DIPLOMA IN MEDICAL ASSISTANT

HPSF MUAR

CASE STUDY: ACUTE KIDNEY INJURY

Section 1: STUDENT PARTICULAR

NAME: MOHAMMAD SYAFIQRI BIN

HAFIZ BANAH

MATRIC NUMBER: DMA_002271

YEARS /SEMESTER: YEAR 3 SEMESTER 6

CLINICAL PLACEMENT HOSPITAL PAKAR SULTANAH

AREA: FATIMAH, MUAR, JOHOR

MACP 6092
SUBJECT CODE: (EMERGENCY AND TRAUMA
PRACTICE)

DATE OF SUBMISSION: 1 DECEMBER 2022

 TABLE OF CONTENT

NO TOPIC PAGE
ACUTE KIDNEY INJURY (CASE STUDY)
Table Content i
Acknowledgement ii
1. Introduction 1
2. Definition 1
3. Etiology 4
4. Pathophysiology 6
5. Risk Factor 6
6. Sign and Symptoms 7
7. Physical Examination 8
8. Investigation 10
9. Differential Diagnosis 12
10. Management and Care Plan 12
11. Complications 14
12. Prognosis 15
13. Conclusion 15
Reference iii
Attachment iv

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ACKNOWLEDGEMENT

Assalammualaikum W.B.T

I am thankful to Allah S.W.T because with His permission I was able to complete the
course work successfully. First of all, I would like to thank Hospital Pakar Sultanah
Fatimah, where I underwent Obstetric Practice internship for giving me the opportunity
to produce this course work by providing various facilities to facilitate the process for me
to complete this assignment perfectly.

I would also like to thank my clinical instructor, Sir Mazlan Bin Dali who has given me
guidance and information from the beginning of this assignment until the process of
completing this assignment. Apart from that, I would also like to thank Sir Mazlan Bin
Dali for giving me the confidence to carry out this task successfully.

Not to be mentioned are both my parents who have provided a lot of emotional support
throughout the process of completing this assignment. Without support and
encouragement from them, it was difficult for me to complete the assignment within the
stipulated period. In fact, I would also like to thank my beloved partner, Nur Hiqmah
Hafiza Binti Matlau for the moral support and sharing her knowledge with me. Also not
to mention my friends and the parties involved for helping me a lot in completing this
assignment.

Finally, I hope that the assignments that I have been produce will further increase my
knowledge in this medical field as well as be a knowledgeable human being. In addition,
I hope that readers can also understand and utilize the knowledge that will be gained
and provide awareness to the community.

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1.0 INTRODUCTION

The kidney are two reddish-brown bean-shaped organs found in vertebrates. They are
located on the left and right in the retroperitoneal space, and in adult humans are about
12 centimetres in length. This organ receive blood from the paired renal arteries; blood
exits into the paired renal veins. Each kidney is attached to a ureter, a tube that carries
excreted urine to the bladder. An acute kidney injury (AKI) is where the kidneys
suddenly stop working properly. It can range from minor loss of kidney function to
complete kidney failure. Acute kidney injury normally happens as a complication of
another serious illness. It is not the result of a physical blow to the kidneys, as the name
might suggest.

2.0 DEFINITION

Acute kidney injury (AKI) refers to an abrupt decrease in kidney function, resulting in the
retention of urea and other nitrogenous waste products and in the dysregulation of
extracellular volume and electrolytes.

It also can define as a syndrome of decreased renal function, measured by serum

creatinine or urine output, occuring over hours-days. It includes different etiologies and
may be multifactorial.

The Kidney Diseases: Improving Global Outcomes (KDIGO) guidelines define acute
kidney injury as:

• Rise in creatinine >26μmol/L within 48 hours

• Rise in creatinine >15 x baseline (i.e, before the AKI) within 7 days.
• Urine output <0.5mL/kg/hour for >6 consecutive hours.

The severity of AKI is then staged according to the highest creatinine rise or longest
period/severity of oliguria.

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 2.1 TYPE OF KIDNEY INJURY

Depending on the cause, acute kidney injury (AKI) can be prerenal, instrinsic, or
postrenal. The table below describes each type and its causes.

