ICU Management of Acute Pancreatitis

Departeman Anestesiologi dan Reanimasi
Fakultas Kedokteran Universitas Airlangga
ICU Management
of Severe Acute Pancreatitis
: a Case Report
oleh :
Andri Subiantoro
Pembimbing :
Bambang Pujo Semedi, dr., Sp.An-KIC
Background
• Severe acute pancreatitis (SAP) remains a very
challenging disease with multiple complications and
high mortality.
• No specific treatment for this disease.
• Supportive therapy  is still the mainstay of
therapy.
• Early identification and aggressive treatment can
have a major impact on outcome.
Wilmer, A. 2004. ICU Management of Severe Acute Pancreatitis : review article. European Journal of Internal
Medicine 15 (2004) 274– 280
Introduction
• Acute pancreatitis is an inflammatory condition of
the pancreas that is characterized by abdominal pain
and elevated levels of pancreatic enzymes (amylase,
lipase) in blood.¹
• 15% to 25%, SAP develops, manifested with
pancreatic parenchymal and/or peripancreatic tissue
necrosis  morbidity  10% to 20% mortality
despite advances in critical care.²
1. David, H. 2014. Pancreatitic and Liver Failure. In : Marino’s ICU Book 4 th Ed. Lippincott Williams & Wilkins, 2014. Chap. 39
2. Maheswari R, Subramanian R. 2015. Severe Acute Pancreatitis and Necrotizing Pancreatitis : a Review Article. Crit Care Clin -
(2015)
Type of Pancreatitis
Edematous Necrotizing
• Most common type • Occurs in 10–15% of cases

• Without involvement of • Characterized by areas of
other organs necrotic destruction in the
• Symptoms  self-limited pancreas
period of abdominal pain, • Progressive systemic
nausea, and vomiting inflammation and inflammatory
• The mortality rate is low injury in one or more extra
(<2%) abdominal organ
• Management rarely requires • The mortality rate can be as
ICU-level care high as 40%
• Management usually requires
ICU-level care
David, H. 2014. Pancreatitic and Liver Failure. In : Marino’s ICU Book 4 th Ed. Lippincott Williams & Wilkins, 2014. Chap. 39
Etiology
Klasifikasi Indian Guidelines & Protocol
• Mild acute pancreatitis : tanpa adanya kegagalan organ

• Moderate acute pancreatitis : tanpa adanya kegagalan
organ namun dengan disertai adanya komplikasi lokal
• Severe acute pancreatitis, digolongkan atas dua yaitu :
- early severe, yaitu disertai dengan kegagalan organ
dalam waktu 72 jam (fulminan), dan disertai dengan
kegagalan organ dalam waktu 4-7 hari (subfulminan)
- late severe, bila kegagalan organ sudah terjadi setelah
7 hari
• Critical acute pancreatitis : disertai kegagalan organ
persisten dan infected pancreatic necrosis11
Banks PA, Bollen TL, Dervenis C. Classification of acute pancreatitis - 2012: revision of the Atlanta
classification and definitions by international consensus. Gut BMJ. 2013; 62: 102-111.
Tenner S, Baillie J, DeWitt J. American College of Gastroenterology Guideline: Management of Acute
Pancreatitis. Am J Gastroenterol. 2013; 1-16.
Case ICU
Tn. Andi Lesmana/ 43 th / 80 kg / 12549741

Dx : Pankreatitis Acute + DM Tipe II
8
Time line 26-11-2016
Pasien tiba di RES RSDS
23-11-2016 Kondisi di RES:
26-11-2016 A : bebas Tube in suara nafas +an (-),
Pasien awalnya mengeluh B : Control RR 20x/menit, simetris,
sesak dan badan lemas, Perawatan hari ke -3 di RS jejas (-), retraksi (-), Rh +/+
disertai panas badan dan WB, pasien bertambah sesak, C: pDKP, CRT <2”, N 180 x/mnt SVT TD
batuk pilek sudah dan pada pemeriksaan 62/43 mmHg,
berlangsung 2 minggu didapatkan BUN/SK  D: GCS Tersedasi, PBI 3/3, refl cahaya
+/+
84/5,5
Dilakukan HD Cito ..?? Tindakan :

