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Presenter: R 蔡逸文
 Literature review.
 MEDLINE/PubMed
 MeSH term keyword: “mesenteric ischemia”,
“bowel ischemia”, and “bowel infarction”
 Exclusion: Isolated colonic ischemia and focal
segmental ischemia secondary to adhesions,
hernias or other forms of extrinsic compression.
 Classification system used to determine
strength of evidence
 Presentation and clinical diagnosis
 etiology
 Diagnosis
 Image
 Treatment
 Vascular procedure
 Damage control surgery
 prevention
Presentation and clinical diagnosis
 Acute abdominal pain is disproportionate to
the physical examination findings
 Early:
 Nausea, vomiting and initial forced evacuation
 Late if transmural infarction:
 Fever, bloody diarrhea and shock
Presentation and clinical diagnosis
 Arterial thrombosis
(TAMI): 25%
 Arterial Embolic
(EAMI): 45%
 Non-occlusive
(NOMI): 20%
 Venous thrombosis
(VAMI): 10%
CHARACTERISTICS
 The sudden onset of severe
pain
 spontaneous emptying of
the bowel (vomiting and
diarrhea)
 no significant physical
findings(40-80%)
RISK FACTOR
 Atrial fibrillation
 Rheumatic heart disease
 Myocardial infarction
 Prosthetic valve
 Ventricular aneurism
CHARACTERISTICS
 Acute episode, may be
recurrent
 Prodromal symptoms of
mesenteric angina
 postprandial abdominal pain
 Nausea
 weight loss
RISK FACTOR
 Atherosclerosis
 Dyslipidemia
 History of other vascular
events, previous vascular
surgery
CHARACTERISTICS
 Subacute abdominal pain
 Vague complaints
 Younger population
 Thromboembolic AMI in the
over 60s
 VAMI in the over 40s
RISK FACTOR
 Hypercoagulability states
 Abdominal trauma
 Acute pancreatitis
 Malignancy
 Nephrotic syndrome,
 portal hypertension or
cirrhosis or splenomegaly
 Oral contraceptives
 Pregnancy and the
puerperium
CHARACTERISTICS
 Critically ill, sedated and
artificially ventilated Vague
complaints
 Acute or insidious pain
(without defecation)
 Mesenteric hypoperfusion
secondary to circulatory
shock or vasoactive drugs
RISK FACTOR
 Shock, hypovolemia,
hypotension
 Digitalis
 Diuretics
 beta-blockers, alpha-
adrenergics
 Enteral nutrition,
 Critical care support
Presentation and clinical diagnosis
 Older age
 Bandemia, Elevated serum aspartate
aminotransferase, Increased blood urea nitrogen,
Metabolic acidosis
 Significant co-morbidities and poor
performance status
 Intestinal necrosis
 Increased elapsed time to laparotomy(24hr)
 When the colon was involved
Aliosmanoglu I et al. Int Surg. 2013
Huang HH, et al. Chin Med Assoc. 2005
Gupta PK et al. Surgery. 2011
Presentation and clinical diagnosis
 Multi-detector computerized tomography
scanning (MDCT) with intravenous contrast
(LOE: III)
 Percutaneous angiography for suspected
NOMI (LOE:III)
Pneumatosis intestinalis +
hepatic portal or portomesenteric venous gas
↑the likelihood of transmural bowel infarction
Lisa M. Ho, et al. American Journal of Roentgenology. 2007
Melanie S. Morris, et al .The American Journal of Surgery. 2008
Treatment
 Vasopressor drugs should be avoided in AMI.
 Minimal effect on the splanchnic circulation
 Dobutamine, low dose dopamine, or milrinone
 Cardiac glycosides should not be used as first
line treatment of atrial fibrillation/flutter in
AMI (LOE: IV).
Treatment
 Open embolectomy
 Endovascular embolectomy
 percutaneous mechanical aspiration or
thrombolysis
 percutaneous transluminal angioplasty (PTA) with
or without stenting
 Endovascular procedure
 PTA and stenting
 Percutaneous aspiration thrombectomy, local
fibrinolysis or intra-arterial drug perfusion
 Retrograde open mesenteric stenting
 After resection of ischemic bowel
 Failed percutaneous treatment
 Bypass procedures
 Antegrade bypass from supraceliac aorta to
superior mesenteric trunk
 Retrograde bypass from the infra-renal aorta and
iliac arteries
 Correcting the underlying cause
 Improving mesenteric perfusion by direct
infusion of vasodilators.