Type of Kidney Injury Causes

Prerenal injury: decrease renal blood flow • Prolonged low-volume states, such
resulting from sepsis, trauma, bleeding, or as sepsis, decreased blood
poor cardiac output. pressure, and hemorrhage
• Such drugs as nonsteroidal anti-
inflammatory agents or
cyclooxygenase inhibitors, which
inhibit prostaglandin synthesis; in
turn, inhibition triggers action of
vasoconstrictors on renal arterioles,
which decrease glomerular filtration
rate

Intrinsic injury: acute tubular necrosis • Nephropathy caused ny contrast

from sepsis and renal ischemia (mean agents
arterial pressure below 70 mmHg) and • Aminoglycoside drug therapy
ultimately, from poor organ perfusion and wihout careful dosage monitoring
multisystemic failure.

Postrenal: obstructive nephropathy • Renal calculi

resulting from mechanical obstruction of • Tumors
urine flow. • Prostatic hypertrophy
• Strictures
• Congenital defects

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 2.2 TYPES OF AKI

This chart describes the features and duartions of the four phases of acute kidney injury
(AKI).

Phase Features Duration

3.0 Hours to days
Onset phase • Common triggering
events: significant
blood loss, burns,
fluid loss, diabetes
isipidus
• Renal blood flow
25% of normal
• Tissue oxygenation
25% of normal
• Urine output below
0.5 mL/kg/hour

Oliguric (anuric) phase • Urine ourput below 8 to 14 days or longer,

400 mL/day, possibly depending on nature of AKI
as low as 100 and dialysis initiation
mL/day
• Increase in blood
urea nitrogen (BUN)
and creatinine levels
• Electrolyte
disturbances,
acidosis, and fluid
overload (from
kidney’s inability to
excrete water)

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Diuretic phase • Occurs when cause 7 to 14 days
of AKI is correted
• Renal tubule
scarring and edema
• Increased glomerular
filtration rate (GFR)
• Daily urine output
above 400 mL
• Possible electrolyte
depletion from
excretion of more
water and osmotic
effects of high BUN

Recovery phase • Decreased edema Several months to 1 year

• Normalisation of fluid
and electrolyte
balance
• Return of GFR to
70% or 80% of
normal

3.0 ETIOLOGY

Cause of acute kidney injury (AKI) can be classified as: Prerenal, Renal, Postrenal.

Prerenal AKI is due to inadequate renal perfusion. The main causes are:

• Extracellular fluid volume depletion (e.g, due to inadequate fluid intake, diarrheal
illness, sepsis)
• Cadiovascular disease (e.g, heart failure, cardiogenic shock)

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 • Decompensated liver disease

Prerenal conditions typically do not cause permanent kidney damage (and hence are
potentially reversible) unless hypoperfusion is severe and/or prolonged. Hypoperfusion
of an otherwise functioning kidney leads to enhanced reabsorption of sodium and water,
resulting in oliguria (urine output <500 mL/day) with high urine osmolality and low urine
sodium.

Renal causes of AKI involve intrinsic kidney disease or damage. Disorders may involve
the blood vessels, glomeruli, tubules, or interstitum. The most common causes are
includes: Acute tubular necrosis, Acute glomerulonephritis, Nephrotoxins (including
prescription and over-the-counter drugs)

Glomerular disease reduces glomerular filtration rate (GFR) and increases glomerular
capillary permeability to proteins and red blood cells; it may be inflammatory
(glomerulonephritis) or the result of vascular damage due to ischemia or vasculitis.

Tubules also may be damaged by ischemia and may become obstructed by cellular
debris, protein or crystal deposition, and cellular or interstitial edema.

Interstitial inflammation (nephritis) usually involves an immunologic or allergic

phenomenon. These mechanisms of tubular damage are complex and interdependent,
rendering the previously popular term acute tubular necrosis an inadequate description.

Postrenal AKI (obstructive nephropathy) is due to various types of obstruction in the

voiding and collecting parts of the urinary system. Obstruction can also occur on the
microscopic level within the tubules when crystalline or proteinaceous material
percipitates.

Obstructed ultrafiltrate, in tubules or more distally, increases pressure in the urinary

space of the glomerulus, reducing GFR. Obstruction also affects renal blood flow,
initially increasing the flow and pressure in the glomerular capillary by reducing afferent
arteriolar resistance. However, within 3 to 4 hours, the renal blood flow is reduced, and
by 24 hours, it has fallen to <50% of normal because of increased resistance of the

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renal vasculature. Renovascular resistance may take up to a week to return to normal
after relief of a 24-hour obstruction. To produce significant AKI, obstruction at the level
of the ureter requires involvement of both ureters unless the patient has only a single
functioning kidney. Bladder outlet onbstruction due to an enlarged prostate is probably
the most common cause of sudden, and often total, cessation of urinary output in men.

