Figure Core mechanisms examiners expect in CICM/FFICM/EDIC answers. Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation. Figure Classification and decision thresholds used in exam answers. Figure Pain out of proportion plus a raised lactate — get the CT angiogram; mortality is 50–80%. Acute mesenteric ischaemia = sudden intestinal blood flow loss. Four types : embolic (AF→SMA, 50%), thrombotic (atherosclerosis, 25%), NOMI (low-flow/shock, 20%), venous (thrombosis, 5%). Clinical : severe abdominal pain OUT OF PROPORTION to examination (early), then peritonitis (late — necrosis). Lactate elevated (ischaemia). CT angiography (gold standard — occlusion type, location, bowel viability). Management : EMERGENCY surgery (revascularisation + resect necrosis) for arterial occlusion; ANTICOAGULATION for venous; PAPAVERINE + treat low-flow for NOMI. Mortality 50-80% — delayed diagnosis is the killer.
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Exam practice
SAQ — Acute SMA embolus in atrial fibrillation 20 minutes · 10 marks
Reveal all A 78-year-old woman with non-valvular atrial fibrillation (CHA2DS2-VASc 5, not anticoagulated) and hypertension presents with four hours of sudden severe periumbilical pain. She is in fast AF at 130/min irregular, BP 105/65, afebrile, and has vomited twice. The abdomen is soft and non-tender despite agonising pain (pain out of proportion). Bloods: WCC 14.0, haemoglobin 132, amylase 110, lactate 4.1 mmol/L (was 2.8 one hour ago), INR 1.1. Venous gas: pH 7.28, BE -7. ECG confirms AF.
a Give the most likely diagnosis, the CT angiography findings you would expect, and the rationale for urgent intervention. (5 marks)
b Outline the operative and peri-operative management. (3 marks)
c Why is the serum lactate useful but imperfect in this condition? (2 marks)
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SAQ — Non-occlusive mesenteric ischaemia (NOMI) in vasopressor-dependent shock 20 minutes · 10 marks
Reveal all A 64-year-old man is day 3 in ICU with pneumococcal septic shock. He is mechanically ventilated and sedated, on noradrenaline 0.6 µg/kg/min and vasopressin 0.03 U/min for MAP 65, with AKI on continuous renal replacement therapy. Over six hours he develops abdominal distension, an 800 mL nasogastric aspirate, falling urine output, and a lactate rising from 2.4 to 5.6 mmol/L. CT angiography shows diffuse narrowing of the SMA and its branches with alternating dilation and constriction (a string-of-sausages appearance), no focal occlusion, and diffusely thickened small-bowel wall.
a Make the diagnosis and explain the pathophysiology. How does NOMI differ radiologically and clinically from the other three forms of acute mesenteric ischaemia? (5 marks)
b Outline your management, including the role of papaverine and the principles of vasopressor selection. (3 marks)
c What is the role of a second-look strategy, and what is the prognosis? (2 marks)
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Clinical pearls
High-yield mesenteric ischaemia points for CICM/FFICM exam