 Prostaglandin E1 (alprostadil): 20 mcg bolus
followed by 60–80 mcg/24 h infusion;
 papaverine (30–60 mg/h)
 Infarcted bowel resection(LOE: III)
 Systemic anticoagulation (LOE: III)
 Vascular
 Failed medical therapy
 Transjugular intrahepatic portosystemic shunting
(TIPS) with mechanical aspiration thrombectomy
and direct thrombolysis
 Percutaneous transhepatic thrombolysis
 Indirect thrombolysis via the SMA
Treatment
 Immediate surgery if comorbidities and
clinical condition make curative treatment
possible (LOE: III)
 Patients considered unsalvageable should
have palliative care (LOE: IV)
Treatment
 Laparotomy with resection of ischemic bowel
(and no anastomosis or stoma)
 open thrombectomy (if indicated)
 A temporary abdominal closure via a negative
pressure wound therapy
 ICU and continue resuscitation
 scheduled ‘second-look’ procedure within 48 h
(LOE: III)
Treatment
 Reassessed after adequate fluid resuscitation
and revascularization.
 Intra-operative assessment:
 Doppler ultrasound of the vascular arcade,
fluorescein angiography, indocyanine
angiography
 A second-look procedure for the doubts of
viability of the bowel(LOE: IV).
Treatment
 Restoration of bowel continuity following
extensive resection (LOE: III).
 Improve functional results
 May avoid the need for long termTPN
 Short bowel syndrome often occurs when
residual small bowel length <200 cm
 The following minimum remaining intestinal
lengths must be respected :
 100 cm for terminal jejunostomy (colon removed)
 65 cm for jejunocolic anastomosis (colon retained)
 35 cm for jejunoileal anastomosis with retention
of the ileocecal region.
Messing B, et al. Gastroenterology.1999
 In the elderly patients and in those with
significant co-morbidities
 Significant risk of resection
 In younger patients
 Long term parenteral nutrition
 The option of subsequent intestinal
transplantation
Treatment
 Anastomosis should be avoided in patients
with shock or multiple organ dysfunction.
(LOE: III)
 Stoma avoid risks of anastomotic failure and
permit easy examination of the bowel by
inspection or endoscopy
Treatment
 Access bowel viability after revascularization
and resuscitation
 possible progression of bowel ischemia?
 If doubt about the viability of the bowel,
resection of it (LOE: IV).
 Bowel anastomosis(LOE: III).
 Close the wound
Treatment
 Symptoms >24hr=> Mortality increases
dramatically
 Symptoms <12hr=> lowest mortality
 Gut viability 100% when <12h
56% when 12~24hr
18% when >24hr
Aliosmanoglu I et al. Int Surg. 2013
Lobo Martinez E , et al. Rev Esp Enferm Dig. 1993
 Revascularization performed within 12 h from
the onset of symptoms. (LOE: III)
 Resection of non-viable bowel should be
performed without delay. (LOE: III)
Treatment
 ~60%TAMI have previous symptoms of
chronic mesenteric ischemia
 ~30% EAMI have inadequately treated atrial
fibrillation at presentation
Edwards MS, et al. AnnVasc Surg. 2003
Edwards MS, et al. AnnVasc Surg. 2003
 Elective revascularization for patients with
proven CMI (LOE: IV)
 Anticoagulants or antiplatelet therapy and
statin therapy for patients with mesenteric
artery thrombosis (LOE: IV).
 High risk of coronary thrombosis
Bj ¨ ornsson S, et al. J Gastrointest Surg 2013
Cho JS, et al. JVasc Surg. 2002
 Life-long anticoagulation, unless
contraindicated, for EAMI, prevent
recurrence (LOE: IV).
 A minimum of 6 months of anticoagulation
and survey for thrombophilia or
hypercoagulability forVAMI. (LOE: III).
