Editing Mesenteric ischaemia


== Approach: ==

* There are four distinct disease processes - embolic, thrombosis, NOMI, and venous thrombosis
* Review the four aetiologies below, and consider what the treatment would be:
** CT will identify '''embolisation''' or '''acute arterial thrombosis''', which needs an urgent laparotomy
** '''Mesenteric venous thrombosis''' is harder to diagnose, but keep in mind that these patients don't need a laparotomy anyway, unless the bowel is necrotic
** '''NOMI''' only needs supportive therapy
* So the ones that we really need to identify urgently are the patients with embolisation/acute thrombosis, and we can see this on CT

== ACUTE ==

=== '''Presentation''' ===

* Acute onset abdominal pain that is out of proportion with physical findings (tenderness to palpation does not develop until full-thickness ischaemia is present)
* May have spontaneous bowel evacuation
** This triad is most seen with SMA embolism ischaemia, but it only is found about a third of the time overall
* May have n/v/d
* 16% have PR bleeding
* Look for recent cardiac events/risk factors for embolisation
* Bowel necrosis presents with tachycardia, hypotension, fever, and systemic sepsis
* '''SMA embolism''' - generally quite abrupt, rapid decline, because no collaterals
** Survival decreases from 50% to 30% when the diagnosis is made >24 hours after symptom onset
* '''Thrombotic''' - insidious progression of symptoms - abdominal pain, distension, diarrhoea, acidosis, sepsis, GIT bleeding
* '''NOMI''' - very unpredictable presentation, often critically ill. 

=== '''Risk factors''' ===

* Women:men 3:1
* Typically seen in elderly patients with multiple comorbidities
* '''Mesenteric embolus:'''
** AF/flutter
** Recent MI
** Ventricular aneurysm
** CCF/cardiomyopathy
** Peripheral arterial emboli
** Proximal arterial sources such as cardiac valvular disease, aortic aneurysm or mural thrombus, or recent DSA
* '''Acute-on-chronic mesenteric thrombosis'''
** History consistent with chronic mesenteric ischaemia previously
* '''NOMI:'''
** More likely to be critically ill and in shock from alternative sources
** Classically cardiac surgery and haemodialysis patients are at risk
* '''Mesenteric venous thrombosis:'''
** Commonly middle-aged or older patients
** Hx VTE/PE
** Primary MVT - spontaneous, idiopathic thrombosis of the mesenteric veins not associated with any other disease or aetiologic factor
** Secondary MVT - those with an underlying condition
*** Direct injury
**** Abdominal trauma
**** Post-surgical, especially splenectomy (thrombus propagates from ligated splenic vein to portomesenteric system
**** Intra-abdominal inflammatory states (occurs with IBD near the inflamed bowel)
**** Peritonitis and abdominal abscess
*** Local venous congestion or stasis
**** Portal hypertension/cirrhosis
**** CCF
**** Hypersplenism
**** Obesity
**** Abdominal hypertension (especially in obese patients post RYGB)
*** Thrombophilia (inherited thrombophilia found in 50% of patients with MVT)
**** Protein C/S deficiency
**** Antithrombin III deficiency
**** FVL
**** Prothrombin 2010 A
**** Cancer
**** COCP
**** Myeloproliferative disorders (polycythaemia vera, essential thrombocytopaenia, JAK2 mutation)
**** HITS
**** Lupus anticoagulant-antiphospholipid syndrome
**** CMV infection
**** Extramesenteric venous thromboembolism