4.0 PATHOPHYSIOLOGY

The pathophysiology of Acute Kidney Injury (AKI) is multifactorial and complex. The
most common cause of AKI is ischaemia, which can occur for a number of reasons.
Physiological adaptations, in response to the reduction in blood flow can compensate to
a certain degree, but when delivery of oxygen and metabolic substrates becomes
inadequate, the resulting cellular injury leads to organ dysfunction. The kidney is highly
susceptible to injury related to ischaemia, resulting in vasoconstriction, endothelial
injury, and activation inflammatory process. This susceptibility can be explained in part
from structural associations between renal tubules and blood vessels in the outer
medulla of the kidney, with ischaemia compromising blood flow to critical nephron
structures present therein. Following the reduction in effective kidney perfusion, the
epithelial cells are unable to maintain adequate intracellular ATP for essential process.
This ATP-depletion leads to cell injury and if it is severe enough can lead to cell death
by necrosis or apoptosis. During an ischaemic insult all segments of the nephrons can
be affected but proximal tubular cells are the most commonly injured. In addition, the
nephron’s natural funtion is to filter, concentrate and reabsorb many substances from
tubular lumen, and the concentration of these substances may reach toxic levels for
surrounding epithelial cells.

5.0 RISK FACTOR

• Aging (Old Age), Diabetes, Hypertension, Chronic Kidney Disease,
Cardiovascular Disease, Chronic Obstructive Pulmonary Disease, Obesity,
Human Immunodeficiency Virus Infection (HIV), Shock, Sepsis, Nephrotoxins,
Surgery, Hyperuricemia, Hypoalbuminemia, Hyperglycemia, Anemia

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6.0 SIGN AND SYMPTOMS

Initially, weight gain and peripheral edema may be the only findings. Often, predominant
symptoms are those of the underlying illness or those caused by the surgical
complication that precipitated renal deterioration.

Symptoms of uremia may develop later as nitrogenous products accumulate. Such

symptoms include anorexia, nausea, vomiting, body wekaness, myoclonic jerks,
seizures, confusion, and coma.

Asterixis and hyperreflexia may be present on examination. Chest pain (typically worse
and inspiration or when recumbent), a pericardial friction rub, and findings of pericardial
tamponade may occur if uremic pericarditis is present. Fluid accumulation in the lungs
may cause dypsnea and crackles on auscultation.

Other findings depend on the cause. Urne may be cola-coloured in glomerulonephritis

or myoglobinuria. A palpable bladder may be present with outlet obstruction. The
costovertebral angle may be tender if the kidney is acutely enlarged.

6.1 CHANGES IN URINE OUTPUT

Amount of urine output during acute kidney injury (AKI) does not clearly differentiate
between prerenal, renal, or postrenal causes.

In acute tubular injury, urine output may have 3 phases:

• The prodromal phase usually has normal urine output and varies in duration
depending on causative factors (e.g, the amout of toxin ingested, the duration
and severity of hypotension).
• The oliguric phase has urine output typically between 50 and 500 mL/day. The
duration of the oliguric phase is unpredictable, depending on etiology of AKI and
time to treatment. However, many patients are never oliguric. Nonoliguric
patients have lower mortality and morbidity and less need for dialysis.

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 • In the postoliguric phase, urine output gradually returns to normal, but serum
creatinine and urea levels may not fall for several more days. Tubular dysfunction
may persist for a few days or weeks and is manifested by sodium wasting,
polyuria unresponsive to vasopressin, or hyperchloremic metabolic acidosis.
7.0 PHYSICAL EXAMINATION

Patients with acute kidney injury usually appear ill. Physical examination of patients with
acute kidney injury is usually remarkable for hypotension, edema of the lower
extremities, maculopapular rash and rales on chest auscultation. Apply and adopt an
ABCDE approach, monitor patient’s potassium levels, fluid status for accurate physical
examination.