Indikasi ? • Pasien SVT  ambil alih O2 Jackon
Rees bagging manual kesan
Post HD Pasien bertambah obstruksi  Plugging  Suction
Pasien dibawa ke RS sesak  dilakukan Intubasi  SpO2 99%, SVT (-), ECG Sinus
William Booth dan  Karena ICU Penuh, dirujuk • Pastikan IV line tetap lancar
dilakukan perawatan di ke RSUD Dr. Soetomo loading cairan dan vasopressor
RSWB • Pertahankan kateter urine  cek
RPD : DM Tipe II , HT (-)
produsi urine (target 0,5-1
ml/jam)
• Monitoring dan diagnostik
Time line
Laboratorium Secondary survey (RES)

- Hb/Ht/L/T : 11,8/ 34,3 / 11,2/ B1: A: Bebas, tube in
114 B: Ventilator Support, Mode PCV rate 25 PC 10 Peep 8
- Na/K/Cl: 126/ 4 ,5/ 95 FiO2 50%  rate 25 TV 600 - 650 MV 15-16
B2: pHKP, N 145 x/menit, Sinus TD 77/54 mmHg
- GDA : 280
- OT/PT/alb: 45/54/2.23 B3: GCS 3-X-6
- BUN/SK: 65/ 6,94 B4: BAK kateter, PU 80 mL initial  PU 0 ml/Jam
- APTT/PPT: 41 (26)/11,2 (11,3) B5: datar, soepel, defans muskuler (-), BU (+),
B6: edema (-)
FiO2 50%
pH 7,28
PO2 132
PCO2 27
HCO3 12,7
BE -14
SO2 99%
P/F 264
10
Assesment Awal
• Severe Pneumonia + Syok Septic + DMND
Stage V + Asidosis Metabolik + Abses Perianal
Problem List
1. Gagal Nafas
2. Pneumonia
3. Syok
4. Sepsis
5. Anuria
6. Peningkatan RFT
7. DM Type 2
8. Hipoalbumin
9. Elektrolit imbalance
10. Abses Perianal
Terapi awal
• Terapi :
– Posisi Slight Head Up
– O2 Ventilator Support
– Nebul + Suction sesuai indikasi
– Chest Fisioterapi Nafas
– Drip Metronidazole 500 mg/8 jam i.v
– Drip Levofloxacin 750 mg/48 Jam i.v
– Inj. Omeprazole 40 mg/12 jam i.v
– Inj. Paracetamol 1 gram/8 jam i.v
– NE pump sesuai HD
– Infus Aminofluid 1000 ml/24 jam
– Sonde Diabetasol 6 x 100 ml
– Transfusi Albumin s/d target Alb > 3,0
– Regulasi Gula darah dengan Yale Protocol
KONDISI MINGGU PERTAMA
Hemodynamic Condition 1st Week
160
140
120
100
80
60
40 • Norepinephrine Pump
20 • Dobutamin Pump
0
25-Nov 26-Nov 27-Nov 28-Nov 29-Nov 30-Nov 1-Dec
25- 26- 27- 28- 29- 30-

1-Dec
Nov Nov Nov Nov Nov Nov
TD Sistol 77 113 126 112 121 108 127
TD Diastol 44 76 75 60 67 55 58
Heart Rate 147 113 114 111 112 100 115
20
BGA 1st Week 450
15 400
10 350
300
5
250
0
26-Nov 27-Nov 28-Nov 29-Nov 30-Nov 1-Dec 200
-5
150
-10 100
-15 50
-20 0
26-Nov 27-Nov 28-Nov 29-Nov 30-Nov 1-Dec
pH 7.42 7.45 7.362 7.309
BE -8.8 -8.3 -14.2 -10.5
HCO3 15 15.9 14.5 16
P/f Ratio 168 217 384 316.5
Renal Function Test + Kalium 1st Week
140 8
120
100 6
80
4
60
40
2
20
0 0
BUN 65 79 114 123
SK 6.94 7.38 5.85 4.8
Kalium 4.49 4.5 5.6 5.3
Produksi Urine
4500 180.0
4000 160.0
3500 140.0
3000 120.0
2500 100.0
2000 80.0
1500 60.0
1000 Furosemide 40.0
500 20.0
0 0.0
25-Nov 26-Nov 27-Nov 28-Nov 29-Nov 30-Nov 1-Dec
25- 26- 27- 28- 29- 30-