=== '''Aetiology, pathophysiology and presentation''' ===

* '''Specific causes:'''
** '''Embolisation'''
*** Think about source - see RFs above
*** Historically accounts for 40-50% of acute mesenteric ischaemia
*** Emboli most commonly lodge in proximal SMA due to oblique angle of SMA origin, but can happen in coeliac axis
*** Most commonly (50%) lodge distal to the middle colic artery, creating an ischaemic pattern sparing the first portion of the small intestine and ascending colon
*** Atheroembolic emboli tend to be smaller and lodge in more distal mesenteric circulation - can get quite localised ischaemic areas
** '''Acute thrombosis (most common now)'''
*** Typically have a history of chronic mesenteric ischaemia (post-prandial abdominal pain, history of food avoidance leading to weight loss)
*** Can happen with recent endovascular procedures (trauma/dissection), and can happen to patients with previous SMA stents or interventions
*** Also typically have other manifestations of atherosclerotic disease
*** Any clinical scenario leading to low flow or hypotension can result in thrombosis of SMA stenosis and mesenteric ischaemia
*** Occasionally might see a patient presenting subacute acute mesenteric ischaemia - which could be thought of as 'intestinal rest pain' - these patients still need to be managed urgently to avoid the need for laparotomy. Less dramatic due to long-term development of collaterals.
** '''Intense splanchnic vasoconstriction (non-occlusive mesenteric ischaemia) (15%)'''
*** Usually not sudden onset pain - tends to wax and wane depending on haemodynamic stability
*** Caused by mesenteric vasospasm, perhaps resulting from excessive sympathetic activity during shock. This can be caused by noradrenaline, adrenaline and vasopressin.
*** Can persist even after the inciting event is resolved.
*** They can also have mesenteric atherosclerosis, but that is not the primary inciting cause.
*** Frequently associated with cardiac failure, peripheral hypoxaemia, paradoxical splanchnic vasospasm and reperfusion injury.
** '''Mesenteric venous thrombosis (16%)'''
*** Vague, difficult to diagnose
**** Diffuse abdominal pain
**** Nausea/vomiting
**** Diarrhoea/GIT bleeding are uncommon
*** Generally non-acute symptoms
**** <4 weeks duration - acute MVT
**** >4 weeks - chronic MVT
*** Patients with portal vein thrombosis without SMV thrombus are generally asymptomatic, and almost never experience intestinal infarction
*** Seen at operation as a limited segment of intestinal ischaemia with oedema and reddish discolouration of the small bowel and mesentery, with a palpable SMA pulse. Involved intestinal segment is poorly demarcated. 
* '''Common outcome:'''
** Normal bowel oxygen consumption can be maintained with only 20% of usual blood flow, so the degree of compromise required is significant
** Intestinal injury develops when there is insufficient delivery of oxygen and nutrients for cellular metabolism
** Four stages
*** Mucosal surface affected first - ischaemia and relative hypoxia, with anaerobic metabolism and generation of toxic byproducts
*** Disruption of microvascular integrity
**** Haemorrhagic foci and bowel wall thickening
**** Increased mucosal permeability
*** Progressive mural injury
**** Disruption of the intestinal mucosal barrier (via ROS and neutrophils)
**** Bacterial translocation
**** Leakage of protein/fluids/electrolytes
*** Reperfusion
**** Free radicals
**** Neutrophil infiltration
** Presents clinically with malabsorption and haematochaezia before other symptoms

=== Laboratory tests ===

* Not particularly helpful in diagnosis
* Patients will generally have leucocytosis, acidosis and high lactate
* Patients are often hypovolaemic and haemoconcentrated
* D-dimer can potentially help differentiate SBO and mesenteric ischaemia

=== Imaging ===

* CT - arterial and venous phase
** Excellent in diagnosis of acute and chronic mesenteric ischaemia - se 93% sp 96%
** Emboli often lodge a couple of cm along SMA - look for 'meniscus sign' with abrupt occlusion of SMA
** In SMA thrombosis (i.e. underlying chronic disease) the lesion occurs near the origin and tapers off after a few cm, and often enlarged collaterals are seen
** NOMI - normal SMA, few areas of vasospasm
** MVT - SMA intact, but no delayed images of mesenteric veins
** Commonest finding is bowel wall thickening
* MRA
** Can test for both functional and anatomical causes of vascular disease
** Not very good for assessing bowel
** Takes a long time
* Catheter-based angiography
** Mostly used for intervention rather than diagnosis
** May have a limited role in identifying NOMI where that diagnosis is in doubt and the question is clinically significant
*** Narrowing of the origins of multiple SMA branches
*** Alternate dilatation and narrowing of the intestinal branches - the 'string of sausages' sign
*** Spasm of mesenteric arcades
*** Impaired filling of intramural vessels
* AXR
** Fairly useless
** Ischaemia - ileus, bowel wall oedema (thumb printing), pneumatosis
* DUS
** Accurate in identifying stenosis of coeliac and SMA
** Identifies alternative pathologies
** Can't see emboli beyond the proximal segment, can't assess bowel
** Optimal evaluation requires fasting
** Best for chronic disease




