred care (Berger, 2006).
Scenario Objectives:
1. Regular monitoring of observations and physical assessments
2. Stabilise fluids and electrolyte balance by assessing and monitoring Jack’s intake and output
3. Care for activity daily living (ADL) and emotional wellbeing
4. Educating healthy lifestyle and monitor compliancy towards treatment
5. Referral to multidisciplinary teams and implement appropriate discharge care educations
5. 5
Critical Elements:
1. Jack’s – restless, anxious and complains of pain. Final year student nurse (FYSN) will provide
reassurance whilst senior registered nurse (SRN) will perform physical assessment and record
findings
2. During admission, SRN and FYSN will introduce self, perform vital signs
3. FYSN will perform BSL, urinalysis and weight
4. SRN will inform doctor, administer PRN (when necessary) medications and perform ward
transfer checklist
5. In an hour, SRN will obtain bloods, achieve diagnostic assessments and administer medications
6. FYSN will assist SRN by titrating Jack’s oxygen therapy, enquire pain levels, auscultate heart
sound and perform another set of observation
7. FYSN will assist Jack will his diet and personal hygiene, documenting his intake and output
8. Within 2-4 hours, SRN will interpret blood results, monitor Jack’s physical, emotional status and
perform focus assessments
9. FYSN will educate on healthy eating and advise harms on substance misuses, ensuring that he
is compliant towards care
10. Within next 4 hours, SRN will refer Jack to social worker (SW), dietitian, physiotherapist,
pharmacist, psychiatric and community services to assist in holistic care
11. FYSN will continue with routine observations, document care in progress notes, with SRN
supervision and perform handover using ISOBAR
Scenario Cast/Confederate Roles
Patient/Client
ü Mid-Level Simulator
ED nurse Performing handover to ward
staff
Patient care attendant (PCA)
SRN Transfer checklist, physical
assessments, routine care
and referral to other
disciplinary teams
Ward clerk
FYSN Cleaner and PCA
Renal medical team Diagnosis, Treatment and
management
Multi-disciplinary teams
Props and Equipment
Manikin: Supplies:
Simman 3G Gloves, alcohol wipes, urine collection bottle,
urinalysis dip, intravenous cannula (IVC),
indwelling catheter (IDC), vomiting bag, jug of
water
Props: Vital signs monitoring, stethoscope, BSL
machine, weighing machine, ECG machine,
oxygen masks (non-rebreather mask [NRM],
Hudson mask [HM], nasal prong [NP]), bladder
scan, fluid restriction notice place above patient’s
bedhead, identity band (ID), clothing on Simman,
patient’s belongings- wallet and cigarette
Medications:
Normal saline flushes, Normal saline 500mls
(*2), IV Fentanyl 25 mg, IV metoclopramide 10
mg, Glucagon 1 mg, 10 units of Lantus
Brief Narrative Report Learners Will Receive Before Simulation Begins:
● ED nurse will conduct handover using ISOBAR to ward SRN and FYSN about Jack current
conditions
● Old notes and radiology results
6. 6
● Admission form from ED
● Personal information list
● Bedside file: consist of medication chart, observation chart, weight chart, neurovascular
assessment (NVA), fluid balance chart (FBC), peripheral intravascular score (PIVAS), fall risk
assessment and care plan
Part B: Complex Scenario
Original setup : Blood pressure (BP): 100/52,
heart rate (HR): 115, 97% on HM 8L,
temperature: 36.5 ̊C, respiration (RR): 27
- Dyspnoea, dry lips and vomiting
- IVC line on right forearm: running stat
normal saline (N/S) 500mls over 1 hour
- IDC: 20-30mls/hour
Patient Responses: Jack is restless, anxious,
confused and complain of pain 8/10 in right
lumbar region
FYSN Responses: Introduce self and SRN,
provide reassurance by informing reason for
admission, educating on deep breathing
exercises to reduce anxiety, providing comfort
and advise sips of water when tolerated
1. Initial assessment of vital signs
✓ BP: A drop in BP indicates a shortage in
fluid volumes, whilst tachycardia and
tachypnoea are due to electrolyte
imbalances (Baird & Bethel, 2011).