Klempnauer J, Surgery. 1997
Daniel G. et al. N Engl J Med 2016
Acosta S, et al. Br J Surg 2008;
 History, physical examination
 prompt diagnosis should be achieved and
revascularization performed within 12 h from
the onset of symptoms.
 Resection of non-viable bowel should be
performed without delay
Presentation and clinical diagnosis
 Routine laboratory tests reflect disease
progression in AMI (LOE: III).
 Leukocytosis, metabolic acidosis with high anion gap
 High level of Lactate, amylase, AST(GOT), lactate
dehydrogenase(LDH) and creatine
phosphokinase(CPK)
 A normal serum lactate level does not exclude
AMI and not be used for diagnosis (LOE: III).

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Guideline: Acute mesenteric ischemia

  • 2.  Literature review.  MEDLINE/PubMed  MeSH term keyword: “mesenteric ischemia”, “bowel ischemia”, and “bowel infarction”  Exclusion: Isolated colonic ischemia and focal segmental ischemia secondary to adhesions, hernias or other forms of extrinsic compression.
  • 3.  Classification system used to determine strength of evidence
  • 4.  Presentation and clinical diagnosis  etiology  Diagnosis  Image  Treatment  Vascular procedure  Damage control surgery  prevention
  • 6.  Acute abdominal pain is disproportionate to the physical examination findings  Early:  Nausea, vomiting and initial forced evacuation  Late if transmural infarction:  Fever, bloody diarrhea and shock
  • 8.  Arterial thrombosis (TAMI): 25%  Arterial Embolic (EAMI): 45%  Non-occlusive (NOMI): 20%  Venous thrombosis (VAMI): 10%
  • 9. CHARACTERISTICS  The sudden onset of severe pain  spontaneous emptying of the bowel (vomiting and diarrhea)  no significant physical findings(40-80%) RISK FACTOR  Atrial fibrillation  Rheumatic heart disease  Myocardial infarction  Prosthetic valve  Ventricular aneurism
  • 10. CHARACTERISTICS  Acute episode, may be recurrent  Prodromal symptoms of mesenteric angina  postprandial abdominal pain  Nausea  weight loss RISK FACTOR  Atherosclerosis  Dyslipidemia  History of other vascular events, previous vascular surgery
  • 11. CHARACTERISTICS  Subacute abdominal pain  Vague complaints  Younger population  Thromboembolic AMI in the over 60s  VAMI in the over 40s RISK FACTOR  Hypercoagulability states  Abdominal trauma  Acute pancreatitis  Malignancy  Nephrotic syndrome,  portal hypertension or cirrhosis or splenomegaly  Oral contraceptives  Pregnancy and the puerperium
  • 12. CHARACTERISTICS  Critically ill, sedated and artificially ventilated Vague complaints  Acute or insidious pain (without defecation)  Mesenteric hypoperfusion secondary to circulatory shock or vasoactive drugs RISK FACTOR  Shock, hypovolemia, hypotension  Digitalis  Diuretics  beta-blockers, alpha- adrenergics  Enteral nutrition,  Critical care support
  • 14.  Older age  Bandemia, Elevated serum aspartate aminotransferase, Increased blood urea nitrogen, Metabolic acidosis  Significant co-morbidities and poor performance status  Intestinal necrosis  Increased elapsed time to laparotomy(24hr)  When the colon was involved Aliosmanoglu I et al. Int Surg. 2013 Huang HH, et al. Chin Med Assoc. 2005 Gupta PK et al. Surgery. 2011
  • 16.  Multi-detector computerized tomography scanning (MDCT) with intravenous contrast (LOE: III)  Percutaneous angiography for suspected NOMI (LOE:III)
  • 17.
  • 18. Pneumatosis intestinalis + hepatic portal or portomesenteric venous gas ↑the likelihood of transmural bowel infarction Lisa M. Ho, et al. American Journal of Roentgenology. 2007 Melanie S. Morris, et al .The American Journal of Surgery. 2008
  • 20.  Vasopressor drugs should be avoided in AMI.  Minimal effect on the splanchnic circulation  Dobutamine, low dose dopamine, or milrinone  Cardiac glycosides should not be used as first line treatment of atrial fibrillation/flutter in AMI (LOE: IV).