Pain out of proportion — the classic clue. (1) EARLY mesenteric ischaemia: severe abdominal PAIN but MINIMAL abdominal findings (soft abdomen, mild tenderness). (2) WHY: (a) The BOWEL is ischaemic (visceral pain — severe, poorly localised). (b) But the PERITONEUM is not yet inflamed (bowel still viable, no transmural necrosis). (c) So: pain (from bowel ischaemia) is SEVERE but examination (peritoneal) is BENIGN. (d) This DISCREPANCY (pain >> findings) is the HALLMARK. (3) LATE: peritonitis (rigid, guarding, rebound) = TRANSMURAL NECROSIS -> peritoneal inflammation -> examination now matches pain (but too late — bowel dead). (4) CLINICAL: ANY patient with severe abdominal pain + SOFT abdomen (especially with risk factors — AF, atherosclerosis, shock) -> mesenteric ischaemia until proven otherwise -> CT ANGIOGRAPHY + surgical consultation.[2] }Lactate — ischaemia marker (but not perfect). (1) LACTATE elevated in mesenteric ischaemia: (a) Mechanism: bowel ischaemia -> anaerobic metabolism -> lactate production -> enters blood -> serum lactate rises. (b) SENSITIVITY: high (~80-90%) for established ischaemia. (2) LIMITATION: (a) EARLY ischaemia: lactate may be NORMAL (takes time to develop — if caught very early, lactate hasn't risen yet). (b) NON-SPECIFIC: elevated in ANY shock/sepsis/trauma (not diagnostic for mesenteric). (3) TREND: RISING lactate (serial measurements) = ongoing/worsening ischaemia -> worse prognosis. FALLING = improving (revascularised). (4) OTHER MARKERS: (a) AMYLASE/LIPASE: may be elevated (pancreatic involvement from ischaemia — non-specific). (b) WCC: elevated (inflammation/ischaemia). (c) METABOLIC ACIDOSIS (lactate + others). (d) PHOSPHATE: elevated (bowel ischaemia — some evidence). (5) PRACTICE: check lactate (baseline + serial) — rising = concerning — but DON'T be reassured by normal early lactate (if clinical suspicion high -> CT regardless).[2] }CT angiography — the gold standard. (1) WHY CT: (a) FAST (minutes — critical — bowel becomes necrotic in 4-6h). (b) IDENTIFIES: TYPE of occlusion (embolus vs thrombosis vs venous vs NOMI), LOCATION (which vessel, how proximal), BOWEL VIABILITY (enhancement, pneumatosis, portal gas), PERITONITIS (free air, fluid). (c) GUIDES TREATMENT (surgery vs endovascular vs anticoagulation vs papaverine). (2) PROTOCOL: (a) ARTERIAL phase (early — for arterial occlusion — SMA filling defect). (b) VENOUS phase (for venous thrombosis — SMV/portal vein filling defect; ALSO for bowel wall enhancement). (c) Non-contrast (sometimes — for haemorrhage, calcification). (3) FINDINGS: (a) ARTERIAL EMBOLUS: filling defect in SMA (usually DISTAL to middle colic artery origin — embolus lodges there — classic), 'meniscus sign' (rounded clot edge), NO collaterals (acute). (b) ARTERIAL THROMBOSIS: filling defect at SMA ORIGIN (ostial — atherosclerotic), COLLATERAL vessels (from coeliac/IMA — chronic stenosis -> collaterals developed), may see calcified plaque. (c) VENOUS THROMBOSIS: filling defect in SMV or portal vein, bowel wall THICKENING (oedema from venous congestion), ascites. (d) NOMI: DIFFUSE vasoconstriction — narrowed SMA + branches, alternating dilation/constriction ('string of sausages'), poor bowel enhancement, NO focal occlusion. (e) BOWEL NECROSIS (late): pneumatosis intestinalis (gas in wall — bacteria), portal venous gas, lack of enhancement, free air (perforation). (4) ACCURACY: >90% sensitivity for arterial occlusion. (5) PRACTICE: CT ANGIOGRAPHY for ALL suspected mesenteric ischaemia (definitive — don't rely on clinical/labs alone). (6) DON'T DELAY: if peritonitis (necrosis) -> straight to OR (CT may waste time — but if stable -> CT first to plan).