2. FYSN will perform BSL, measure Jack
weight (using weight scale electrical hospital
bed), perform urinalysis and record findings in
observation chart
SRN Responses:
1. Inform Jack about performing physical
assessments
ü Airway: It is important to address if airway is
compromised because an obstruction can result in
circulatory arrest (Thim et al., 2012). Oxygen
administration and removal of vomitus is necessary
in ensuring a patent airway (Thim et al., 2012).
ü Breathing: It is essential to monitor HR, RR
and saturation levels to assess for abnormalities
(Thim et al., 2012). Nurses can observe for use of
accessory muscles, abnormal breathing and
conduct auscultation to evaluate respiratory
distresses (Baird & Bethel, 2011).
ü Circulation: Health professionals need to
observe facial features to inspect signs of cyanosis
(Baird & Bethel, 2011). It is necessary to monitor
capillary refill and assess heart sounds to evaluate
underlying heart diseases (Baird & Bethel, 2011).
ü Disability: Nurses can assess pain levels
using the ‘numeric rating scale’ to describe severity
of pain (Baird & Bethel, 2011, p. 137). This
includes Glasgow Coma Scale monitoring where
individual’s conscious levels are assessed (Baird &
Bethel, 2011).
ü Exposure: Nurses need to maintain
patient’s dignity and privacy whilst performing
physical checks (Thim et al., 2012). Patient’s
temperature can be monitored through use of
thermometer, whilst visualising for signs of
abnormalities or trauma (Thim et al., 2012).
2. Informing doctor about Jack’s admission and
completing transfer checklist
3. Offer PRN medications as documented by ED
doctors
✓ SRN will administer IV Fentanyl 25 mg (for
pain), IV metoclopramide 5 mg (for nausea and
7. 7
vomiting) (MIMS, 2015).
Vital Sign (post 1 hour): BP: 110/55, HR:
110, 96% on HM 6L, temperature: 36.6 ̊C,
RR: 25
- Tolerating sips of water, vomited 50mls of
gastric content
- IDC: 30mls/hour
- BSL: 3mmol/L
Patient Responses: Jack is still anxious but
verbalise that pain has decreased scoring 6/10
FYSN Responses:
1. Assist SRN in conducting observations,
titrating oxygen mask to NP 3L
2. Offer support with diet and attend to his
personal hygiene
✓ Assessing and documenting his intake and
output in FBC
SRN Responses:
1. Obtain bloods as requested by ward doctors
✓ Full blood count: It is used to detect any source
of infections resulting in AKI (Griffiths &
Kanagasundaram, 2011).
✓ Serum creatinine: It is used to detect
progressive kidney failures and to check if
patient is receiving appropriate treatment
(Thakar, Christianson, Freyberg, Almenoff &
Render, 2009).
✓ Blood urea nitrogen (BUN): It evaluates the
level of nitrogen in our blood and monitor
kidney’s functions (Macedo & Mehta, 2014).
✓ Estimated glomerular filtration rate (eGFR): It
assess kidney’s function therefore results will
show a declination if patient is at risk or has
AKI (Griffiths & Kanagasundaram, 2011).
Decreased blood pressure, vomiting and
diarrhoea can minimise blood flow to the
kidney and decrease eGFR (Kellum &
Lameire, 2013).
✓ Urine analysis: It is used to determine the
causes of AKI (Kellum & Lameire, 2013).
✓ Weight: AKI patients need to be weight daily
for fluid management, because patient is at
risk of fluid overload (Griffiths &
Kanagasundaram, 2011).
2. Perform diagnostic tests
✓ ECG is to rule out any potential hypo or
hyperkalaemia
✓ Kidney ultrasonography helps to visualise
kidney’s size and detect any urinary tract
abnormalities (Griffiths & Kanagasundaram,
2011).
3. SRN will administer subcutaneous (SC)
glucagon 1 mg to treat hypoglycaemia, re-
check BSL in 10 minutes to ensure efficiency of
medication (Diabetes Australia, 2012).
✓ Change fluids to 500 mls of N/S 6 hourly to aid
in electrolyte balance (Griffiths &
Kanagasundaram, 2011).
