CASE PRESENTATION

SHOCK SEPSIS ON COMMUNITY-ACQUIRED PNEUMONIA

Arranged by:
Florence Low (0906550751)

Resource Person:
dr. Dita Aditianingsih, Sp,An-KIC

Intensive Care Elective Practice Module

Faculty of Medicine, Universitas Indonesia
May 2015

Case Illustration
Patients Identity
Nama

: Mr. R

No. Rekam Medis

: 404-01-92

Tanggal Lahir

: 12 September 1962 (52 tahun

Jenis Kelamin

: Laki-laki

Pekerjaan

: Ketua RT

Pendidikan

: SD

Status Perkawinan

: Menikah

Agama

: Islam

Alamat

: Kramat Jati

Tanggal masuk

: 14 Mei 2015

Ananmnesis
Data didapat dari anamnesis dan rekam medis pada tanggal 18 Mei 2015.
Keluhan Utama
Penurunan kesadaran sejak 7 jam sebelum masuk rumah sakit.
Riwayat Penyakit Sekarang
Pasien dirujuk ke RSCM dari RS daerah karena pneurunan kesadaran yang membutuhkan
perawatn ICU. 3 hari SMRS, pasien mengeluhkan sesak yang memburuk. Sesak tidak
dipengaruhi posisi ataupun aktivitas. Mengi disangkal. Terdapat demam namun suhu tidak
diukur. Pasien sebelumnya hanya minum obat warung untuk mengurangi demam.
Satu hari SMRS, pasien tampak mengantuk dan lemas. Pasien masih dapat diajak berbicara
namun lebih memilih untuk tidur terus. Nafsu makan pasien juga menurun. 7 jam SMRS,
sesak bertambah parah, nafas bertambah cepat dan pasien tidak dapat berbicara. Kesadaran
pasien juga menurun dan pasien tidak menjawab bila dipanggil. Sakit kepala disangkal, mulut
mencong dan kelemahan satu sisi juga disangkal, kejang disangkal. Pasien lalu dibawa ke RS
daerah.
2 minggu SMRS, pasien mulai batuk berdahak, batuk darah disangkal. Pada waktu itu,
demam belum muncul. Pasien tidak berobat dan hanya mengkonsumsi obat warung. Riwayat

batuk lama, keringat pada malam hari, dan penurunan berat badan disangkal. Psien
menyangkal riwayat sakit paru ataupun asma.
Pasien didiagnosis diabetes mellitus type II sejak 2,5 tahun yang lalu. Pasien tidak rutin
berobat. Pasien mengaku bahwa gula darah rata-rata 300 mg/dL..
Riwayat Penyakit Dahulu
Terdapat riwayat darah tinggi, stroke dan penyakit jantung sebelumnya. Pasien tidak
memiliki pengobatan apapun.
Riwayat Penyakit dalam Keluarga
Riwayat DM, hypertensi, asma dan penyakit jantung dalam keluarga disangkal.
Riwayat Sosioekonomic
Pasien sudah menikah, memiliki 4 anak. Pasien bekerja sebagai ketua RT. Untuk pembiayaan,
pasien menggunakan KJS.
Pemeriksaan Fisik
(Dilakukan tanggal 18 Mei 2015)
Status Generalis

: tampak sakit berat

Kesadaran

: coma (dalam pengaruh obat)

Tanda Vital
Tekanan darah
Nadi
Pernapasan
Suhu
Berat badan
Pemeriksaan
Kepala
Mata

Hidung
Mulut
Leher
Dada
Jantung
Paru

: 182/41 mmHg
: 104x/minute,
: 20x/minute, on ventilator
: 36.7C
: 60 kg
: normocephal, tidak ada tanda deformitas
: konjuntiva pucat +/+, sklera ikterik -/-, pupil isokor 3mm, RCL +/+,
RCTL +/+
: on NGT
: on ETT
: tidak teraba pembesaran KGB, terpasang CVC
: simetris statis dinamis
: S1 S2 normal, murmur -/-, gallop -/: simetris, perkusi kiri sama dengan perkusis kanan, vesikuler +/+,

terdengar rhonki basah halus pada kedua lapang paru

Abdomen
Ekstremitas
Kulit

: buncit, kenyal, tidak teraba massa, bising usus normal

: akral hangat, CRT< 2, edema pada kedua lengan
: pada region inguinal bilateral hingga skrotim, tampak lasi plakat
multiple diskret ireguler, batas tegas denga lesi satelit