1-Dec
Nov Nov Nov Nov Nov Nov
Produksi Urine / Hari 80 450 802 2280 2585 2540 3860
Produksi Urine / Jam 11.4 18.8 33.4 95.0 107.7 105.8 160.8
CXR
CXR
Tren Laboratorium
• Laboratorium
KONDISI MINGGU KEDUA
3 Desember 2016
(Perawatan di ICU hari ke-5)
• Visite dr. Bambang Pujo, Sp. An KIC :
– Melakukan pemeriksaan fisik palpasi abdomen 
pasien merasa kesakitan
– Advis beliau : cek Amylase dan Lipase
– Kecurigaan suatu Pankreatitis Acute.
Diagnosis
Definition of diagnosis of acute pancreatitis :
1. Abdominal pain consistent with acute
pancreatitis (acute onset of a persistent, severe,
epigastric pain often radiating to the back)
2. Serum lipase activity (or amylase activity) at
least three times greater than the upper limit of
normal
3. Evidence of pancreatitis on contrast-enhanced
computed tomography
Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis – 2012: revision of the
Atlanta classification and definitions by international consensus. Gut 2012; 62:102–111
• If abdominal pain suggests strongly that acute
pancreatitis is present but :
– serum amylase and/or lipase activity is less than
three times the upper limit of normal  may be
it’s a delayed presentation
Imaging  Confirm Diagnosis
Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis – 2012: revision of the
Atlanta classification and definitions by international consensus. Gut 2012; 62:102–111
Tren Laboratorium
(Minggu ke 2)
Pancreatic Enzymes
• Amylase :
– Sources of amylase are the pancreas, salivary
glands, and fallopian tubes
– Serum amylase levels begin to rise 6–12 hours
after the onset of acute pancreatitis,
– An increase in serum amylase  high sensitivity
(>90%) but a low specificity (as low as 70%)
Pancreatic Enzymes
• Lipase :
– Sources of lipase are the tongue, pancreas, liver, i
intestine, and circulating lipoproteins.¹