Vital sign Changes (in 2-4 hours): BP: SRN Responses:
8. 8
128/68, HR: 90, 96% on NP 3L, temperature:
36.2 ̊C, RR: 21
- Tolerating clear fluids, nil vomiting seen
- IDC: 50-60mls/hour
- BSL: 8.9mmol/L
Patient Responses: Jack will verbalise a
reduction in pain level scoring 4/10
FYSN Responses:
1. Routine assessments of physical
observations
✓ FBC: Hourly intake and output is essential
in AKI to ensure that patients are
compliant towards fluid restrictions and
avoid fluid retentions (Baird & Bethel,
2011).
✓ Vital signs: Nurses can perform 4 hourly
observations to monitor alterations in
patient’s condition (Government of
Western Australia Department of Health,
2010b).
✓ Pain assessment: It is essential to
recognise type and triggers of pain and
evaluate if rating correlates with vital signs
(Government of Western Australia
Department of Health, 2010b).
2. Advise Jack to comply towards care as
to prevent worsening in health.
1. Interpretation of blood results
✓ Serum creatinine level: 27 µmol/l
An increase in serum creatinine level >26.5 µmol/l
within 24 hours and decrease urine output
indicates AKI (Kellum & Lameire, 2013).
✓ Blood urea nitrogen (BUN) level: 18mg/dl
The normal range of blood urea nitrogen level is 7-
20mg/dL (Macedo & Mehta, 2014).
✓ eGFR: 70 mL/min/1.73 m2
The normal range of eGFR is 90 - 120 mL/min/1.73
m2, but eGFR will decrease due to age (Kidney
health Australia, 2012).
Rationale: Fluid resuscitations can restore patient's
hydration levels, increase blood flow to kidneys
and elevate eGFR whilst decreasing serum
creatinine level, thus, urine production will improve
(Godin, Bouchard & Mehta, 2013).
2. Conduct focus assessments
✓ Cardiac: Regular monitoring of patient’s BP is
essential thus if blood volume is deprived,
placing patient in supine position together with
fluid resuscitation can help to improve
condition (Thim et al., 2012).
✓ Skin, abdomen and limb: Oedema occurs in
independent tissues due to overloaded fluids in
AKI patients, conducting focus assessment is
essential to detect any abnormalities (Schnabl
et al., 2009).
3. Re-check of BSL as part of standardised
practice, ensuring a target of 4-8mmol/L pre-food
consumption (Diabetes Australia, 2012).
✓ Administer 10 units of SC Lantus at initial use to
achieve glycaemic stability (Diabetes Australia,
2012).
Vital Sign Changes/events (Next 4 hours):
BP: 136/78, HR: 88, 97% on NP 2L,
temperature: 36.0 ̊C, RR: 18
- Maintaining fluid restriction of 2.5L/day
- IDC: urine output 90-100mls/hour
Patient Responses: Jack will express his
SRN Responses:
1. Referral to multidisciplinary teams
2. Care towards prevention of chronic renal failure
Education in relation to:
9. 9
desire in maintaining a healthy lifestyle whilst
being compliant to treatments.
FYSN Responses
1. Educate healthy eating and minimising
substance misuse
ü Incorporating high fibre diet and regular
exercise to achieve wellness (Heart
Foundation, 2008).
ü Compliance towards medication and
treatment such as nicotine replacement
therapy (Royal Australian College of
General Practitioners, 2008).
ü Setting goals to reduce number of cigarette
per day and limit alcohol consumptions
(Hodge, 2011).
2. Documentation of care in progress notes,
with SRN supervision and perform
handover using ISOBAR to next shift staff.
✓ Smoking reduction
✓ Alcohol withdrawal
✓ Social support
✓ Manage HTN and type 2 diabetes
✓ Changing lifestyle
10. 10
2. Section two
2.1. Pathophysiology of acute kidney injury (AKI)
The cause of Jack's AKI is due to presence of toxins and loss of fluid volume. The
kidney's functions are to return water and nutrients to body as to restore blood volume and
pressure whilst removing unwanted waste, expelling it as urine (Yaklin, 2011). However,
poor renal perfusion and decreased volume causes a decline in uresis and glomerular
filtration rate [GFR] (Yaklin, 2011). The use of ACEi, vomiting and dehydration also results in
prerenal causes of AKI (Rahman, Shad & Smith, 2012). ACEi expands efferent arterioles
and deprive ‘intraglomerular pressure’ (p. 362) resulting in kidney hypoperfusion (Rahman,
Shad & Smith, 2012). Furthermore, these drugs restricts renal homeostasis reactions
towards fluid imbalances causing a fall in kidney’s performances (Rahman, Shad & Smith,
2012). Severe dehydration is classified as a diminished renal intravascular volume which
causes a drop in blood pressure, weakening GFR and intraglomerular pressure (Monaghan,
Nolan, Labato, 2012).
