Laki-laki 52 tahun dengan keluhan nyeri perut disertai dengan

perut kembung, dan riwayat melena sebelumnya.

Tensi 100/60 mmHg, Nadi : 100x/mnt. Pernapasan : 24x/mnt.
Pemeriksaan Fisis :
Abdomen : Distended dengan tanda-tanda peritonitis
generalisata
Laboratorium :
Hb : 8,7 gr%, Leukosit : 30.400/mm ;
fibrinogen : 294.
Albumin 2 mg/dl
USG : tidak didapatkan kelainan.
Foto polos abdomen : Ileus obstruksi.
Diagnosis : Trombosis vena mesenterik
 Dilakukan reseksi masif
usus halus
Sisa ileum 50 cm
Sisa jejunum 30 cm
MASALAH DURANTE
OPERASI

????
MASALAH PASCA OPERASI

????
PERLUKAH OPERASI LANJUT ???
Post operasi 3 bulan
 ACUTE MESENTERIC
ISCHEMIA

HERMANSYUR KARTOWISASTRO SpB

KBD
 MORTALITY RATE A.M.I

REFERENCE THN N MRATE

Ottinger & Austen 1967 51 84%
Singh et al 1975 30 81%
Smith & Patterson 1976 23 91%
Kairaluoma et al 1977 44 70%
Ottinger 1978 136 85%
Boley et al 1977 35 45%
Krausz & Manny 1978 40 75%
Sachs et al 1982 37 76%
Finucane et al 1989 32 78%
Levy et al 1990 62 40%
Batellier & Kieny 1990 65 52%
Klempnauer et al 1997 60 80%
 A.M.I
3 ARTERI UTAMA MENDARAHI USUS
A. Celiaka
A. Hepatika, A. Lienalis dan A. Gastrika Sin
A.Mesenterika Superior (SMA)
mendarahi jejunum sampai dengan kolon
transversum
vasa rekta
A. Mesenterika Inferior (IMA)
mendarahi kolon descendens, sigmoid, rektum atas
vasa rekta
 A.M.I
Faktor penting dalam terjadinya AMI
anatomi dan fungsi dalam hubungan 3 arteri
utama usus
kualitas kolateral yang terbentuk
lokasi dan luas obstruksi arteri
A.M.I

gbr.HK2
A.M.I

gbr.HK1
 A.M.I
3 MEKANISME TERJADINYA A.M.I
emboli yang berasal dari tempat lain,
terutama jantung
trombosis arteri`dengan stenosis
arteroskelotik yg sebelumnya telah
terbentuk
nonocclusive mesenteric ischemia
krn vasokonstriksi hebat vasa rekta
tanpa oklusi arteri proksimal
 A.M.I
Sebab infark mesenterik pada 1500 otopsi
62% arterial; 33% venous; 5% kombinasi
62% arterial
26 % emboli 12 nonocclusive 24% trombosis
55% A. Kolika media 33% vasa rekta
18% SMA 66% 2-4 cm dari
16% A. Kolika dextra cab utama
arteri
7% A. Ileokolika
4% vasa rekta
(Jackson 1963)
 A.M.I
DIAGNOSIS
KLINIS
2/3 wanita --beda dgn penyakit kardivasculer
lain
faktor risiko
penyakit jantung
aneurisma aorta torakal
penurunan berat badan kronis dengan nyeri abdomen
postprandial----- terutama pada penyakit aterosklerotik
nyeri perut akut tak spesifik pada satu tempat
dapat disertai : mual, muntah diare
 A.M.I
DIAGNOSIS
KLINIS
abdomen
nyeri abdomen yang ringan yang tak sesuai
dengan keluhannya yang hebat pain out of
proportion to the physical findings (waspadai
pada pasien penyakit jiwa)
bising usus dapat pos atau neg, digital rectal
exam darah dapat pos
bila peritonitis sudah jelas umumnya sudah ada
infark dan tanda yang buruk
 A.M.I
DIAGNOSIS
LABORATORIUM
lab rutin tak membantu penegakan diagnosa
lekositosis pada 90 %
50% lekosit antara 10.000 20.000
50% lekosit > 20.000
lekosit > 25.000 umumnya menandakan usus
sudah infark
serum amilase, phosphate, lactae dehydrogenase
da creatine phosphokinase potensial untuk
diagnosa tetapi tak selalu dapat dipercaya
 A.M.I
DIAGNOSIS
RADIOLOGIK
plain photo abdomen tak spesifik tetapi diperlukan
untuk menyingkirkan kausa lain (obstruksi usus)
ct scan abdomen terutama untuk diagnosis kausa
lain dari nyeri abdomen
penemuan yang menyokong AMI tetapi tak spesifik
dilatasi dan penebalan dinding usus
engorgement v.mesenterika
udara pada dinding usus atau v porta
non-filling a. mesenterika dgn pemberian kontrast iv
pemeriksaan agar tak menyebabkan penundaan
tindakan
 A.M.I
DIAGNOSIS
RADIOLOGIK
mesenterik angiografi
harus biplanar untuk dapat melihat a.celiaka dan SMA
umumnya dapat membedakan trombosis akut, emboli
atau nonocclusive
trombosis sumbatan pada pangkal SMA yg keluar dari aorta
emboli umumnya pada cabang a kolika media atau
distalnya sedang SMA sepanjang 2 3 cm bebas
nonocclusive arteri proksmal baik , cabangnya
irregular/sempit
sangat spesifik
pelaksanaan angiografi yang lama dapt memperburuk
kondisi karena dalam waktu 6 8 jam usus tak viable
lagi
 A.M.I