– Serum lipase levels begin to rise earlier than serum
amylase (at 4 to 8 hours)  remain elevated longer.¹
– An increase in serum lipase has a sensitivity and
specificity of 80–100% for acute pancreatitis.¹
– Serum Lipase, unlike amylase, is reabsorbed by the
kidney tubules and hence remains elevated for
prolonged period which may be helpful in late
presenting patients.²
2. Anish MS et al, 2010. Acute Pancreatitis with Normal Serum Lipase: A Case Series. JOP. Journal of the Pancreas . Vol. 11,
No. 4 - July 2010
Sources of Elevated Pancreatic Enzyme
Recommendation
• Amylase and lipase remain important tests in
the diagnosis of AP.¹
• Lipase, which was initially thought to be more
specific.¹
• Pancreatic enzyme assays cannot be used to
evaluate the severity of illness than amylase.²
2. Yadav D, Agarwal N, Pitchumoni CS. A critical evaluation of laboratory tests in acute pancreatitis. Am J Gastroenterol 2002;
97:1309–1318.
Assesment
• Pankreatitis Akut + Pneumonia + DMND +
Sepsis + Abses Perianal
Renal Function Test + Kalium
140 8
120 7
100 6
5
80
4
60
3
40 2
20 HD I 1
0 0
2-Dec 3-Dec 4-Dec 5-Dec 6-Dec 7-Dec 8-Dec
BUN 123 101 107
SK 3.23 4.94 2.5
Kalium 4.42 6.2 5 6.3 5.8 7.5 7.5
Produksi Urine
4500 180.0
4000 160.0
3500 140.0
3000 120.0
2500 100.0
2000 80.0
1500 60.0
1000 40.0
500 HD I 20.0
0 0.0
Produksi Urine /
2880 3230 3850 3170 3440 2710 1360
Hari
Produksi Urine /
120.0 134.6 160.4 132.1 143.3 112.9 56.7
Jam
• Acute kidney injury (AKI) is a known complication of SAP  AKI is one of
the most common causes of death in patients with SAP.
• AKI was defined and classified according to the RIFLE (Risk, Injury, Failure,
Loss, and End-stage) criteria based on urine production <400 mL/d or
serum creatinine level >2 mg/dL.
• Cause  systemic inflammation, cytokine production, free radicals and
other factors influencing the microcirculation play a role.
• Other cause  Hypoxemia, decrease in renal perfusion pressure due to
abdominal compartment syndrome, intraabdominal hypertension and
hypovolemia
Kumar R, Pahwa N, Jain N. 2015. Acute Kidney Injury in Severe Acute Panceatitis : An Experience from a tertiary care
center. Saudi J Kidney Dis Transpl 2015;26(1):56-60 2015 Saudi Center for Organ Transplantation
Treatment AKI
1. Treatment of underlying disease (pancreatitis),
2. Intraabdominal hypertension and abdominal
compartment syndrome treatment measures,
3. Renal function supportive measures
4. Renal replacement therapy (RRT).
Kumar R, Pahwa N, Jain N. 2015. Acute Kidney Injury in Severe Acute Panceatitis : An Experience from a tertiary care
center. Saudi J Kidney Dis Transpl 2015;26(1):56-60 2015 Saudi Center for Organ Transplantation
Hemodynamic Condition
180
160 HD I
140
120
100
80
60
40
20
0
TD Sistol 133 126 131 159 135 128 131
TD Diastol 54 63 68 74 87 73 83
Heart Rate 110 109 96 110 110 98 119
BGA
20 HD I 600
15
500
10
400
5
0 300
-5
200
-10
100
-15
-20 0
pH 7.32 7.39 7.33 7.32
BE -10.2 -12.5 -11.4 -13.9
HCO3 16.2 13.5 14 12.4
P/f Ratio 377.25 535.5 282 430
Severe Pancreatitis
• Severe acute pancreatitis (SAP) is defined as
acute pancreatitis associated with other end
organ failure and/or local complications such
as necrosis, abscess, or pseudo cyst.¹
• The cause of the extra pancreatic organ injury
is progressive systemic inflammation (similar
to severe sepsis and septic shock).²
1. Wilmer, A. 2004. ICU Management of Severe Acute Pancreatitis : review article. European Journal of Internal Medicine 15 (2004) 274– 280
General Management
• Fluid Rescucitation
• Respiratory Care
• Cardiovascular Care
Pharmacologic • Metabolic
Complications
• Infectious Disease
and Antibiotic
• Pain Management
General • Endosopic
Non Pharmacologic
Management • Nutrition
Radiologic & Surgical Treatment
Maheswari R, Subramanian R. 2015. Severe Acute Pancreatitis and Necrotizing Pancreatitis : a Review Article. Crit Care Clin : 2015
Fluid Rescucitation
• SAP  usually volume-depleted  poor oral intake,
third space loss, and increased vascular permeability.¹
• The goal is to provide enough intravascular volume 
to maintain pancreatic perfusion.²
• Which type of fluid (colloid or crystalloid) is best?
• Initial Regiments :³
– infuse crystalloid 20 mL/kg (about 1.5 liters) over 60 to 90 minutes 
infusion rate up to 250 ml/hr for the next 24-28 h.
– maintain a mean arterial pressure ≥65 mm Hg, and a urine output ≥0.5
mL/kg/hr
2. Maheswari R, Subramanian R. 2015. Severe Acute Pancreatitis and Necrotizing Pancreatitis : a Review Article. Crit Care Clin : 2015
Caution !!
• Aggressive volume infusion has not been shown to
improve outcomes in severe pancreatitis.²
• The infusion rate should be titrated to the desired
blood pressure and urine output Not exceed to
250 ml/h.¹
• If hemodynamic goals does not achieve 
Vasopressor.¹
1. David, H. 2014. Pancreatitic and Liver Failure. In : Marino’s ICU Book 4 th Ed. Lippincott Williams & Wilkins, 2014.
Chap. 39
2. Haydock MD, Mittal A, Wilms HR, et al. Fluid therapy in acute pancreatitis: anybody’s guess. Ann Surg 2013;
257:182–188
Respiratory Care
Severe Acute Pancreatitis
Systemic Inflammatory Severe Pancreatic