PRERENAL AKI
• Any obvious causes of decrease volume
a) History Taking
(Haemorrhage/haematoma, Gastrointestinal loss, renal
loss, skin loss (burns/erythema), third spacing
(pancreatitis), dehydration)
• Cardiac failure (recent echo?, recent ischaemic insult
to heart? etc.)
• Sepsis (what is the source of it?)
• Cool peripheries
b) Examination
• Warm to touch indicates sepsis ongoing
• Capillary refill time greater than 2 second implies
volume depletion or poor cardiac function
• Peripheral pulses
• Lying and standing blood pressure, significant drops
indicates hypovolaemia
• Jugular venous pressure may be low if volume deplete
or raised if heart failure or AKI causing significant
volume overload (an emergency)
• Face – sunken eyes imply dehydration

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 • Reduced skin turgor
• Dry mouth and mucous membranes, dry lips –
systemic hypovolaemia
• Signs of peripheral edema – pitting edema
• Lungs: signs of fine basal crepitations – pulmonary
edema. Signs of pneumonia imply source of sepsis
• Heart – listen for an S3, fluid overloaded escpecially in
Congestive cardiac failure (CCF) patients
• Abdomen : shifting dullness, source of sepsis
• Urine output – catheterised if necessary

RENAL AKI
• Cardivascular history (smoking, diabetes mellitus,
a) History
cholesterol, hypertension, PVD/IHD/CCF/stroke, AF,
prosthetic valves)
• Nephrotic syndrome (renal vein thrombosis)
• Recent infection of skin or throat
• “B type” symptoms such as night sweats, weight loss
and fevers
• Rashes, joint swellings
• Known autoimmune disease
• Easy bruising (myeloma)
• As for prerenal but be wary of rashes, skin changes,
b) Examinations
arthropathy, uveitis, oral ulceration, epistaxis, new
neurology including hearing loss, stigmata of
endocarditis

POST RENAL AKI

• Lower urinary tract symptoms (LUTS) – frequency,
a) History
urgency, dysuria, nocturia, poor stream, hesitancy,
terminal dribbling, strangury

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 • Prostate disease
• Malignancy
• Haematuria (visible and non-visible)
• Loin pain
• As for pre-renal AKI but examine for palpable
b) Examinations
abdominal massess, palpable bladder, visible
haematuria, rectal examination for prostate in males.

8.0 INVESTIGATION

A thorough patient history and physical examination, with a focus on evaluating the
patient's volume status, are essential for determining the aetiology of acute kidney
damage. The history should reveal any usage of nephrotoxic drugs or systemic
diseases that may have resulted in poor renal perfusion or directly impairing renal
function. A physical examination should be performed to determine intravascular
volume status and any skin rashes that may indicate systemic disease. Urinalysis,
complete blood count, serum creatinine level, and salt fractional excretion should all be
included in the first laboratory examination (FENa). Imaging studies can assist in ruling
out blockage. A summary of useful tests is provided in provides an overview of the
diagnosis and treatment of acute renal damage.

i. SERUM CREATININE LEVEL

To establish the length and severity of the condition, compare the patient's
current blood creatinine level to prior readings. The diagnosis of acute kidney
damage requires that a spike in creatinine occurred within 48 hours, albeit
this may be difficult to determine in the outpatient context. A high blood
creatinine level in a patient who previously had a normal reported level
indicates an acute event, but a gradual rise over weeks to months indicates a
subacute or chronic condition.

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ii. URINALYSIS

The most significant noninvasive test in the early workup of acute renal
damage is urinalysis. Urinalysis results suggest the differential diagnosis and
additional workup.

iii. FULL BLOOD COUNT

In the case of acute kidney damage, the development of acute hemolytic

anaemia with schistocytes on the peripheral smear should raise the potential
of hemolytic uremic syndrome or thrombotic thrombocytopenic purpura.

iv. URINE ELECTROLYTES

In patients with oliguria, measurement of FENa is helpful in distinguishing

prerenal from intrinsic renal causes of acute kidney injury. FENa is defined by
the following formula:

There are other online calculators accessible. A number of less than 1%

denotes a prerenal cause of acute kidney damage, whereas a value larger
than 2% denotes an intrinsic renal cause. However, in patients on diuretic
medication, a FENa greater than 1% may be generated by diuretic-induced
natriuresis and is a less accurate marker of a prerenal state. In such
circumstances, fractional urea excretion may be useful, with levels less than
35% indicating a prerenal origin. FENa levels less than 1% are not selective
for prerenal causes of acute kidney damage since they can be found in other
disorders such as contrast nephropathy, rhabdomyolysis, acute
glomerulonephritis, and urinary tract obstruction.

v. IMAGING STUDIES

Several patients with acute kidney damage, particularly older males, should
have a renal ultrasonography to rule out obstruction (i.e., a postrenal
cause). The presence of more than 100 mL of postvoid residual urine (as
measured by a bladder scan or urethral catheterization if a bladder scan is
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 not available) signals postrenal acute kidney damage and necessitates renal
ultrasonography to detect hydronephrosis or outlet blockage. Other imaging
modalities, such as computed tomography or magnetic resonance imaging,
may be necessary to determine extrarenal sources of blockage (e.g., pelvic
tumours).