=== '''Treatment''' ===

* Resuscitation
** Don't delay intervention for resuscitation
** Fluid + NBM
** Correct acidosis
** Antibiotics (translocation)
** Anticoagulation - heparin as soon as a plan is in place, to prevent propagation of thrombus
** Try to avoid pressors - splanchnic vasoconstriction may worsen the problem. Preference those with less impact on splanchnic flow - dopamine, dobutamine, milrinone; and avoid pure alpha-adrenergic agents, even after successful revascularisation
** ICU, GOC
** Bloods incl G+H
* '''Embolic or thrombotic mesenteric ischaemia'''
** '''Principles:'''
**# Resect ischaemic bowel
**#* Complete bowel necrosis - non-survivable - usually close and palliate. Usually from SMA thrombosis.
**#** Could technically anastomose duodenum to colon and make the patient dependent on TPN, which would be appropriate in some patients, especially if young and not actively dying once the bowel is resected.
**#* Shorter segment necrosis or multiple short segments of necrosis - resect the minimum possible, leave disconnected, revascularise, relook later. Usually from emboli. 
**#** Could consider re-joining if the patient is stable, nutritionally replete, there is no established peritoneal infection, and the bowel is unquestionably viable.
**#* Dusky bowel - second-look laparotomy the next day.
**# Restore flow
**#* Thrombosis - most likely bypass indicated
**#* Embolus - embolectomy
**# Routine second-look operations in almost all cases where ischaemia is confirmed (unless patient is dead or dying)
** '''Surgical'''
*** Laparotomy
*** Assess bowel and act
*** Identify vascular problem and fix it
**** Expose SMA - lateral or anterior
***** Horizontal incision in peritoneum at base of transverse mesocolon
***** Careful dissection in the mesentery - initially see venous tributaries of SMV, autonomic nerve fibres and small lymphatic vessels, that are all divided to expose SMA, which lies to the left of SMV
***** To get to more proximal SMA, need to mobilise the inferior pancreatic border, the splenic vein and its tributaries from the pancreas
**** Proximal and distal control
**** Heparin
**** If the SMA is soft and disease-free, assume acute embolus
***** If soft and large vessel - transverse arteriotomy; if diseased, longitudinal (will need patch)
***** Embolic balloon catheter to remove embolus (3-5Fr proximally; smaller catheter distally)
***** Torrential, pulsatile inflow should be present
***** If the balloon catheter can't be passed distally, you can try to milk thrombotic material out manually
***** Close artery, including patch if needed
**** If SMA has atherosclerotic disease, can check for embolus, but probably needs a bypass graft to SMA
***** When bypass is planned, lateral SMA needs to be exposed
****** Peritoneum opened laterally to duodenum, anterior to the aorta, and onto the left or right CIA (see diagram under 'exposures')
****** Inflow: depends on degree of atherosclerosis present, the lie of the graft, and the patient's overall status. 
******* If patient is critically ill, can't cross-clamp aorta - prefer CIA and use of 'lazy C' orientation
******* If right CIA is diseased, consider left CIA or distal infra-renal aorta
******* Antegrade bypass from supra-coeliac aorta could be considered - often relatively free of disease, but challenging to cross-clamp here
****** Conduit:
******* If no necrotic bowel, 6-8mm Dacron or PTFE are ok
******* If abdominal contamination, autologous vein preferred
******* Prone to kinking and external compression, especially if a small graft is used
**** Retrograde open mesenteric stenting - for acute on chronic SMA thrombosis
***** Successful and safe alternative to bypass or percutaneous stenting
**** If distal thrombus is not completely removed, give 0.5-1mg of TPA through the arteriotomy
*** Reassess bowel and resect as necessary
*** Leave abdomen open for presumed second look in 24-48 hours
** '''Endovascular (selective - only in patients with no peritonism)'''
*** All patients with possible bowel ischaemia should be assessed with laparoscopy/laparotomy
*** For endovascular treatment to be beneficial, can't be any gangrenous bowel
*** However these patients seem to fare better than open approach if it's manageable, so likely future trend towards endovascular management 
*** Thrombolysis
**** TPA contraindicated in those with open abdomen, recent surgery and need for bowel resection or further surgery
*** Embolectomy
**** Mechanical or pharmacological
*** Angioplasty
**** Angioplasty alone is rarely recommended
**** Might be suitable for patients with occlusion or stenosis of a previously placed stent
*** Stenting
**** Good for restoring inline flow to those with proximal stenosis
**** Can be performed antegrade or retrograde
**** Covered stents better for chronic ischaemia, but need to weight that against the risk of infection if necrosis is present
* '''NOMI'''
** Largely non-op and supportive
** Treat underlying precipitative cause
** Optimise cardiac output, eliminate vasopressors
** Direct injection of vasodilators to SMA can be done, but the only evidence is from small studies and case reports, and this is not standard practice
** Operative exploration reserved for necrotic bowel
* '''Mesenteric vein thrombosis'''
** Heparin infusion, NGT, fluid/electrolyte replacement, consider TPN, antibiotics
** Refer to gastro (at Austin, anyway), especially for Budd Chiari syndrome. Can possibly have TIPS or stents.
** Evaluate for hypercoagulopathy incl cancer
*** Scopes, chest imaging
*** Refer haem for thrombophilia screen - need to do lupus anticoagulant, cardiolipin, antiphospholipid antibodies, hereditary thrombophilias (FVL, prothrombin mutation, protein C/S, antithrombin III), and JAK2. If all negative and no other factor found, consider PNH screen and CALR mutation analysis. Consider BM biopsy.
** ?need to operate - to resect bowel if ischaemic signs
*** Admission - late presentation with peritonitis and necrotic bowel
**** Peritonitis
**** Severe bleeding
**** Perforation 
*** After some weeks due to failure of anticoagulation
*** Months later due to ischaemic bowel stricture
*** Difficult decision whether to resect - bowel will often be dark blue but not frankly dead
** Catheter-directed thrombolytic therapy can be considered for patients who have abdo pain despite resus and anticoagulation
** Therapeutic anticoagulation in all patients for minimum 3-6 months, but longer in patients with persisting risk factors
*** LMWH 1mg/kg BD initially. Lower dose LMWH in thrombocytopaenia.
*** Warfarin in patients with non-malignancy MVT
*** Continue LMWH in malignancy-associated MVT
*** DOACs unproven for this indication, and not on PBS yet