Pemeriksaan Penunjang
Pemeriksaan Laboratorium
14/4/15

18/5/15

18/5/15

19/5/15

20/5/15

21/5/15

22/5/15

(post
Hb (g/dL)
Ht (%)
Leukosit

7.75
25,2
9970

10,5
32,7
17500

HD)
9,2728,7
28,7
20100

9,92
30,7
21300

8,48
24
12400

11,1
33,4
12200

9.74
30.4
25200

(/L)
Trombosit

427000

198000

131000

118000

102000

54800

71.900

73,1
23,7

70,0
22,6
11,2

70,0
22,6
11,9

72
25,4
13,8

73,6
24,4
13,0

74,4
23,8
14,0

APTT

(11,8)
69,9

(11,8)
53,2

(11,2)
65,2

(12,7)
55,7

(10,8)
>180

Na

132

135

(35,5)
125

(32,5)
135

(34,5)
130

(36,3)
127

(35,1)
127

(mmol/dL)
K

4.5

5,0

4,2

4,3

3,8

4,8

4,4

(mmol/dL)
Cl

106

106

103

102

100

96

97

25,2
1,392

7,9
2,26
81,4
3,5

66,7
3,1

8,4
2,04
74,9
3,347

8,3
2,8
92,9
3,863

89
3,39
117,2
4,104

94
3,316

7,213
28,4
149,5
11,5
-14,2
98,9
2,05

7,190
47,1
189,3
17,2
-9,3
97,9

54,4
188,4
15,9
-13,5
97,4
2,27

6,864
93,1
117,6
17,7
-15,6
92,5
2,16

(L)
MCV (fL)
MCH (Pg)
PT

12,4
(12,6)

(mmol/dL)
Ca
Mg
Ur (mg/dL)
Cr (mg/dL)
AGD
pH
pCO2
pO2
HCO3
BE
SaO2
Albumin

7,272
26,4
206,5
12,3
95,9

7,076
34,9
158,4
10,3
-17,5
96,1

(g/dL)
Keton
GDS
Prokalsitoni

4
17,93

n
Laktat

0,7

0,5

1,5

1,1

Urinalisis
Pada urinalisis ditemukan protein +2, keton +1, darah +1 dan leukosit 1-2
Pemeriksaan Radiologis

Chest X-ray (18/5/15)

o 18/5/15: Tampak inflitrat di parakardial kanan dan suprhiler kiri, sugestif
gambaran tanda awal bendungan paru
o 20/5/15: dibandingkan dengan foto sebelunya, infiltrate di parakardial kanan
berkurang

Daftar Masalah
1.
2.
3.
4.

Penurunan Kesadaran ec sepsis dd metabolik

Shock sepsis ec CAP
Ketoacidosis diabetikum pada DM type II tidak terkontrol
AKI dd Acute on CKD

Rencana Diagnosis
1. Kultur sputum dan darah
2. Tes resistensi and sensitivitas antibiotic
Rencana Terapi
1.
2.
3.
4.

Rawat ICU dengan ventilator pemantauan hemodinamik

IVFD RF 50cc/jam
Diet per NGT nutriflex
Atasi sepsis dan CAP
a. Stabilisasi hemodinamik: norepinephrine 0,1 mcg/kg/min IV, dobutamin
20mcg/kg IV
b. Antibiotik: meropenem 3 x 1gr IV dikombinasikan dengan levofloxacin 1 x
750mg IV
c. Anti-fungal fluconazole 1 x 400mg IO
d. Pengeluaran mucus: fluimucyl 3 x 1 sach, suction aktif / 4jam dan inhalasi
B:V:N / 6jam
e. Atasi demam: paracetamol 3 x 500mg

5. Anti stress-ulcer
a. omeprazole 2 x 40mg
b. Sucralfat 4 x 1 Corig
c. Metoclopramid 3 x 1amp
6. Atasi hiperglikemia: Ringer Insulin 1Unit/jam, GDS per 6 jam
7. Sedasi midazolam 15 mg
8. Anuria dengan fluid overload furosemide 20 mg IV, balans diuresis negatif
9. Jaga higienis mulut dan kulit