  • 22.  Open embolectomy  Endovascular embolectomy  percutaneous mechanical aspiration or thrombolysis  percutaneous transluminal angioplasty (PTA) with or without stenting
  • 23.  Endovascular procedure  PTA and stenting  Percutaneous aspiration thrombectomy, local fibrinolysis or intra-arterial drug perfusion  Retrograde open mesenteric stenting  After resection of ischemic bowel  Failed percutaneous treatment
  • 24.  Bypass procedures  Antegrade bypass from supraceliac aorta to superior mesenteric trunk  Retrograde bypass from the infra-renal aorta and iliac arteries
  • 25.  Correcting the underlying cause  Improving mesenteric perfusion by direct infusion of vasodilators.  Prostaglandin E1 (alprostadil): 20 mcg bolus followed by 60–80 mcg/24 h infusion;  papaverine (30–60 mg/h)  Infarcted bowel resection(LOE: III)
  • 26.  Systemic anticoagulation (LOE: III)  Vascular  Failed medical therapy  Transjugular intrahepatic portosystemic shunting (TIPS) with mechanical aspiration thrombectomy and direct thrombolysis  Percutaneous transhepatic thrombolysis  Indirect thrombolysis via the SMA
  • 28.  Immediate surgery if comorbidities and clinical condition make curative treatment possible (LOE: III)  Patients considered unsalvageable should have palliative care (LOE: IV)
  • 30.  Laparotomy with resection of ischemic bowel (and no anastomosis or stoma)  open thrombectomy (if indicated)  A temporary abdominal closure via a negative pressure wound therapy  ICU and continue resuscitation  scheduled ‘second-look’ procedure within 48 h (LOE: III)
  • 32.  Reassessed after adequate fluid resuscitation and revascularization.  Intra-operative assessment:  Doppler ultrasound of the vascular arcade, fluorescein angiography, indocyanine angiography  A second-look procedure for the doubts of viability of the bowel(LOE: IV).
  • 34.  Restoration of bowel continuity following extensive resection (LOE: III).  Improve functional results  May avoid the need for long termTPN
  • 35.  Short bowel syndrome often occurs when residual small bowel length <200 cm  The following minimum remaining intestinal lengths must be respected :  100 cm for terminal jejunostomy (colon removed)  65 cm for jejunocolic anastomosis (colon retained)  35 cm for jejunoileal anastomosis with retention of the ileocecal region. Messing B, et al. Gastroenterology.1999
  • 36.  In the elderly patients and in those with significant co-morbidities  Significant risk of resection  In younger patients  Long term parenteral nutrition  The option of subsequent intestinal transplantation
  • 38.  Anastomosis should be avoided in patients with shock or multiple organ dysfunction. (LOE: III)  Stoma avoid risks of anastomotic failure and permit easy examination of the bowel by inspection or endoscopy
  • 40.  Access bowel viability after revascularization and resuscitation  possible progression of bowel ischemia?  If doubt about the viability of the bowel, resection of it (LOE: IV).  Bowel anastomosis(LOE: III).  Close the wound
  • 42.  Symptoms >24hr=> Mortality increases dramatically  Symptoms <12hr=> lowest mortality  Gut viability 100% when <12h 56% when 12~24hr 18% when >24hr Aliosmanoglu I et al. Int Surg. 2013 Lobo Martinez E , et al. Rev Esp Enferm Dig. 1993
  • 43.  Revascularization performed within 12 h from the onset of symptoms. (LOE: III)  Resection of non-viable bowel should be performed without delay. (LOE: III)
  • 45.  ~60%TAMI have previous symptoms of chronic mesenteric ischemia  ~30% EAMI have inadequately treated atrial fibrillation at presentation Edwards MS, et al. AnnVasc Surg. 2003 Edwards MS, et al. AnnVasc Surg. 2003
  • 46.  Elective revascularization for patients with proven CMI (LOE: IV)  Anticoagulants or antiplatelet therapy and statin therapy for patients with mesenteric artery thrombosis (LOE: IV).  High risk of coronary thrombosis Bj ¨ ornsson S, et al. J Gastrointest Surg 2013 Cho JS, et al. JVasc Surg. 2002
  • 47.  Life-long anticoagulation, unless contraindicated, for EAMI, prevent recurrence (LOE: IV).  A minimum of 6 months of anticoagulation and survey for thrombophilia or hypercoagulability forVAMI. (LOE: III). Klempnauer J, Surgery. 1997 Daniel G. et al. N Engl J Med 2016 Acosta S, et al. Br J Surg 2008;
  • 48.  History, physical examination  prompt diagnosis should be achieved and revascularization performed within 12 h from the onset of symptoms.  Resection of non-viable bowel should be performed without delay
  • 50.  Routine laboratory tests reflect disease progression in AMI (LOE: III).  Leukocytosis, metabolic acidosis with high anion gap  High level of Lactate, amylase, AST(GOT), lactate dehydrogenase(LDH) and creatine phosphokinase(CPK)  A normal serum lactate level does not exclude AMI and not be used for diagnosis (LOE: III).