Response Inflammation
Noncardiogenic Pulmonary
Edema Increased Abdominal Pressure
Gas Change Abnormalities
Pulmonary Insufficiency & Lung Injury ARDS
Intubation & Ventilator Support Tracheostomy
Maheswari R, Subramanian R. 2015. Severe Acute Pancreatitis and Necrotizing Pancreatitis : a Review Article. Crit Care Clin : 2015
Cardiovascular Care
• SAP  systemic inflammatory response 
distributive shock syndrome  increased in cardiac
index & decreased total peripheral resistance 
hemodynamic disturbances.¹
• If hypotension persists even with appropriate fluid
resuscitation  vasoactive agent (Norepinephrine)¹
• The initial infusion rate is 0.1 μg/kg/hr, then titrated
to maintain a mean arterial pressure ≥ 65 mm Hg.²
• All vasoconstrictor drugs can reduce splanchnic
blood flow  aggravate pancreas necrotic ²
Metabolic Complications
• Hyperglycemia may present during the first
several days of severe pancreatitis but usually
disappears as the inflammatory process
subsides.
• Blood sugars fluctuate, and insulin should be
administered cautiously.
Maheswari R, Subramanian R. 2015. Severe Acute Pancreatitis and Necrotizing

Pancreatitis : a Review Article. Crit Care Clin : 2015
The Role of Antibiotic
• Is the prophylactic antibiotic needed?
– About 1/3 of patients with necrotizing pancreatitis
develop infections in the necrotic areas of the
pancreas.
– These infections are difficult to eradicate, and
associated with increased mortality rates.
– antibiotic prophylaxis does not reduce the
incidence of pancreatic infections, and does not
influence the mortality rate in severe pancreatitis.
David, H. 2014. Pancreatitis and Liver Failure. In : Marino’s ICU Book 4 th Ed. Lippincott Williams &
Wilkins, 2014. Chap. 39
The Role of Antibiotic
• Infections typically appear 7–10 days after the onset
of illness.¹´²
• Antibiotics would be appropriate in pancreatic sepsis
& non-pancreatic sepsis.¹
• These septic conditions are major sources of
morbidity and mortality in patients with SAP.¹
• Imipenem, fluoroquinolones, and metronidazole are
the drugs that achieve the highest inhibitory
concentrations in pancreatic tissue.¹
Pada Pasien ini ?
• Saat awal  Levofloxacin dan Metronidazole
• Kultur I keluar  AB Sesuai kultur Cefo
Sulbactam  Metronidazole stop ganti Cefo
Sulbactam
• Klinis masih tidak membaik  advis dr.
Edward Sp. An KIC (Konsultan ICU Mingguan)
 Meropenem
• Minggu ke 5, Visite dr. Bambang Wahyu Sp. An
KIC  Stop Antibiotik.
Endoscopic
• When acute pancreatitis is associated with
gallstones  Gallstone Pancreatitis
• Early Endoscopic Retrograde Cholangio
Pancreatography (ERCP) is indicated for biliary
obstruction or evidence of cholangitis
(Jaundice & Fever)
David, H. 2014. Pancreatitis and Liver Failure. In : Marino’s ICU Book 4 th Ed. Lippincott Williams &
Wilkins, 2014. Chap. 39
Nutrition
• Formerly, total parenteral nutrition was the standard