The physiological processes of AKI are described in four distinctive stages. In the first
stage, insults to kidneys are due to multiple factors like use of medications, infections or
presence of sepsis (Monaghan, Nolan, Labato, 2012). There is minimal symptoms seen at
this stage and it occurs for hours or days showing a declination in GFR (Monaghan, Nolan,
Labato, 2012). Poor circulation and renal ischaemia is seen at outer parts of renal medulla
because of overwhelming vasoconstriction and blockage of small vessels as a result of
endothelial-leukocyte adhesion and stimulation of coagulatory processes (Bonventre &
Yang, 2011). This results in oedema and cause obstruction at proximal convoluted tubule
(PCT) and ascending loop of Henle (Bonventre & Yang, 2011). Furthermore, direct injury to
kidneys reduce cellular functions resulting in hypoxaemia and adenosine triphosphate (ATP)
dysfunctions at PCT and wide segment of ascending limb (Monaghan, Nolan, Labato, 2012).
Dysfunctional ATP results in an elevated calcium balance which trigger proteases and
phospholipases thus aggravating renal cellular destruction (Monaghan, Nolan, Labato,
2012). The body goes through an inflammatory response worsening renal activities
(Monaghan, Nolan, Labato, 2012). The damage endothelium expels proinflammatory
cytokines and chemokines thus stimulating immune cell responses and intensifying
inflammation (Bonventre & Yang, 2011). Electrolyte imbalances are observable as elevated
levels of sodium transportation to distal tubular nephron results in narrowing of blood vessels
in afferent arteriole and worsening of ischaemia (Monaghan, Nolan, Labato, 2012). Cellular
permeability and renal integrity is diminished reflecting a reduction in GFR levels
(Monaghan, Nolan, Labato, 2012).
11. 11
Renal cellular activities continue to deprive in extensive phase lasting over a 48 hour
period (Monaghan, Nolan, Labato, 2012). In this instance, programmed cell death, renal
tubular necrosis and exacerbation of GFR is observed with presence of endothelial cellular
damage and impairments (Monaghan, Nolan, Labato, 2012). This results in augmented
reactions towards vasoconstrictive properties, disregarding vasodilation actions and further
depressing renal functions (Monaghan, Nolan, Labato, 2012). It is important intervene
appropriate treatments at this period to avoid cellular infarctions (Monaghan, Nolan, Labato,
2012).
The aim of stage three, is to achieve a balance in GFR thus this is accomplished
within one to two weeks (Monaghan, Nolan, Labato, 2012). Programmed cell death is still
visible with existence of renal complications, however renal perfusion is established by
enhancing cellular restorations (Monaghan, Nolan, Labato, 2012). It is important that health
professionals are able to restore fluid balances and discontinue use of ACEi medications to
regain normal renal functions (Rahman, Shad & Smith, 2012).
In the last stage, GFR is improved with presence of normal urine productions
(Monaghan, Nolan, Labato, 2012). The restoration of kidney functions are achieved through
the division and substitution of necrotic cells therefore regenerating normal polarity of
epithelium (Bonventre & Yang, 2011). It is important to acknowledge that improvement of
GFR is highly dependent on types of insults that cause AKI (Monaghan, Nolan, Labato,
2012).
2.2. Signs and Symptoms
In Jack’s case, he presents with sign and symptoms of prerenal AKI. Hypotension and
tachycardia are due to ineffective circulating blood volume which reduces systolic blood
pressure therefore balancing low stroke volume by elevating HR (Qureshi et al., 2012). Urine
output less than 0.5ml/kg/hour in 12 hours, is related to renal vasoconstriction that leads to a
reduction in GFR during prerenal stages (Bellomo, Kellum & Ronco, 2012). Nausea,
vomiting, dry lips, fatigue and confusion is due to dehydration, which is related to sodium
and potassium losses, leading to metabolic alkalosis (Raebel et al., 2010). Pain on right
lumbar region is related to nephrolithiasis causing papillary necrosis, hydronephrosis and
expansion of renal fibrous capsule around kidneys lead by kidneys infection (Tang & Lieske,
2014). Breathlessness, restlessness and anxiety are related to pain and stress in the
hospitalisation stay. Bouchard et al. (2009) stated that patients feel physically and mentally
vulnerable when faced with unfamiliar environment.