Editor's Notes

  1. 可以透國臨床狀況去預測prognosi來幫助我們做決定嗎?
  2. occlusion of mesenteric vessels and the non-specific appearance of bowel wall thickening and intestinal pneumatosis Pneumatosis Intestinalis (often indicate transmural infarction in AMI, particularly if it is associated with portomesenteric venous gas), but this sign is not specific for either infarction or ischemia.
  3. Consideration should be given to the use of drugs such as dobutamine, low dose dopamine and milrinone, which have been shown to have less impact on mesenteric blood flow [39]. Vasopressors should not be used until the patient has been adequately volume resuscitated. Cardiac output can also be improved by rate control in atrial fibrillation. However, digoxin and other cardiac glycosides also reduce flow in the splanchnic circulation and should be avoided for the control of atrial fibrillation/flutter in patients with AMI [40, 96, 98].
  4. Open embolectomy is usually performed via a midline incision approaching the SMA just below the pancreas at the mesenteric root [98]. A transverse arteriotomy is then made after proximal and distal clamping and embolectomy catheters are used to clear the artery proximally and distally. High pressure proximal flushing should be avoided so as not to dislodge the thrombus in the aorta and produce further emboli. After completing the thrombectomy the artery should be flushed gently with heparinized saline. The arteriotomy is then closed in a standard fashion.
  5. There are a variety of bypass procedures, providing either antegrade or retrograde flow, with vein or synthetic grafts. An antegrade bypass from supraceliac aorta to superior mesenteric trunk using an endogenous vein graft will give the best result. An alternative approach would be a renal mesenteric bypass. However, the most practical option for proximal mesenteric atherosclerotic occlusive disease is a retrograde bypass from common iliac with a synthetic graft.
  6. The treatment of NOMI is based on correcting the clinical or pharmacological conditions that generate splanchnic vasoconstriction, improving mesenteric perfusion and early recognition and resection of infarcted bowel [99]. The main factor in improving mesenteric perfusion is the restoration of circulatory volume and hemodynamic stability coupled with the use of vasodilators administered directly into the SMA in order to reverse the intestinal vasospasm that causes ischemia. The diagnosis of NOMI should be confirmed by selective mesenteric angiography and, if there are no contraindications, the infusion of vasodilators directly into the SMA [90]. The best vasodilator drug appears to be prostaglandin E1 (alprostadil) given as a 20 mcg bolus followed by 60–80 mcg/24 h infusion [90]; papaverine (30–60 mg/h) has been shown to reduce the mortality rate for NOMI from 70 to 50–55 % and is an acceptable alternative [1, 10]. Other prostacyclin analogues have also been used [61]. The decision to intervene surgically is based on the presence of peritonitis, perforation, or overall worsening of the patient’s condition [99].
  7. Contraindications to thrombolytic treatment Absolute (central nervous system tumors, recent hemorrhagic stroke, gastrointestinal bleed and uncontrolled hypertension) Relative (pregnancy, remote history of GI bleeding, and recent major surgery).
  8. 在severe sepsis or septic shock下life saving damage control surgery
  9. Intra-operative assessment with Doppler ultrasound of the vascular arcade, [128, 129], fluorescein angiography [127, 130] and indocyanine green angiography [131] have shown promise, but not been used extensively.