Preparasi pra-bedah
resusitasi cairan
monitor urine output dgn memasang Foley catheter
monitor hemodinamik yang tak meyebabkan penundaan
operasi
umumnya tak dapat dicapai keadaan optimum prabedah
penundaan akan menyebabkan infark usus yang irreversible
 A.M.I
OPERASI --- EMBOLI
umumnya SMA yg terkena
embolectomi dengan Fogarty kateter
penutupan dengan vein-patch bila perlu
bypass bila perlu dengan graft
reseksi usus yang jelas nonviable kemudian
anastomosis, bila yang meragukan panjang
jangan reseksi tetapi nilai kembali dengan
relaparotomi 24 jam kemudian
 A.M.I
OPERASI TROMBOSIS
MESENTERI
karena atherosclerosis ------sulit
bypass arteri yang tersumbat dengan
graft
A. Celiaka dan SMA harus di-
revaskularisasi
 A.M.I
0PERASI NONOCCLUSIVE
operasi hanya dilakukan bila ada tanda
infark atau kematian usus
direct infusion ke SMA papaverin 30-60
mg/j selama 24 jam bila perlu
diperpanjang
supportive terapi optimal
resusitasi cairan
cardiac output dimaksimalkan
vasopressor dihentikan
terapi underlying diseases
 A.M.I
ASESMEN VIABILITAS USUS
penting untuk menentukan panjang reseksi
asesmen fisik (clinical judgment)---89%
warna

peristaltik

pulsasi arteri
insisi arteri : aliran ; warna
asesmen dengan Doppler -------84%
usus yang meragukan : nilai ulang dengan
relaparotomi 24 jamkemudian
A.M.I