Follow up 16/5/2015
S

: perawatan hari ke-1; pasien masuk ICU

: BP 100-120/60-80; MAP 50-89 CVP +17,5 cmH2O

RR 12-16x; Pola ventilator PC 12, PEEP +5, RR 12, FiO2 40%,
GDS 109, 85, 162, 325
Input: 2221,2 cc
Output 420 cc Rate diuresis 0,29/kgBB/jam
Balans/24 jam +1801,2 cc

: Shock sepsis ec CAP, KAD, AKI dd acute on CKD

: RDx: cek PCT, kultur sputum dan darah, sputum BTA 3x

RTh
1. Lanjutkan terapi
2. Sedasi morfin 1mg/jam dan midazolam 1mg/jam
3. IVFD NS 500cc/24jam
4. MC 30cc/jam
5. Nutriflex 1 /24jam
6. RI 1 unit/jam
7. NE 0,05mcg/kgBB/min

Follow up 17/5/2015
S

: perawatan hari ke-2; pasien arrest dan di-RJP, re-intubasi karena mucus plug

: BP 120-140/60-80; MAP 66-103 CVP +15 cmH2O

RR 12-16x; Pola ventilator SIMV 14, PC 12, PEEP +7, RR 16, FiO2 40%,
GDS 324, 304, 311, 219, 150, 118
Input: 3183,3 cc
Output 781 cc Rate diuresis 0,54cc/kgBB/jam
Balans/24 jam +2402,3 cc

: Shock sepsis ec CAP, KAD, AKI dd acute on CKD

: RDx: DPL, Ur/Cr, P/APTT, AGD, elektrolit, GDS

RTh
1. MC 50cc/jam
2. Nutriflex 1/24jam
3. RF 50cc/jam
4. RI 1 unit/jam titrasi
5. Midazolam 2mg/jam
6. MAP 50 NE dinaikkan darri 0,15mcg ke 0.75mcg
7. Arrest bradicardi 36x; BP 36/29
Dilakukan RJP 2 siklus, mendapat SA 6 ampul, Adrenalin 1 amp
NE 1,1 mcg, dobutamin start dosis 5-10mcg
Reintubasi ETT ditemukan sekret kental putih (mucus plug)

Follow up 18/5/2015
S

: perawatan hari ke-3, pasien HD, ditarik cairan sebanyak 1500cc

: BP 182/82; MAP 90-124; CVP +22cmH2O

RR 16-20x; Pola ventilator PC 14, PEEP +7, RR 16 FiO2 50%,
GDS 188, 207, 306, 203
Input: 3984,4 cc
Output 2520cc Rate diuresis 0,63/kgBB/jam
Balans/24 jam +1464,4cc

: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrest

: RDx: cek ulang PT/APTT, konsul nefrologi

RTh:
1.
2.
3.
4.
5.
6.
7.
8.

lanjutkan terapi
Peptamen 30cc/jam per NGT
Nutriflex 1/24jam
RF 50cc/jam
RI 1 unit/jam titrasi
NE 0,3mcg/kgBB
Lasix 2mg/jam
MAP >100 Titrasi Norepinephrine 0,1mcg

Follow up 19/5/2015
S

: perawatan hari ke-4, residu makanan keluar dari NGT

: BP 140-120/80-90; MAP 92-100; CVP +12cmH2O

RR 16-20x; Pola ventilator PC 12, PEEP +7, RR 12, FiO2 50%,
GDS 146, 104, 157, 38, 75
Input: 2358,6 cc
Output 550cc Rate diuresis 0,38/kgBB/jam
Balans/24 jam +1808,6 cc

: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrest

: RDx: GDS berkala, rencana echocardiography

RTh:
o
o
o
o
o
o
o
o

RI 1U/jam titrasi
NE 0,4mcg/kgBB
RF 20cc/jam
Lasix drip 2mg/jam
miloz 1mg/jam
GDS menurun, stop RI
pasien dipuasakan
GDS menurun, stop RI; pasien dipuasakan

Follow up 20/5/15
S

: perawatan hari ke-5; GDS menurun, residu makanan keluar dari NGT

: BP 140-110/80-90; MAP 50-89 CVP +17,5 cmH2O

RR 12-16x; Pola ventilator PC 12, PEEP +7, RR 12, FiO2 60%,

GDS 75, 68, 121, 112,
Input: 2412 cc
Output 830 cc Rate diuresis 0,26/kgBB/jam
Balans/24 jam +1582,2 cc
Balans kumulatif +9058,7
A