vi. RENAL BIOPSY

Renal biopsy is reserved for individuals who have had prerenal and postrenal
causes of acute kidney damage ruled out and the source of intrinsic renal
injury is unknown. Renal biopsy is especially crucial when clinical evaluation
and laboratory studies reveal a diagnosis that has to be confirmed before
disease-specific treatment (e.g., immunosuppressive medicines) is started.
Patients with oliguria who have quickly developing acute kidney damage,
hematuria, and red blood cell casts may require an immediate renal biopsy. If
Goodpasture syndrome is present, the biopsy may support the
implementation of specific treatments, such as plasmapheresis, in addition to
identifying a diagnosis that needs immunosuppressive medication.

9.0 DEFFERENTIAL DIAGNOSIS

• Acute Tubular Necrosis
• Azotemia
• Chronic Kidney Disease
• Renal Calculi
• Sickle Cell Anemia
• Acute Glomerulonephritis
10.0 MANAGEMENT AND CARE PLAN

Effective engagement among primary care physicians, nephrologists, hospitalists, and

other subspecialists involved in the patient's care is required for optimal therapy of acute
kidney injury. Management is mostly supportive once acute kidney injury has been
diagnosed.

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Patients with acute kidney injury generally should be hospitalized unless the condition is
mild and clearly resulting from an easily reversible cause. The key to management is
assuring adequate renal perfusion by achieving and maintaining hemodynamic stability
and avoiding hypovolemia. In some patients, clinical assessment of intravascular
volume status and avoidance of volume overload may be difficult, in which case
measurement of central venous pressures in an intensive care setting may be helpful.

If fluid resuscitation is required because of intravascular volume depletion, isotonic

solutions (e.g., normal saline) are preferred over hyperoncotic solutions (e.g., dextrans,
hydroxyethyl starch, albumin). A reasonable goal is a mean arterial pressure greater
than 65 mm Hg, which may require the use of vasopressors in patients with persistent
hypotension. Renal-dose dopamine is associated with poorer outcomes in patients with
acute kidney injury; it is no longer recommended. Cardiac function can be optimized as
needed with positive inotropes, or afterload and preload reduction.

Attention to electrolyte imbalances (e.g., hyperkalemia, hyperphosphatemia,

hypermagnesemia, hyponatremia, hypernatremia, metabolic acidosis) is important.
Severe hyperkalemia is defined as potassium levels of 6.5 mEq per L (6.5 mmol per L)
or greater, or less than 6.5 mEq per L with electrocardiographic changes typical of
hyperkalemia (e.g., tall, peaked T waves). In severe hyperkalemia, 5 to 10 units of
regular insulin and dextrose 50% given intravenously can shift potassium out of
circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused
intravenously over five minutes) is also used to stabilize the membrane and reduce the
risk of arrhythmias when there are electrocardiographic changes showing hyperkalemia.
In patients without electrocardiographic evidence of hyperkalemia, calcium gluconate is
not necessary, but sodium polystyrene sulfonate (Kayexalate) can be given to lower
potassium levels gradually, and loop diuretics can be used in patients who are
responsive to diuretics. Dietary intake of potassium should be restricted.

The primary indication for using diuretics is to control volume excess. Intravenous loop
diuretics, administered as a bolus or continuously, can be beneficial in this situation.
However, in the absence of volume overload, diuretics do not improve morbidity,

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mortality, or renal outcomes and should not be used to prevent or treat acute kidney
injury.

All medications that have the potential to impair renal function by direct toxicity or
hemodynamic mechanisms should be avoided if at all feasible. Metformin
(Glucophage), for example, should not be administered to diabetic individuals who
suffer acute renal damage. The doses of critical drugs should be changed to account for
the decreased renal function. It is critical to avoid iodinated contrast medium and
gadolinium, and noncontrast tests are indicated if imaging is required.