gbr.HK7
 A.M.I
HASIL OPERASI------PROGNOSIS
mortality rate tinggi ----keterlambatan
diagnosis
prognosis
emboli 50 - 76 % mortalitas
trombosis 100%
nonocclusive 67 87 %
long term prognosis
80% early mortality
50% 3 years survival dari yang hidup setelah early
mortality
 A.M.I
3 KASUS
Laki-laki 60 thn
riwayat operasi jantung
dilakukan observasi
nyeri perut, peritonitis tak jelas
hari ke 4 peritonitis jelas
operasi: necrosis dari jejunum s/d kolon transversum
second operation 48 jam kemudian daerah necrosis
bertambah
parenteral nutrition selama 2 bulan
meninggal dengan sepsis dan multi organ failure
 A.M.I
Laki-laki 63 thn
nyeri abdomen hebat berulang, harus duduk
bila nyeri timbul
riwayat atherosclerosis dan penyakit
jantung
peritonitis tak jelas
operasi : nekrosis segmen usus halus ,
reseksi anastomosis
6 bulan berulang kembali : operasi reseksi
anastomosis usus halus yang nekrosis
meninggal 1 tahun kemudian karena gagal
jantung
 A.M.I
Laki-laki 68 thn
riwayat atherosclerosis, Buerger disease,
bypass arteri perifer
nyeri abdomen hebat, peritonitis
angiografi multiple atherosclerosis
operasi : ulcus pepticum perforasi; simple
closure, usus tampak pucat
meninggal 2 minggu pasca bedah dengan
multiple organ failure
 A.M.I
ISCHEMIC TOLERANCE TIME
A Celiaka
trunk ----------unlimited
cabang ---------120 180 menit
SMA
120 180 menit
IMA
unlimited
A.M.I

gbr.HK4
A.M.I

gbr.HK5
TERIMA KASIH
Pathophysiology
Mesenteric
Thrombosis
A.Harryanto Reksodiputro

Hematology-Medical-Oncology
Department of Internal Medicine
School of Medicine-University of Indonesia
Jakarta
Definition
Mesenteric ischemia
failure of normal oxygenation of the small or large
intestine due to interruption of vascular flow
>>Ho and Walls 2001

ischemic small bowel and mesentery

ischemic large bowel / colon

acute and chronic varieties

additional variants
intestinal angina
SMA syndrome
Anatomy
- Mesentrik ischemia is caused by an interruption in blood flow to all or
part of the small intestine or the right colon
- SMA occlusion or not full occlusion
- IMA occlusion, venous thrombosis, arteritis
- Pain may be acute (embolism) or chronic (usually the case)
- Older patients with CHF, hypovolemia, CAD, CHF, digoxin,
hypercoagulable states are at risk
- The classic triad of superior mesenteric artery (SMA) embolism includes
GI disease emptying, abdominal pain, and underlying cardiac disease
- The sine qua non of mesenteric ischemia is a relatively norm abdominal
examination in the face of severe abdominal pain
The intestinal epithelium dies :
It can no longer prevent the intestinal contents from
entering the dying circulation
Noxious materials are absorbed, including bacterial
enterotoxins, lysosomal hydrolases, cathepsins
Toxin + Severe intestinal ischemia shock and death
Epidemiology
1 / 1000 admissions
50+ % mortality; up to 90 % if infarction
risk factors: age <-> comorbidities
atherosclerotic disease
arrhythmia
AMI / CHF
renal failure / hemodialysis
hypercoagulability
+ vasoactive medications (digoxin, pressors, cocaine,
diuretics)
+ recent hypoperfusive state (eg major surgery, cardiac
arrest)
Classification
occlusive
arterial
70-80% of occlusive cases
10% SMA thrombosis
50% SMA embolic
venous
5-15% of occlusive cases
non-occlusive / hypoperfusion
primary low-flow state, secondary vasospasm
increasingly diagnosed, may account for majority of
venous occlusive cases
Pathophysiology
insufficient regional perfusion of bowel

tissue hypoxia / dysfunction

shock / MSOF
mucosal / epithelial sloughing + ulceration

loss of bowel wall integrity

bacterial translocation -> bacteremia

luminal content permeation through bowel wall

perforation -> peritonitis / abscess formation

reperfusion injury
Different(ial) Diagnosis?
ED patients over 50y with acute abd pain are more
likely to have a significant structural explanation

40% 70+%

>>also 42% surgical management of 127pts with acute abd pain age > 65y in
Bugliosi TF et al. Ann Emerg Med 1990; 19(12):1383-6.
Atherosclerosis

Most common cause of mesenterial Arterial

Thrombosis
Rupture Thrombocyte Aggregation
Fibrin Formation
Endothelial Dysfunction
Endothelial Dysfunction