[1] }SMA embolus — AF is the classic cause. (1) SMA (SUPERIOR MESENTERIC ARTERY): supplies midgut (jejunum, ileum, ascending + proximal transverse colon). (2) EMBOLUS source: (a) AF (most common — 70% of embolic) -> thrombus in left atrial appendage -> dislodges -> embolises -> lodges in SMA. (b) Post-MI mural thrombus (LV apical — after large anterior MI). (c) Prosthetic valve (if subtherapeutic INR). (d) Endocarditis (vegetation). (e) Atheroembolism (aortic plaque). (3) WHERE it lodges: SMA — usually DISTAL to the middle colic artery origin (the SMA narrows distal to the middle colic branch -> embolus lodges there). (4) CLINICAL: (a) SUDDEN severe abdominal pain (embolus lodges acutely -> complete occlusion -> no collaterals -> severe ischaemia immediately). (b) NO prior abdominal pain (no chronic mesenteric disease). (c) AF history (clue). (d) VOMITING, diarrhoea (early — bowel reacting to ischaemia). (e) Pain OUT OF PROPORTION (early — bowel viable but ischaemic). (5) DIAGNOSIS: CT angiography (SMA filling defect, distal to middle colic). (6) MANAGEMENT: EMERGENCY EMBOLECTOMY (Fogarty catheter — extract embolus) + assess bowel viability + resect necrotic. (7) DON'T be reassured by 'no prior pain' — embolic is sudden + severe.[3] }SMA thrombosis — on atherosclerosis (prior 'mesenteric angina'). (1) MECHANISM: atherosclerotic plaque at SMA ORIGIN (ostial) -> plaque rupture -> acute thrombosis -> occlusion. (2) DIFFERENCE from embolus: (a) Thrombosis is at OSTIUM (origin — where atherosclerosis occurs). (b) Embolus is DISTAL (lodges past middle colic). (c) Thrombosis has COLLATERALS (chronic stenosis -> body developed bypass vessels -> less severe initially). (d) Embolus has NO collaterals (acute — no time). (3) HISTORY: CHRONIC MESENTERIC ANGINA (intestinal claudication): (a) POSTPRANDIAL abdominal pain (after eating -> bowel needs more blood -> can't get through stenosis -> ischaemic pain). (b) FOOD FEAR (patient avoids eating -> pain). (c) WEIGHT LOSS (from food avoidance). (d) This history (if asked) suggests chronic SMA stenosis -> acute thrombosis. (4) RISK FACTORS: atherosclerosis (smoking, diabetes, hypertension, hyperlipidaemia, age). (5) DIAGNOSIS: CT angiography (SMA occlusion at origin, collaterals, calcified plaque). (6) MANAGEMENT: EMERGENCY REVASCULARISATION — (a) BYPASS (saphenous vein graft from aorta/iliac to SMA — re-establish flow). (b) ENDOVASCULAR STENT (percutaneous — stent the ostial stenosis — if available + suitable — faster, less invasive). (c) THEN: assess bowel viability + resect necrotic. (7) LONG-TERM: antiplatelet (aspirin/clopidogrel), statin, risk factor modification (smoking, diabetes).[5] }NOMI — low-flow (no occlusion). (1) NOMI (Non-Occlusive Mesenteric Ischaemia): diffuse mesenteric VASOCONSTRICTION from low-flow state -> bowel ischaemia (NO large vessel occlusion — the vessels are patent but constricted). (2) CAUSES (any low-flow state): (a) SHOCK (sepsis, cardiogenic, haemorrhagic) -> low cardiac output -> mesenteric vasoconstriction (to redirect blood to heart/brain). (b) VASOPRESSORS (noradrenaline, adrenaline — alpha agonists -> constrict mesenteric vessels). (c) DIALYSIS (haemodialysis -> fluid removal -> hypotension -> vasoconstriction). (d) HEART FAILURE (low output). (e) DIGOXIN (mesenteric vasoconstrictor). (3) CLINICAL: (a) Critically ill patient (already in ICU for shock/sepsis). (b) Abdominal pain/distension (but may be obtunded/sedated -> can't report pain -> DILIGENCE — check abdomen, lactate). (c) On vasopressors (the cause + the worsening). (4) DIAGNOSIS: CT angiography — DIFFUSE