The signs and symptoms of intrinsic and postrenal AKI are hypervolemia cause by the
kidney’s insufficiency to excrete adequate fluids out of the body, which causes fluid
accumulation in peripheral and pulmonary area (Bouchard et al., 2009). Nephritic syndrome
12. 12
of proteinuria, hypertension and oedema are seen at damaged glomeruli and reduced
kidney’s functions (Orozco et al., 2011). Rash is due to accumulation of waste products in
blood stream (Tang & Lieske, 2014). Fever is related to the secretion of cytokine response
towards hypothalamus causing an increase in body temperature (Haas et al., 2013).
Palpitation or malaise is associated with hyperkalemia due to decrease urinary potassium
excretion (Raebel et al., 2010).
2.3. Treatment Modalities
2.3.1. Treatment of AKI
Nadeau-Fredette and Bouchard (2013) state that most treatments are supportive
interventions aimed to restore patient’s fluid and acid-base balance, and minimise damage
to kidneys. However, the treatment focused on AKI is dependent on the cause and patient’s
condition (Griffiths & Kanagasundaram, 2011). In this scenario, the cause of AKI is severe
dehydration that results in inadequate blood flow to the kidney. Therefore, the treatment for
Jack would be fluid resuscitation, avoid nephrotoxic - ACEi and nutrition therapy (Goldstein,
2012).
2.3.2. Fluid management
The key treatment of AKI is intravenous fluid therapy, which is aimed to restore
patient’s intravascular volume to assure adequate tissue perfusion (Godin, Bouchard &
Mehta, 2013). Colloid and crystalloid are the common fluids used to prevent and manage
AKI (Ingham & Forni, 2011). Colloids maintain plasma volume in our body, which can reduce
risk of renal failure (Roche & James, 2009). Yet, colloid can increase risk of AKI if patient
has sepsis (Ingham & Forni, 2011). In addition, crystalloid is used to balance electrolytes,
and it aids in immediate restoration of fluid imbalances (Ingham & Forni, 2011). However,
large amount of crystalloid can causes hyperchloremic metabolic acidosis that minimise
urine productions (Roche & James, 2009). It can results in risk of sodium overloading
(Roche & James, 2009). Therefore, nurses have to monitor AKI patient’s volume status,
which includes BP, capillary refill time, and hourly input and output (Ingham & Forni, 2011). If
volume overload occurs, diuretic, such as furosemide, might be required to increase urine
production (Nadeau-Fredette & Bouchard, 2013).
2.3.3. Avoid nephrotoxic - ACEi
Patient with AKI have weak kidneys as certain drugs causes nephrotoxic reaction
(Tomlinson et al., 2013). In this case, Jack was prescribed Ramipril that is an ACEi
medication. It is used for hypertension, which decreases arterial pressure that influence
blood flows to the kidney and reduces GFR (Tomlinson et al., 2013). Hence, nephrotoxic
13. 13
drug should be avoided for AKI patients as to avoid risk of developing chronic kidney
disease (Tomlinson et al., 2013).
2.3.4. Nutrition therapy
People with AKI are at high risk of developing malnutrition that will influence in a delayed
recovery (Saxena, 2012). Patient at any stage of AKI, should achieve a total of 20 – 30
kcal/kg/day energy intake (Khwaja, 2012). Therefore, nutrition therapy is essential for Jack to
balance his macro and micro nutrition levels (Saxena, 2012).
2.4. Discharge care/plan
According to Queensland Government (2014), providing education to be independent
and self-reliant, and promoting the prevention of illness to individuals is ideally useful in
achieving optimal quality of life. The discharge plan for Jack should include smoking
reduction as to smoking cessation programs (Royal Australian College of General
Practitioners, 2008). Nicotine replacement therapy (NCT) helps to minimise cigarettes uses
before cessation, therefore application of nicotine gum or inhaler are advisable (Royal
Australian College of General Practitioners, 2008). Moreover, health professionals involved
in promoting and encouraging smoking cessation needs to provide intense interventions
(Royal Australian College of General Practitioners, 2008). Telephone counseling and quit-
lines support are appropriate measures for Jack to utilise. Specialised counselors provide
advice and support to smokers who want to quit as they will follow up with proactive calls
(Royal Australian College of General Practitioners, 2008).