of care for feeding patients with SAP  because enteral
nutrition can stimulate pancreatic and intestinal secretions.¹
• However, bowel rest is associated with intestinal
atrophy and bacterial overgrowth  elevated
endotoxin and cytokines levels, bacterial
translocation, and SIRS induction  a higher risk of
infected pancreatic necrosis. ¹
• Enteral feeding maintains the barrier function of the
intestinal tract. ²
Nutrition
• Nowadays, enteral nutrition (EN) is favored.²
• The use of early enteral nutrition (within 48
hours of admission) has proven to be
beneficial in patients with acute pancreatitis
 it improves clinical outcomes by reducing
the number of infections, particularly
pancreatic infections ¹´²´³
3. Li JY, Yu T, Chen GC, et al. Enteral nutrition within 48 hours of admission improves clinical outcomes of acute pancreatitis by reducing
complications: a meta-analysis. LoS One 2013;8
Pada Pasien ini?
• Saat Minggu I  Pasien sudah langsung dicoba sonde
diabetasol bertahap hingga dapat dinaikkan sampai 6 x 200 ml
ditambahkan infus aminofluid 1000 ml/24 jam
• Regulasi Gula dengan insulin pump
• Hiperkalemia  dikoreksi dengan Inj. Ca Gluconas 3 x 1 amp
• Minggu ke II  advis dr. Philia (Konsultan Mingguan ICU)
Aminofluid diganti dengan Clinimix NG20E 1000 ml/24 jam
ditambahkan ekstra kuning telur ayam kampung 3 x 1 hari,
dan sonde tetap diberikan
– Advis beliau cek Lipid Profile
Pada Pasien ini?
• Minggu ke II  pada perjalanannya pasien keluar hematin
dari NGT  dicurigai SRMD
• Advis konsultan mingguan  Sementara Puasa, lakukan
Gastric Cooling 3 x 1 hari sebanyak 100 ml, berikan
Omeprazole 2 x 40 mg, dan tambakan Syrup Sucralfat 4 x 30
ml
• Nutrisi  Infus Triofusin E1600 sebanyak 1000 ml/24 jam dan
Infus Kidmin 200 ml/24 jam,
• Sonde tetap diberikan diganti dengan clear water (D5) mulai
50 ml dinaikkan bertahap disesuaikan dengan retensinya.
KONDISI MINGGU KETIGA
160
140
120
100
80
60
40 HD II
20
0
10- 11- 12- 13- 14- 15-
9-Dec
Dec Dec Dec Dec Dec Dec
TD Sistol 102 103 122 113 134 119 116
TD Diastol 58 74 61 68 76 73 64
Heart Rate 114 130 100 121 115 114 103
140 8
120 7
100
6
5
80
4
60
3
40
2
20
HD II
1
0 0
BUN 110 119 89 94 81
SK 3.2 4.8 3.03 2.67 2.1
Kalium 7.2 6.8 7.5 5.7 4.53 5
BGA
20 500
15
400
10
5 300
0
-5 9-Dec 10-Dec 11-Dec 12-Dec 13-Dec 14-Dec 15-Dec 200
-10
100
-15 HD II
-20 0
9-Dec 10-Dec11-Dec12-Dec13-Dec14-Dec15-Dec
pH 7.38 7.32 7.4
BE -8.4 -13.9 -8
HCO3 17 12.4 17
P/f Ratio 373.5 396.2 321.2
Produksi Urine
3500 160.0
3000 140.0
2500 120.0
100.0
2000
80.0
1500
60.0
1000 40.0
500 HD II 20.0
0 0.0
10- 11- 12- 13- 14- 15-
9-Dec
Produksi Urine /
1634 3225 2800 2350 1700 2965 2200
Hari
Produksi Urine /
68.1 134.4 116.7 97.9 70.8 123.5 91.7
Jam
CXR
KONDISI MINGGU KEEMPAT
160
140
120
100
80
60
40
20
0
TD Sistol 106 132 135 130 143 132 128
TD Diastol 65 79 81 74 84 89 74
Heart Rate 120 133 132 125 118 133 137