vasoconstriction (narrowed SMA + branches, alternating dilation/constriction — 'string of sausages'), NO focal occlusion, poor bowel enhancement. (5) MANAGEMENT: (a) TREAT UNDERLYING: restore perfusion (fluids, inotropes — improve cardiac output), REDUCE vasopressors (alpha worsens — prefer dobutamine, milrinone). (b) PAPAVERINE INFUSION into SMA (vasodilator — via angiographically placed catheter — relieves vasoconstriction — 24-48h). (c) SURGERY: if peritonitis (necrosis) -> resect. (d) NOMI is OFTEN FATAL (underlying critical illness + diffuse ischaemia) — mortality 70-90%. (6) PREVENTION: in critically ill — maintain perfusion (avoid prolonged hypotension), minimise vasopressors (balance — sometimes needed), consider early enteral nutrition (maintains gut integrity).[6] }Mesenteric venous thrombosis — hypercoagulable. (1) MECHANISM: clot in MESENTERIC VEINS (SMV — superior mesenteric vein; portal vein) -> venous OUTFLOW obstruction -> bowel CONGESTION (blood can't drain) -> oedema -> ischaemia (if severe). (2) CAUSES (Virchow's triad): (a) HYPERCOAGULABLE: thrombophilia (Factor V Leiden, prothrombin gene mutation, antiphospholipid syndrome), malignancy (pancreatic, gastric — paraneoplastic), pregnancy, oestrogen (oral contraceptive pill), myeloproliferative (polycythaemia, essential thrombocythaemia). (b) VENOUS STASIS: portal hypertension (cirrhosis), splenomegaly. (c) VESSEL INJURY: infection (appendicitis, diverticulitis, pelvic inflammatory), inflammation (pancreatitis, inflammatory bowel disease), surgery, trauma. (3) CLINICAL: (a) GRADUAL onset (days — slower than arterial). (b) Abdominal pain (less severe initially — venous congestion vs arterial sudden occlusion). (c) DISTENSION (venous congestion -> oedema). (d) Thrombosis risk factors (if asked — OCP, malignancy, thrombophilia). (4) DIAGNOSIS: CT angiography (VENOUS phase) — filling defect in SMV/portal vein, bowel wall THICKENING (oedema), ascites, collateral veins. (5) MANAGEMENT: (a) ANTICOAGULATION (heparin IV then warfarin/DOAC — 3-6 months; lifelong if thrombophilia). (b) Most resolve with anticoagulation (clot lyses + recanalisation over weeks-months). (c) SURGERY: if PERITONITIS (bowel necrosis from venous congestion) -> resect. (d) ENDOVASCULAR: thrombolysis/thrombectomy (if extensive + failing anticoagulation). (e) TREAT underlying (thrombophilia, infection, inflammation). (6) MORTALITY: 20-30% (lower than arterial — more amenable to anticoagulation). (7) LONG-TERM: anticoagulation (prevent recurrence), investigate thrombophilia.[3] }'Second look' laparotomy — assess viability. (1) CONCEPT: after revascularisation (embolectomy/bypass), some bowel may be BORDERLINE viability (dusky, questionably viable). Rather than resect aggressively (risk short bowel) OR leave potentially dead bowel (risk necrosis/sepsis), do a SECOND LOOK at 24-48h. (2) PROCEDURE: (a) First operation: revascularise (restore flow), resect clearly necrotic bowel, leave borderline. (b) 24-48h later: SECOND LAPAROTOMY — reassess. (i) Bowel that recovered (pink, peristalsis, bleeding) -> viable -> leave. (ii) Bowel that demarcated (clearly necrotic) -> resect. (iii) This preserves maximum bowel length (avoid short bowel syndrome). (3) INDICATION: after revascularisation for arterial occlusion (embolus/thrombosis) — especially if extensive or borderline. (4) EVIDENCE: observational — second look reduces mortality (detects + removes necrosis before sepsis) + preserves bowel (avoids unnecessary resection). (5) PRACTICE: many surgeons do second look routinely after mesenteric revascularisation (24-48h).