  10. Short bowel syndrome requiring total parenteral nutrition (TPN) has been reported in 13–31 % of long-term survivors of AMI [9, 21, 31] and weight loss has been documented in 38 % [31]. SBS generally occurs when less than 200 cm of functioning bowel remains [106]. Restoring bowel continuity will improve the functional results of extensive small bowel resection and may avoid long term TPN. It has been suggested that while permanent intestinal failure is likely with a residual 100 cm of small bowel and an end jejunostomy, the need for permanent TPN may be avoided with a minimum 65 cm of jejunum and a jejunocolic anastomosis, and 35 cm where the ileocaecal region is preserved and a jejunoileal anastomosis performed [133]. When a residual small bowel length of 200 cm cannot be obtained, careful consideration should be given to the significant risk of resection, particularly in the elderly patients and in those with significant co-morbidities. In younger patients the option of long term parenteral nutrition or the option of subsequent intestinal transplantation could make a more extensive resection reasonable.
  11. Messing B, Crenn P, Beau P, Boutron-Ruault MC, Rambaud JC, Matuchansky C. Long-term survival and parenteral nutrition dependence in adult patients with the short bowel syndrome. Gastroenterology.1999;
  12. Anastomosis 需再adequate resuscitation and stable condition而且
  13. The use of second look procedures is associated with a significant reduction in morbidity (p = 0.002) [9] and mortality in selected patients leading to resection of ischaemic bowel in 38–71 % of cases [14,17, 18, 24, 29, 126, 135]. It is currently the best method to assess bowel viability after revascularization and resuscitation and may be the best time to perform an anastomosis and to close the abdomen after DCS.
  14. Mortality increases dramatically when symptoms have been present for more than 24 h in AMI. Numerous studies have shown that mortality is lowest if intervention is performed within 12 h of the onset of symptoms. [18, 22, 25, 58, 136–139]. This is supported by experimental work which has shown gut viability to be 100 % within the first 12 h of ischaemia. This drops to 54 % between 12 and 24 h and 18 % beyond 24 h The development of symptoms in VAMI is usually slower than the other forms of AMI. A small retrospective study of VAMI over 23 years suggested that patients presenting within 3 days of the onset of symptoms had poorer outcomes than those presenting with symptoms of longer duration. The first group were more likely to undergo laparotomy within 12 h of hospital admission (83 vs. 20 %) [52]. This reflected rapid disease progression in the group that presented sooner. In studies comparing the four aetiological types of AMI, VAMI has the lowest mortality (11– 30 %) [5, 22, 30].
  15. Mortality increases dramatically when symptoms have been present for more than 24 h in AMI. Numerous studies have shown that mortality is lowest if intervention is performed within 12 h of the onset of symptoms. [18, 22, 25, 58, 136–139]. This is supported by experimental work which has shown gut viability to be 100 % within the first 12 h of ischaemia. This drops to 54 % between 12 and 24 h and 18 % beyond 24 h The development of symptoms in VAMI is usually slower than the other forms of AMI. A small retrospective study of VAMI over 23 years suggested that patients presenting within 3 days of the onset of symptoms had poorer outcomes than those presenting with symptoms of longer duration. The first group were more likely to undergo laparotomy within 12 h of hospital admission (83 vs. 20 %) [52]. This reflected rapid disease progression in the group that presented sooner. In studies comparing the four aetiological types of AMI, VAMI has the lowest mortality (11– 30 %) [5, 22, 30].
  16. The liver can clear large quantities of L-lactate from the porto-mesenteric circulation and as a result serum lactate level does not correlate with intestinal infarction [74]. Serum L-lactate is a specific marker of tissue hypo-perfusion [73]. Lactic acidosis develops late in the course of AMI with extensive transmural infarction and tissue hypoperfusion due to sepsis. At that point mortality is already in the order of 75 % [75]. The fibrinolytic marker D-dimer does not differentiate patients with AMI from those with non-acute mesenteric ischemia and that there is no difference in D-dimer levels between patients with resectable and irresectable bowel necrosis [76].