-Thrombocyte Aggregation
- Fibrin Formation
-Leucocyte Mobilization
-SMC Mobilization
-Vasoconstrion
-Angiogenesis
-Thrombus Enlargement
Risk Factor of Mesentric Arterial
Thrombosis

History Thrombosis : - Stroke

- MCI
- Peripheral TH
Smoking
Diabetes Mellitus
Atherosclerosis Risk Factor
Hypovolemia
Heart Failure
MCI
Cancer
Old Age
2/3 Are Female
Endhothelial Disfunction
 endothelium
intima

media

Modified
LDL
Cytokines
Cytokines
Growth factors
foam cell
Risk Factor of Endothelial dysfunction :

1. Stres oksidatif
2. Radikal bebas
3. Sitokin (ILK, TNF, dsb)
4. Hormon
5. Infeksi
6. Trombin
7. Histamin
Vascular Endothelial
lumen cells

fibrinogen Fibrous
Fibrous cap
cap
Fibrin
Collagen
Proteoglycans
IL-4
IL-10
IL-13 cytokines
Macrophage
Macrophage
foam
foam cells
cells

Th2 IFN
IL-4
IL-10
CD40
Th1

Smooth muscle
cells
Endothelial Dysfunction

-Thrombocyte Aggregation
- Fibrin Formation
-Leucocyte Mobilization
-SMC Mobilization
-Vasoconstrion
-Angiogenesis
-Thrombus Enlargement
Risk Factor of Mesentric Arterial
Thrombosis

History Thrombosis : - Stroke

- MCI
- Peripheral TH
Smoking
Diabetes Mellitus
Atherosclerosis Risk Factor
Hypovolemia
Heart Failure
MCI
Cancer
Old Age
2/3 Are Female
Endhothelial Disfunction
Outcomes
embolic SMA occlusion (21 pts)
<12h until reperfusion -> 100% had viable gut
12-24h 56%
>24h 18%
>>Lobo-Martinez 1993, all pts Tx with surg
embolectomy
acute mesenteric ischemia (43 pts)
67% mortality overall
time from pain until diagnosis # pts survivors
< 12h 21 10
> 12h 22 4
>>Deehan DJ et al 1995, all pts Tx with laparotomy
morbidity: short gut syndrome, recurrent ischemia
Diagnosis
lack of reliable, accurate, early clinical diagnostic
findings
abdominal pain or discomfort
not necessarily sudden
not necessarily constant or colicky
not necessarily present
bloody stool / diarrhea
nausea / vomiting
lack of reliable, accurate, early physical exam findings
pain out of proportion to exam... ...until perforation
Treatment
basic supportive
oxygenation / ventilation
fluid resuscitation
address co-morbid / precipitant conditions; pre-op
antibiotics
early diagnosis
operative vs. angio vs. pharmacologic support (+/- anti-
coag)
late diagnosis
? invariably poor prognosis of significant infarction in
vulnerable population intolerant of surgery, with
predisposing conditions
31 of 75 operative cases had exploration only (non-
salvageable) >>Wadman et al. 2000
Take Home Points
think of mesenteric ischemia
if you think of it, be aggressive about working it up
likely mesenteric ischemia -> surg consult, ? I+ CT vs.
angio
possible mesenteric ischemia -> surg consult, I+ CT
labs and XRs are diagnostic only late in course (if ever)
elderly acute abd pain -> y ou will likely find something

leaking AAA
aortic dissection
volvulus / strangulated bowel
perforated DU
etc etc etc
Watershed areas :

Splenic flexure (M colic-SMA and L colic-IMA

R colon (decreased arcade supply)

Sigmoid colon (L colic and superior rectal watershed)

Treatment
basic supportive
oxygenation / ventilation
fluid resuscitation
address co-morbid / precipitant conditions; pre-op
antibiotics
early diagnosis
operative vs. angio vs. pharmacologic support (+/- anti-coag)
late diagnosis
? invariably poor prognosis of significant infarction in
vulnerable population intolerant of surgery, with
predisposing conditions
31 of 75 operative cases had exploration only (non-
salvageable) >>Wadman et al. 2000