: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrest

: RDx: cek PCT, konsul radiologi untuk USG abdomen

RTh:
o GDS menurun stop RI, bolus D40%, cek GDS berkala
o Peptamen stop, ganti CF 30cc/jam, konsul IPD
o Rencana HD
Koreksi albumin untuk persiapan HD
Hb 8,48 Transfusi PRC 1 bag
o Ganti ETT
o MAP 50 dosis NE 0,8mcg, dobutamin 15mcg
o Rencana HD menjadi CVVH karena hemodinamik tidak stabil start
epinephrine 0,1 mcg

Follow up 21/5/15
S

: Perawatan hari ke-6, pasien mulai CVVH

: BP 96-105/58-66; MAP 50-70; CVP +12cmH2O

RR 16-20x; Pola ventilator PC 12, PEEP +7, RR 15, FiO2 60%,
Input: 2579,4 cc
Output 400cc Rate diuresis 0,27/kgBB/jam
Balans/24 jam +2179,4 cc

: Shock sepsis ec CAP, KAD, AKI dd acute on CKD, riwayat cardiac arrest

: RDx: rencana USG abdomen

RTh: MAP 70 titrasi epinephrine hingga 0,5mcg, bila tercapai mulai titrasi NE

Literature Review
Community-Acquired Pneumonia
Pneumonia is defined as infection of lung parenchyma. Clasically, pneumonia can be
classified to 3 type: community-acquired (CAP), hospital-acquired (HAP), and ventilatorassociated (VAP). Each types have different pathogens causing the infection. Streptococcus
pneumonia, Mycoplasma pneumonia, Haemophilus pneumonia are the most common typical
bacteria associated with CAP. Less common typical bacteria include Staphylococcus aureus
and Pseudomonas aeruginosa.
Pneumonia results from combination of pathogens activity at alveoli and hosts
response to these activities. Normally, when pathogens are inhaled, mechanical factors of
respiratory system will act to capture the particles. Then mucociliary clearance and local
antibacterial factor will response to either clear or kill the pathogens. If the pathogens
managed to reach the alveolar level, local alveolar macrophages then act to eliminate it.
However, if macrophages are overwhelmed by thse pathogens, colonization of pathogens
occurs. Inflammation response are triggered causing release of inflammatory mediators
causing the clinical manifestation of pneumonia. Interleukin (IL)-1 and tumour necrosis
factors (TNF) wresults in fever while chemokines stimulates the release of neutrophils,
resulting in increase of leukocytes and production of purulent and mucus. These mediators
also caused capillary leakage which can be seen in radiographic examination as infiltrate and
rales which are detectable on auscultation. The leakage will cause alveolar filling which in
turn caused hypoxemia. All this contributes to dyspnoea.
Clinical manifestations of CAP are fever with tachycardia, productive or nonproductive cough, and shortness of breath. Pleuritic chest pain and haemoptysis may also
occurs. In cases of atypical pneumonia, low-grade fever and non-productive cough may be
seen. American Thoracic Society (ATS) recommend laboratory testing such as sputum and
blood culture to identify the aetiology accompanied by chest radiographic to appropriately

diagnose pneumonia. Initial assessment of severity is important in determining whether

patient can be managed as outpatients or in the hospital.
British Thoracic Society (BTS) recommends the CURB-65 score for this assessment
while ATS used Pneumonia Severity Index (PSI) to assess the severity of CAP. Below are the
scoring system of CURB-65 and PSI.

The decision of ICU treatment for CAP patients is performed on second-level

admission. Based on ATS guidelines, patients with septic shock requiring vasopressor or
those with acute respiratory failure requiring intubation and mechanical ventilation fulfilled
the criteria for ICU. Patients with severe CAP are also recommended for ICU admission.

Determining the severity of CAP is also important for the antibiotic selection.
Empirical antibiotic therapies are given before responsible pathogens are identified by
culture. For inpatient in non-ICU settings, respiratory fluroquinolone are -lactam plus
macrolide can be used for hospitalized patients without complication. In ICU settings,
antibiotic of choice are -lactam (cefotaxime, ceftriazone, ampicillin-sulbactam) plus either
azithromycin or fluoroquinolone. In the suspicion of pseudomonas infection, antipseudomonas -lactam such as carbapenem plus fluoroquinolones can be given. As soon as
specific pathogen responsible for CAP are identified, therapy should be switch to
antimicrobial therapy directly targeted for the specific pathogens.