Nurses should encourage Jack to participate in cognitive behavioral therapy which
helps him to improve behaviours and coping skills through observations (Hodge, 2011). In
addition, motivational enhancement therapy is useful in discontinuing alcohol consumptions
by setting goals with a therapist or counselor, which motivates patients to change their
behaviours and achieve positive attitudes (Myrick et al., 2008).
Nurses can encourage Jack to maintain healthy lifestyle by performing 30 minutes of
exercise daily (Heart Foundation, 2008). Achieving a salt intake with <4 per day and
recommendation to low-salt diets, in addition limiting alcohol consumption with maximum of
2 standard drinks per day can facilitate healthy regimes (Heart Foundation, 2008).
Nurses can educate Jack to self-monitor his BGL daily before food and monitor correct
technique with insulin administration (Royal Australian College of General Practitioners,
2014).
14. 14
2.5. Multi-disciplinary Care
Multidisciplinary team involved a collaborative panel with each professional playing a
critical role within their own scope of practice to manage patient’s care efficiently. Social
worker is highly recommend for Jack as he has a deprived living situation. They can provide
information about homeless services, follow-up, promote social support and activities
(Claure & Bouchard, 2012). Dietitian play an essential role in maintaining optimal nutrition
and tailoring diet considering patient’s catabolic rate, in order to enhance nutritional status
(Claure & Bouchard, 2012). Pharmacists must be familiarise with medication therapies and
manage treatments of abnormal haemodynamic associated with AKI. Pharmacists play a
vital role in educating appropriate use of medications in treating AKI and regular monitoring
to prevent medication-induced injury (Claure & Bouchard, 2012).
15. 15
3. References
Agency for clinical innovation. (2014). Male indwelling urinary catheterisation (IUC)- Adult.
Retrieved from
http://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0020/256133/ACI_Male_IU
C.pdf
Baird, M. S., & Bethel, S. (2011). Manual of critical care nursing (6th ed.). Missouri, USA:
Elsevier Mosby
Bellomo, R., Kellum, J. A., & Ronco, C. (2012). Acute kidney injury. The Lancet, 380, 756-
766. doi:10.1016/S0140-6736(11)61454-2
Berger, J. L. (2006). Incorporation of the tidal model into the interdisciplinary plan of care: A
program quality improvement project. Journal of Psychiatric and Mental Health
Nursing, 13, 464-467. Retrieved from
http://edocs.library.curtin.edu.au/eres_display.cgi?url=DC65089371.pdf
Bonventre, J. V., & Yang, L. (2011). Cellular pathophysiology of ischaemic acute kidney
injury. The Journal of Clinical Investigation, 121, 4210-4221. doi:10.1172/JCI45161
Bouchard, J., Soroko, S. B., Chertow, G. M., Himmelfarb, J., Ikizler, T. A., Paganini, E. P., &
Mehta, R. L. (2009). Fluid accumulation, survival and recovery of kidney function in
critically ill patients with acute kidney injury. Kidney International, 76, 422-427.
doi:10.1038/ki.2009.159
Claure, R., & Bouchard, J. (2012). Acid-base and electrolyte abnormalities during renal
support for acute kidney injury: Recognition and management. Blood Purification, 34,
186-193. doi:10.1159/000341723
Queensland Government. (2014). Homelessness Program Guidelines. Retrieved from
http://www.hpw.qld.gov.au/SiteCollectionDocuments/homelessness-program-
guidelines.pdf
Diabetes Australia. (2012). Diabetes management in general practice. Retrieved from
http://www.diabetesaustralia.com.au/Documents/DA/What%27s%20New/12.10.02%
20Diabetes%20Management%20in%20General%20Practice.pdf
ECGs 1: Carrying out. (2011). Nursing Times, 107, 12-14. Retrieved from
http://www.nursingtimes.net/Journals/2012/03/30/o/z/d/110712ECG1.pdf
Godin, M., Bouchard, J., & Mehta, R. (2013). Fluid balance in patients with acute kidney
injury: Emerging concepts. Nephron Clinical Practice, 123, 238-245.