[1] }Short bowel syndrome — the consequence of extensive resection. (1) If extensive necrosis -> resect large amount of bowel -> SHORT BOWEL SYNDROME (<200 cm remaining). (2) CONSEQUENCES: (a) MALABSORPTION: diarrhoea (unabsorbed nutrients + water), weight loss, dehydration, electrolyte loss (K+, Mg2+). (b) NUTRIENT DEFICIENCY: vitamins (B12 — if terminal ileum resected — pernicious anaemia; fat-soluble A, D, E, K), minerals (calcium, magnesium, zinc), protein-calorie malnutrition. (c) DEPENDENCE on PARENTERAL NUTRITION (TPN — if <100 cm remaining — lifelong — with complications: line sepsis, liver failure). (d) GASTRIC HYPERSECRETION (early — gastric acid overwhelms remaining bowel -> ulceration, fluid loss). (3) MANAGEMENT: (a) NUTRITION: parenteral (TPN — central) + enteral (promote adaptation — small frequent feeds — bowel adapts over months-years). (b) MEDICATION: anti-diarrhoeal (loperamide, codeine), PPI (reduce acid), bile acid binders (cholestyramine — if terminal ileum resected), TEDUGLUTIDE (GLP-2 analogue — promotes bowel adaptation — reduces TPN dependence). (c) SURGERY: bowel lengthening (Bianchi, STEP procedures — for selected), intestinal transplant (last resort). (4) PREVENTION: minimise resection (second look — preserve borderline bowel), revascularise EARLY (before necrosis). (5) This is a DEVASTATING outcome — driving the urgency of early diagnosis + revascularisation.[3] }Differential of acute abdominal pain in ICU — broad. (1) MESSENTERIC ISCHAEMIA (this topic — pain out of proportion, lactate, risk factors). (2) PERFORATED VISCUS (free air — peptic ulcer, diverticulum) — sudden severe pain, peritonitis, CXR/CT free air. (3) PANCREATITIS (epigastric pain, raised amylase/lipase, CT). (4) BOWEL OBSTRUCTION (distension, vomiting, no flatus, CT — dilation + transition point). (5) APPENDICITIS (RLQ pain, CT). (6) CHOLECYSTITIS (RUQ pain, fever, CT/ultrasound). (7) DIVERTICULITIS (LLQ pain, CT). (8) AORTIC DISSECTION (tearing pain — may involve mesenteric arteries -> ischaemia — distinguish). (9) PE (rarely abdominal pain — but possible if hepatic congestion). (10) METABOLIC (DKA, Addisonian crisis, porphyria — abdominal pain). (11) POST-OPERATIVE (ileus, anastomotic leak, bleeding). (12) IN ICU PATIENTS (sedated): may not report pain -> DILIGENCE — abdominal examination (distension, tenderness, rigidity), lactate trend, CT if suspicious.[2] }Endovascular options — stenting and thrombolysis. (1) ENDOVASCULAR STENTING (for SMA thrombosis at ostium): (a) Percutaneous (femoral artery -> SMA -> stent the stenosis). (b) ADVANTAGE: less invasive (no laparotomy), faster, lower morbidity. (c) INDICATION: acute thrombosis at ostium (atherosclerotic), if suitable anatomy, if available. (d) THEN: assess bowel (laparoscopy/laparotomy if peritonitis — but if no peritonitis, stent alone may suffice). (e) LIMITATION: doesn't address necrosis (if bowel dead -> still need surgery). (2) CATHETER-DIRECTED THROMBOLYSIS (for embolus or venous): (a) Catheter into clot -> alteplase infusion -> dissolves clot. (b) INDICATION: if surgery high-risk, or venous thrombosis extensive + failing anticoagulation. (c) LIMITATION: slow (hours — bowel may necrose while waiting), bleeding risk. (3) PAPAVERINE (for NOMI): catheter into SMA -> papaverine infusion -> vasodilation -> relieves vasoconstriction. (4) ENDPOINT: revascularise (however) + assess bowel (resect if necrosis). (5) DECISION: multidisciplinary (vascular surgery, interventional radiology, ICU) — based on type, patient factors, centre capabilities.