Sepsis and Septic Shock

Sepsis is defined as systemic inflammation in response to infection. The diagnosis of sepsis
can be established when systemic inflammation response syndrome (SIRS) are documented
along with the presence of infection. Severe sepsis occurs when one or more signs of organ
dysfunction is found. Organ dysfunction occurs due to lack of tissue perfusion induced by
sepsis. When sepsis-indeuced hypotension cannot be manage despite adequate fluid
resuscitation, septic shock occurs.
Inflammation Condition
Systemic Inflammation Response Syndrome

Criteria
1. Fever more than 38.3oC or hyperthermia

(SIRS)

<36oC
2. Tachycardia (HR> 90x/min)
3. Tachypnoea (RR> 24x/min)
4. Leukocytosis >12000/L, leukopenia
<4000/L or normal leukocytes with
increase 10% of immature forms

Sepsis
Sepsis-induced hypotension

Infection + SIRS
Hypotension with SBP< 90mmHg, MAP <

Sever Sepsis or Sepsis-induced

70mmHg
Sepsis induced hypotension with organ

Hypoperfusion

dysfunction
1. Elevated lactate (> 1mmol/L)
2. Oliguria (output < 0.5ml/kgBW/h)

3.
4.
5.
6.
7.

ALI with hypoxemia (PaO2< 300)

Creatinine> 2mg/dL
Bilirubin >2mg/dL
Thrombocytopenia <100000/ L
Coagulopathy (INR >1.5)

In patient with severe sepsis, initial resuscitation is important in preventing further organ
dysfunction. The target for resuscitation includes CVP 8-12mmHg, MAP >65mmHg, urine
output >0.5mL/kgBW/h, central venous or mixed vein oxygen saturation 70% or 65%
respectively and normalized lactate. Further management should be identification of
microbes by culture along with initial empirical anti-infective therapy. Anti-microbes
recommended in cases of respiratory failure and septic shock is combination of broadspectrum beta-lactam and aminoglycoside or fluoroquinolone.

Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus (DM). Although it
is usually found in DM type I patients, it can also be seen several DM type II patients.
Clinical manifestation of DKA includes nausea-vomiting, thirst, decrease of consciousness,
Kussmaul breathing, abdominal tenderness, lethargy, tachycardia and signs of dehydration.
DKA is usually precipitated by certain condition in the patient such acute myocardial
infarction, stroke or acute infection. Laboratory findings of DKA includes hyperglycemia
with blood glucose of >250mg/dL, metabolic acidosis and ketosis in the form of ketonemia or
ketonuria.
Pathophysiology of DKA can be seen from hormonal onbalance betwenn regulatory
hormones of blood glucose. Deficit in insulin hormone, coupled with excess in its
counterregulatory hormones such as glucagon cause increase in gluconeogenesis,
glycogenolysis causing increase in glucose synthesis. Reduced insulin level and elevation of
catecholamine promoted release of free fatty acids from adypocutes, which is metabolized in
the liver, forming ketone body due to hyperglucagonemia, causing ketosis.
In the management of DKA, monitoring of electrolytes, acid-base status and renal
functions are important. Fluid therapy at the first 6 hours of hospital admission is important
along with management of hyperglycemia with insulin. Based on guidelines by Indonesian
Society of Endocrinology (PERKENI), 2-3 L of NaCl 0.9% must be given in the first 3 hours,
then on the second hour, insulin must be administered with dosage of 280mU/kgBW bolus,
continued with drip of dosage 90mU/kgBW/hours in NaCl0.9%. Dosage can be lowered

based on the level of blood glucose. Correction of potassium and bicarbonate can be given of
necessary. Since potassium stores are depleted in DKA, hypokalemia commonly occurred. 50
mEq/6 hours can be given then after administration, addition of potassium can be added if
hypokalemia still occurring. Vital signs and blood glucose level must be monitored every
hour while blood gas analysis and electrolyte level can be measured every 6 hours until
patient is stable.