60 7
50 6
5
40
4
30
3
20
2
10 1
0 0
BUN 55 41 34
SK 1.8 1.4 1.08
Kalium 5.3 6.6 5.4 5.4
BGA
25 600
20
500
15
400
10
5 300
0
200
-5 16-Dec 17-Dec 18-Dec 19-Dec 20-Dec 21-Dec 22-Dec
100
-10
-15 0
16- 17- 18- 19- 20- 21- 22-
Dec Dec Dec Dec Dec Dec Dec
pH 7.3 7.39 7.3
BE -10.1 -9.6 -10.9
HCO3 15.9 15.5 19.3
P/f Ratio 390 445 479.1
Produksi Urine
3000 150.0
2000 100.0
1000 50.0
0 0.0
16- 17- 18- 19- 20- 21- 22-
Dec Dec Dec Dec Dec Dec Dec
Produksi Urine /
2570 2080 2050 2480 2350 2750 1980
Hari
Produksi Urine /
107.1 86.7 85.4 103.3 97.9 114.6 82.5
Jam
CXR
CT Scan Abdomen
21/12/2016
Hasil CT SCan
• Hepatomegali
• Edema Pancreas dengan permukaan
lobulated merupakan gambaran pankreatitis
• Kista Lien
• Multiple nodul dan cavitas dengan cairan
kental di dalamnya, membentuk air fliud level
di paru bagian kiri, dapat merupakan
gambaran proses infeksi dd metastasis
• Efusi Pleura kiri
Computed Tomography
Edematous Pancreatitis Necrotizing Pancreatitis
The pancreas is enlarged & enhances The area that is not contrast enhanced
completely. There is also blurring of the represents necrotizing the neck and
pancreatic border which is characteristic of body of pancreas.
edema formation.
KONDISI MINGGU KELIMA
160
140
120
100
80
60
40
20
0
23-Dec 24-Dec 25-Dec 26-Dec 27-Dec 28-Dec
TD Sistol 131 138 142 116 116 128
TD Diastol 73 74 95 77 77 86
Heart Rate 130 121 131 127 138 131
47 5
46 4
45
3
44
43
2
42 1
41 0
BUN 43 46
SK 0.94 1.07
Kalium 4.6 4.7
BGA
20 500
15
Ekstubasi 400
10
5 300
0 200
-5 23-Dec 24-Dec 25-Dec 26-Dec 27-Dec 28-Dec 29-Dec
100
-10
-15 0
pH 7.357 7.34
BE -12.2 -11.7
HCO3 13.9 14.3
P/f Ratio 463 346.4
Produksi Urine
3000 120.0
2500 100.0
2000 80.0
1500 60.0
1000 40.0
500 20.0
0 0.0
23- 24- 25- 26- 27- 28-
Produksi Urine /
2190 2690 2250 1490 1410 1210
Hari
Produksi Urine /
91.3 112.1 93.8 62.1 58.8 50.4
Jam
Abses Perianal
Post-Rawat luka
Tgl 28 Desember 2016
• Pasien pindah Ruangan UPI Interna
• 2 minggu dirawat di UPI  membaik pindah
ke ruangan biasa Interna 1
• 2 minggu di ruangan Interna 1  baik  ACC
KRS.
77

ICU Management of Acute Pancreatitis

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ICU Management of Acute Pancreatitis

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Departeman Anestesiologi dan Reanimasi

Fakultas Kedokteran Universitas Airlangga

• Most common type • Occurs in 10–15% of cases

• Mild acute pancreatitis : tanpa adanya kegagalan organ

Tn. Andi Lesmana/ 43 th / 80 kg / 12549741

Dilakukan HD Cito ..?? Tindakan :

Laboratorium Secondary survey (RES)

25- 26- 27- 28- 29- 30-

25- 26- 27- 28- 29- 30-

Imaging  Confirm Diagnosis

intestine, and circulating lipoproteins.¹

Radiologic & Surgical Treatment

Systemic Inflammatory Severe Pancreatic

Gas Change Abnormalities

Pulmonary Insufficiency & Lung Injury ARDS

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