doi:10.1159/000354713
Goldstein, S. (2012). Fluid management in acute kidney injury. Journal of Intensive Care
Medicine, 29(4), 183-189. doi:10.1177/0885066612465816
Government of Western Australia Department of Health. (2006). Nursing practice standard
for medication administration. Retrieved from
https://lms.curtin.edu.au/bbcswebdav/courses/313045-HlthFac-
415036218/RPH%20NPS%202015/M%20-
%20Medication%20Admin%20NPS%202014%20v5.pdf
Government of Western Australia Department of Health. (2010a). Royal Perth Hospital
nursing practice standard for essential patient care (hygiene management).
16. 16
Retrieved from https://lms.curtin.edu.au/bbcswebdav/courses/313045-HlthFac-
415036218/RPH%20NPS%202015/P%20-
%20Patient%20Care%20Essential%20NPS%202013.pdf
Government of Western Australia Department of Health. (2010b). Royal Perth Hospital
nursing practice standard for vital signs. Retrieved from
https://lms.curtin.edu.au/bbcswebdav/courses/313045-HlthFac-
415036218/RPH%20NPS%202015/V%20-%20Vital%20Signs%20NPS%202013.pdf
Griffiths, L., & Kanagasundaram, N. (2011). Assessment and initial management of acute
kidney injury. Medicine, 39, 390-397. doi:10.1016/j.mpmed.2011.04.010
Haas, C. S., Lehne, W., Muck, P., Boehm, A., Rupp, J., Steinhoff, J., & Lehnert, H. (2013).
Acute kidney injury and thrombocytopenic fever-Consider the infrequent causes. The
American Journal of Emergency Medicine, 31, 441.e5- 441.e9.
doi:10.1016/j.ajem.2012.04.007
Heart Foundation. (2008). Guide to management of hypertension. Retrieved from
http://www.heartfoundation.org.au/SiteCollectionDocuments/HypertensionGuidelines
2008to2010Update.pdf
Hodge, D. R. (2011). Alcohol treatment and cognitive-behavioural therapy: Enhancing
effectiveness by incorporating spirituality and religion. Social work, 56, 21-31.
doi:10.1093/sw/56.1.21
Ingham, V., & Forni, L. (2011). The management of acute kidney injury. Medicine, 39, 398-
401. doi:10.1016/j.mpmed.2011.04.013
Kellum, J., & Lameire, N. (2013). Diagnosis, evaluation, and management of acute kidney
injury: A KDIGO summary (Part 1). Critical Care, 17, 204. doi:10.1186/cc11454
Khwaja, A. (2012). KDIGO clinical practice guidelines for acute kidney injury. Nephron
Clinical Practice, 120, 179-184. doi:10.1159/000339789
Kidney health Australia. (2012). eGFR - estimated glomerular filtration rate [Factsheet].
Retrieved from
http://www.kidney.org.au/LinkClick.aspx?fileticket=ndIOAsF1Bjo%3D&tabid=841&mi
d=1952
Macedo, E., & Mehta, R. (2014). Clinical approach to the diagnosis of acute kidney injury.
National Kidney Foundation Primer on Kidney Diseases, 294-303. doi:10.1016/b978-
1-4557-4617-0.00033-9
MIMS. (2015). MIMS Online. Retrieved from www.mimsonline.com.au
Monaghan, K., Nolan, B., & Labato, M. (2012). Pathophysiology, etiology and etiology-
specific management considerations. Journal of Feline Medicine and Surgery, 14,
775-784. doi:10.1177/1098612X12464458
Murphy, F., & Byrne, G. (2010). The role of the nurse in the management of acute kidney
injury. Br J Nursing, 19, 146-152. doi:10.12968/bjon.2010.19.3.46534
Myrick, H., Anton, R. F., Li, X., Henderson, S., Randall, P. K., & Voronin, K. (2008). Effect of
naltrexone and ondansetron on alcohol cue–induced activation of the ventral
striatum in alcohol-dependent people. Archives of General Psychiatry, 65, 466-475.
doi:10.1001/archpsyc.65.4.466
17. 17
Nadeau-Fredette, A., & Bouchard, J. (2013). Fluid Management and use of diuretics in
acute kidney injury. Advances in Chronic Kidney Disease, 20, 45-55.
doi:10.1053/j.ackd.2012.09.005
Orozco, R., Fervenza, F. C., Contreras, L., Leung, N., Singh, A., & Fierro, J. A. (2011).