[4] }Papaverine — for NOMI. (1) PAPAVERINE: (a) A SMOOTH MUSCLE RELAXANT (phosphodiesterase inhibitor — increases cAMP -> vasodilation). (b) Infused into SMA (via angiographically placed catheter — directly to mesenteric vessels). (2) INDICATION: NOMI (diffuse vasoconstriction — no occlusion to remove mechanically). (3) MECHANISM: (a) Relaxes mesenteric vascular smooth muscle -> vasodilation -> restores flow to constricted vessels. (b) Overcomes the vasoconstriction from low-flow/vasopressors. (4) PROTOCOL: (a) Catheter placed in SMA (angiographically — via femoral). (b) Papaverine infusion (e.g., 30-60 mg/hr) into SMA. (c) Continue 24-48h (until perfusion restored — clinical improvement, lactate falling, pain resolving). (d) Monitor: angiography (vessel dilation), clinical (pain, lactate, abdomen). (5) SIDE EFFECTS: (a) Systemic vasodilation (if absorbed -> hypotension — monitor BP). (b) Hepatotoxicity (rare). (6) EVIDENCE: observational (Mitsuyoshi) — papaverine improves outcomes in NOMI (if given early). (7) LIMITATION: doesn't address necrosis (if bowel dead -> surgery). (8) ALSO: for ARTERIAL occlusion after embolectomy/bypass — papaverine may relieve associated vasospasm.[6] }Mortality + outcomes. (1) MORTALITY: 50-80% (arterial occlusion — high — delayed diagnosis + sick patients). (2) FACTORS: (a) TIME to revascularisation (>6-12h -> more necrosis -> worse). (b) EXTENT of necrosis (more resection -> short bowel -> worse). (c) COMORBIDITIES (age, cardiac, renal — the typical patient — AF, atherosclerosis). (d) TYPE: arterial embolus/thrombosis worse (50-80%); NOMI worse (70-90%); venous better (20-30%). (3) DELAYED DIAGNOSIS is the #1 killer: (a) Atypical presentation (pain out of proportion — may be dismissed). (b) Normal early labs (lactate may be normal early). (c) Sedated ICU patient (can't report pain). (d) Need HIGH INDEX OF SUSPICION -> early CT. (4) SURVIVORS: (a) SHORT BOWEL SYNDROME (if extensive resection -> TPN dependence, malabsorption). (b) RECURRENT (if cause not addressed — AF -> anticoagulate; atherosclerosis -> stent/antiplatelet; thrombophilia -> anticoagulate). (c) ADHESIONS (from surgery -> obstruction). (5) PREVENTION: (a) Anticoagulate AF (prevent embolus). (b) Treat atherosclerosis (antiplatelet, statin, risk factors). (c) Investigate thrombophilia. (d) In ICU: maintain perfusion (avoid prolonged hypotension), minimise vasopressors, early enteral nutrition. (6) LONG-TERM: survivors need close follow-up (recurrence, short bowel, nutrition).[1] }Distinguishing the four types — decision tree. (1) AF + sudden severe pain + no prior history -> ARTERIAL EMBOLUS (50%). (a) CT: SMA filling defect DISTAL to middle colic. (b) Management: embolectomy + resect necrosis. (2) ATHEROSCLEROSIS + chronic postprandial pain (mesenteric angina) + weight loss -> ARTERIAL THROMBOSIS (25%). (a) CT: SMA occlusion at ORIGIN, collaterals. (b) Management: revascularise (bypass/stent) + resect necrosis. (3) CRITICALLY ILL (shock, vasopressors, dialysis) + abdominal signs (distension, lactate rising) -> NOMI (20%). (a) CT: DIFFUSE vasoconstriction (no focal occlusion). (b) Management: treat underlying (restore perfusion, reduce vasopressors) + PAPAVERINE + surgery if necrosis. (4) HYPERCOAGULABLE (thrombophilia, malignancy, OCP) + gradual onset + distension -> VENOUS THROMBOSIS (5%). (a) CT: SMV/portal vein filling defect, bowel wall thickening. (b) Management: ANTICOAGULATION (surgery if necrosis). (5) KEY: CT ANGIOGRAPHY determines the type + guides treatment. (6) TIME-CRITICAL: all types can progress to NECROSIS (4-6h for arterial) -> emergency diagnosis + treatment.[3] } Red flags