Supportive therapies (e.g., antibiotics, maintenance of adequate nutrition, mechanical

ventilation, glycemic control, anemia management) should be pursued based on
standard management practices. In patients with rapidly progressive glomerulonephritis,
treatment with pulse steroids, cytotoxic therapy, or a combination may be considered,
often after confirmation of the diagnosis by kidney biopsy. In some patients, the
metabolic consequences of acute kidney injury cannot be adequately controlled with
conservative management, and renal replacement therapy will be required. The
indications for initiation of renal replacement therapy include refractory hyperkalemia,
volume overload refractory to medical management, uremic pericarditis or pleuritis,
uremic encephalopathy, intractable acidosis, and certain poisonings and intoxications
(e.g., ethylene glycol, lithium).

11.0 COMPLICATIONS

The most serious consequences of acute kidney injury are as follows:

• High levels of potassium in the blood – in severe cases, this can lead to muscle
weakness, paralysis and heart rhythm problems
• Too much fluid in the body, which can cause build-up of fluid in the arms and
legs (edema) or in the lungs (pulmonary edema)
• Acidic blood (metabolic acidosis) – which can cause nausea, vomiting,
drowsiness and breathlessness
• Chronic kidney disease

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12.0 PROGNOSIS

Acute kidney injury patients are more prone to acquire chronic renal disease in the
future. They are also more likely to develop end-stage renal disease and die
prematurely. Patients with acute renal damage should be closely followed for the
development or progression of chronic kidney disease.

13.0 CONCLUSION

Clinical examination results might, with modest accuracy, predict AKI in severely sick
patients. Clinical examination may be effective as a quick, free, and noninvasive firstline
evaluation, 'triggering' further measures that aid in the prediction of AKI incidence.

AKI is a serious clinical condition that is linked to poor clinical outcomes in hospitalised
patients. Significant progress has been achieved in clarifying the description of this
condition and elucidating the underlying pathophysiologic processes of the various
clinical presentations. All clinical manifestations of AKI cannot be explained by a single
pathophysiologic route. AKI promotes organ cross-talk and damage to distant organs.
These advancements will benefit in the design of epidemiology research and
randomised controlled trials of preventative and therapeutic therapies.

Because of the morbidity and mortality associated with acute kidney injury, primary care
physicians must identify patients who are at high risk of developing this kind of injury
and apply preventative treatments. Adults over the age of 75, those with diabetes or
previous chronic renal disease, those with medical conditions such as heart failure, liver
failure, or sepsis, and those exposed to contrast agents or undergoing cardiac surgery
are at the highest risk. Preventive methods can be adjusted to the clinical conditions of
the particular patient.

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 REFERENCES

Kalantarinia K. (2009). Novel imaging techniques in acute kidney injury. Current

drug targets, 10(12), 1184–1189.

https://doi.org/10.2174/138945009789753246

Makris, K., & Spanou, L. (2016). Acute Kidney Injury: Definition, Pathophysiology

and Clinical Phenotypes. The Clinical biochemist. Reviews, 37(2), 85–98.

Malkina, A. (2022, Jan). Acute Kidney Injury (AKI), retrieve by 7 Nov 2022, from

https://www.msdmanuals.com/professional/genitourinary-disorders/acute-kidney-

injury/acute-kidney-injury-aki

Rahman, M. Shad, F. Smith, M.C. (2012, Oct, 1). Acute Kidney Injury: A Guide to

Diagnosis and Management. American Family Physician. 86(7), 631–639

Wiersema, R., Koeze, J., Eck, R. J., Kaufmann, T., Hiemstra, B., Koster, G.,

Franssen, C., Vaara, S. T., Keus, F., & Van der Horst, I. (2020). Clinical

examination findings as predictors of acute kidney injury in critically ill

patients. Acta anaesthesiologica Scandinavica, 64(1), 69–74.

https://doi.org/10.1111/aas.13465

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ATTACHMENTS

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ATTACHMENT

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 MEDICAL ASSISTANT DIPLOMA COURSE
CASE STUDY SCORING FORMAT
Name: ............................................................................................. No. Matrik: ...................................
Year: ..................... Semester:.................................. Placement Area: ....................................................

BIL. Subject Marks Score Note

1 Introduction and clear statement of the
10
problem
2 Search for complete and relevant
20
literature
3 Discussions & arguments that are clear,
40
sound and show authenticity
4 Compact and conclusive formula 10
5 Appropriate and adequate reference
resources 10
6 Format:
- Clear package skin 2
- Number of words as set 2
- Clear and clean print 2
- Neat binding 2
- Format according to the set 2

Demerit:
- Spelling error > 20 words -5
TOTAL

Note:
Delay in submitting tasks will be checked based on 80

Examiner's Signature : .................................................................

Name : .................................................................
Date : .................................................................

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