Clinico-pathological conference on acute kidney injury in a patient with nephrotic
syndrome. Nephron, 119, c240-c247. doi:10.1159/000329507
Qureshi, A. I., Palesch, Y. Y., Martin, R., Novitzke, J., Flores, S. C., Ehtisham, A., . . . Tariq,
N. (2012). Systolic blood pressure reduction and risk of acute renal injury in patients
with intracerebral hemorrhage. The American Journal of Medicine, 125, 718.e1-
718.e6. doi:10.1016/j.amjmed.2011.09.031
Royal Australian College of General Practitioners. (2014). General practice management of
type 2 diabetes. Retrieved from
http://www.diabetesaustralia.com.au/PageFiles/763/UPdated%20GP%20guidelines.
pdf
Royal Australian College of General Practitioners. (2008). Supporting smoking cessation.
Retrieved from http://www.racgp.org.au/your-practice/guidelines/smoking-
cessation/smoking-reduction-rather-than-smoking-cessation/
Raebel, M. A., Ross, C., Xu, S., Roblin, D. W., Cheetham, C., Blanchette, C. M., . . . Smith,
D. H. (2010). Diabetes and drug-associated hyperkalemia: Effect of potassium
monitoring. Journal of General Internal Medicine, 25, 326-333. doi:10.1007/s11606-
009-1228-x
Rahman, M., Shad, F., & Smith, M. C. (2012). Acute kidney injury: A guide to diagnosis and
management. American Family Physician, 86, 631-639. Retrieved from
http://www.aafp.org/afp/2012/1001/p631.pdf
Roche, A., & James, M. (2009). Colloids and crystalloids: Does it matter to the kidney?
Current Opinion in Critical Care, 15, 520-524. doi:10.1097/mcc.0b013e328332f686
Royal college of Nursing Australia. (2011). Adult urinary obstruction, retention and bladder
scanning. Retrieved from
http://www.health.qld.gov.au/mass/docs/resources/continence/urinaryobstruct.pdf
Saxena, A. (2012). Dietary management in acute kidney injury. Clinical Queries:
Nephrology, 1, 58-69. doi:10.1016/s2211-9477(11)70010-3
Schnabl, K. L., Sibbald, M., Gold, W. L., Chan, P. C., Adeli, K., Richardson, R. M. A., &
Alpers, C. E. (2009). A patient with a leg rash, pedal edema, renal failure, and
Thrombocytopenia/Commentary/Commentary. Clinical Chemistry, 55, 1419-1422.
Retrieved from http://search.proquest.com/docview/213993622?accountid=10382
Tang, X., & Lieske, J. C. (2014). Acute and chronic kidney injury in nephrolithiasis. Current
Opinion in Nephrology and Hypertension, 23(4), 385-390.
doi:10.1097/01.mnh.0000447017.28852.52
Thakar, C., Christianson, A., Freyberg, R., Almenoff, P., & Render, M. (2009). Incidence and
outcomes of acute kidney injury in intensive care units: A Veterans Administration
study. Critical Care Medicine, 37(9), 2552-2558.
doi:10.1097/ccm.0b013e3181a5906f
Thim, T., Krarup, N. H. V., Grove, E. L., Rohde, C. V., & Lofgren, B. (2012). Initial
assessment and treatment with the airway, breathing, circulation, disability, exposure
18. 18
(ABCDE) approach. International Journal of General Medicine, 5, 117-121.
doi:10.2147/IJGM.S28478
Tomlinson, L., Abel, G., Chaudhry, A., Tomson, C., Wilkinson, I., Roland, M., & Payne, R.
(2013). ACE Inhibitor and angiotensin receptor-II antagonist prescribing and hospital
admissions with acute kidney injury: A longitudinal ecological study. Plos one, 8.
doi:10.1371/journal.pone.0078465
Yaklin, K. M. (2011). Acute kidney injury: An overview of pathophysiology and treatments.
Continuing Nursing Education, 38, 13-19. Retrieved from
http://search.proquest.com.dbgw.lis.curtin.edu.au/docview/852514364/fulltextPDF/1E
FE260EB3764972PQ/1?accountid=10382