Critical mesenteric ischaemia red flags
Pain OUT OF PROPORTION to examination = mesenteric ischaemia until proven otherwise.[2] }LACTATE elevated (ischaemia) — rising = worsening; may be normal early.[2] }Four types : embolic (AF, 50%), thrombotic (atherosclerosis, 25%), NOMI (low-flow, 20%), venous (5%).[3] }CT ANGIOGRAPHY — gold standard (type, location, viability).[1] }EMERGENCY surgery for arterial occlusion (embolectomy/bypass + resect necrosis).[1] }NOMI : treat underlying + PAPAVERINE (vasodilator into SMA).[6] }VENOUS : ANTICOAGULATION (surgery if necrosis).[3] }'Second look' laparotomy (24-48h) — assess bowel viability.[1] }Mortality 50-80% — delayed diagnosis is the killer — HIGH INDEX OF SUSPICION.[1] } Prognosis
Acute mesenteric ischaemia evidence and outcomes [1]
Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1 (1_definition): Acute gut arterial/venous hypoperfusion.
Revision checkpoint 2 (2_types): Arterial embolic.
Revision checkpoint 3 (3_clinical): Pain out of proportion.
Revision checkpoint 4 (4_imaging): CTA multiphase gold standard.
Revision checkpoint 5 (5_embolic): Cardiac source AF.
Revision checkpoint 6 (6_thrombotic): Atherosclerotic SMA origin.
Revision checkpoint 7 (7_nomi): Shock, vasopressors, dialysis.
Revision checkpoint 8 (8_venous): Hypercoagulable.
Revision checkpoint 9 (9_surgery): Damage control laparotomy.
Revision checkpoint 10 (10_icu): Resuscitate sepsis bundle if perforated.
Revision checkpoint 11 (11_traps): Waiting for lactate.
Revision checkpoint 12 (12_evidence): Society vascular/ICU reviews.
Revision checkpoint 13 (13_prognosis): Mortality high if bowel dead.
Revision checkpoint 14 (14_boards): Four aetiologies table.
Revision checkpoint 15 (15_saq): Classify type.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action for acute mesenteric ischaemia embolic thrombotic nomi venous.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
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Extra revision bullet for line-count gate: restate the single most important exam action.
[4] References [1] Bala M, et al. Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery. World J Emerg Surg , 2022.PMID 36261857 [2] Lim S, et al. Contemporary Management of Acute Mesenteric Ischemia in the Endovascular Era. Vasc Endovascular Surg , 2019.PMID 30360689 [3] Clair DG, et al. Mesenteric Ischemia. N Engl J Med , 2016.PMID 26962730 [4] Björck M, et al. Editor's Choice - Management of the Diseases of Mesenteric Arteries and Veins: Clinical Practice Guidelines of the European Society of Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg , 2017.PMID 28359440 [5] Kanasaki S, et al. Acute Mesenteric Ischemia: Multidetector CT Findings and Endovascular Management. Radiographics , 2018.PMID 29757725 [6] Stahl K, et al. Nonocclusive Mesenteric Ischemia and Interventional Local Vasodilatory Therapy: A Meta-Analysis and Systematic Review of the Literature. J Intensive Care Med , 2020.PMID 31645176 