Acute Kidney Injury

Based on Kidney Disease Inmproving Global Outcome (KDIGO) guidelines, acute kidney
injury (AKI) is defined as increase in serum creatinine of more than 0.3 mg/dL within 48
hours or increase of more than 1.5x baseline or decrease urine output of less than 0.5
ml/kg/hour for 6 hours. Based on serum creatinine level and urine output, AKI can be divided
to 3 stages. Other criteria which can be used is the RIFLE, stages includes risk, injury, failure,
loss, and end-stage renal disease (ESRD). These stages determined types of treatment AKI
patients should receive. Determination of cause of AKI is important to prevent worsening of
condition, decrease kidney perfusion, glomerulonephritis, urinary tract obstruction are among
the common cause of AKI. Among the cause, persistent hypotension in patient with shock
who are not responsive towards fluid resuscitation increase the risk of development of AKI.
Vassopressor are recommended in septic shock patients for prevention and even treatment of
patient with AKI.. Noreponephrine, dopamine and vasopressin are the drugs of choice used.
Vasopressin are quite effective increasing blood pressure and enhance diuresis. Diuretics are
not recommended in the management of AKI except volume overload is present in the
patient.

Discussion
Since patient was admitted to ICU, the antibiotics of choices are -lactam plus
fluoroquinolone or azithromycin. However, patient has history of hospitalization for 2 days
prior to this admission. P. aeruginosa infection should be considered in this patient. Hence,
anti-pseudomonas is considered in this patient. Therapy given in this patient, which is
levofloxacin and meropenem is appropriate for the settings. Anti-fungal such as fluconazole
can be considered in patient suspected with Candida sp. infection. Length of treatment should
be 3-5 days and can be extended to 7-10 days in patient with slow clinical response.
Procalcitonin can be use as biomarkers for the effectivity of empiric antibiotics.

In case of life-threatening hypotension, vasopressor therapy should be initialized with

target MAP of 65mmHg. The drug of choice used is norepinephrine. Norepinephrine was
used to increase atrial blood pressure, increase myocardial contractility and cardiac output. It
was given in continuous infusion in the range of 1-20 g/min. Vasopressin can be added to
norepinephrine to increase the target MAP while epinephrine can be used as potential
substitute for norepinephrine or as addition to increase cardiac output rather than to increase
MAP.
Managemeent of AKI in patient with fluid overload and increasing creatinine level is
according to the RIFLE criteria. In this patient, the creatinine level is already above 4mg/dL
with decrease urine output less than 0.3cc/kgBW/hour. Based on this criteria, patient is
already classified in AKI stage 3 or RIFLE criteria of failure. Moreover, patient also had acidbase imbalance from the DKA condition with unstable haemodynamic condition. hence
patient is indicated for hemodialysis therapy.
On the day-7, patient has low pH with a high PCO 2 and near normal HCO3. This
shown that patient develop respiratory acidosis due to poor oxygenation despite breathing on
ventilator. The ventilator mode in this patient was pressure control with PEEP. Patient was
shown to be struggling a bit with the ventilator and still have several spontaneous breathing.
Pressure-control is still appropriate in this patient since he showed a poor lung compliance,
hence PC mode can reduce the risk of barotrauma on this patient. SIMV can also be applied
since patient sometimes still has spontaneous breathing and SIMV mode can make sure that
ventilation given does not collide with patients own breathing. It can be given with lower
tidal volume might be more appropriate since in ensures patient to have minimum ventilation
but still protect the lung from further injury due to mechanical ventilation.

References
1. Dellinger RP et al. Surviving sepsis campaign: international guidelines for
management of severe sepsis and septic shock 2012. Crit Care Med 2013;41:580-637.
2. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious diseases society of America/
American thoracic society consensus guidelines on the management of communityacquired pneumonia in adults. Clinical Infectious Diseases. 2007; 44:S2772.
3. KDIGO. KDIGO Clinical practice guidelines for acute kidney injury. KDIGO Kidney
International Supplements. 2012;2:1; doi:10.1038/kisup.2012.2
4. Miller RD, Pardo MC. Basics of anesthesia. 6th edition. Philadelphia (PA): Elsevier
Saunders; 2011.
5. Longo DL, Kasper DL, Fauci AS, et al. Harrisons principle of internal medicine. 18 th
edition. New York (NY): McGraw-Hill; 2012.
6. PERKENI. Petunkuk praktis pengelolaan diabetes mellitus tipe II. Jakarta: PB
PERKENI; 2002.