== '''CHRONIC MESENTERIC ISCHAEMIA''' ==

* inadequate arterial perfusion of abdominal viscera
* Precursor to intestinal infarction

=== '''Aetiology''' ===

* Caused by >70% stenosis of artery, involves at least two of the three visceral arteries and definitely the SMA
** Most commonly SMA + coeliac
** Stenosis is most commonly at their origins
* '''Atherosclerosis (90% of cases of symptomatic CMI)'''
** Usually develops as an extension of aortic plaque, extending 2-3cm into the branches
** Standard atherosclerotic risk factors
* Spontaneous dissection
* Vasculitis
** GCA, Takayasu, polyarteritis nodosa, SLE
** Tend to be younger patients than atherosclerosis
* Buerger disease
* Fibromuscular dysplasia
* Neurofibromatosis
* Radiation enteritis
* Aortic coarctation
* Mesenteric venous stenosis/occlusion
* Drug-induced arteriopathy from cocaine/ergot use

=== '''Pathophysiology''' ===

* 20% of the cardiac output goes through the mesenteric arteries while fasting, and 35% after a meal
* Flow increases shortly after eating and remains high for 3-6 hours
* Symptoms occur when combined primary and collateral circulation is inadequate to provide the post-prandial hyperaemic response
* Most patients only become symptomatic when two out of three mesenteric arteries are severely narrowed/occluded (but some patients do present earlier, especially if SMA is involved)

=== '''Natural history''' ===

* 86% of patients with asymptomatic three-vessel disease either developed AMI, became symptomatic or died within 6 years in one study, suggesting that early intervention is worthwhile

=== '''Presentation''' ===

* Usually in their 60s
* F:M 3:1
* Post-prandial pain (intestinal angina) which begins within 10-15 minutes after eating and lasts for 3-6 hours
** Usually central
** Character can be sharp and debilitating or a dull ache
* Often have sitophobia (food fear)
* Leads to weight loss and cachexia
* Can get nausea, vomiting, diarrhoea
* No pathognomic findings but look for other manifestations of vascular disease
** 50-70% have CAD
** 20-45% have cerebrovascular disease
** 20-35% have peripheral arterial disease
** 20% have renal artery disease
* Check for median arcuate ligament syndrome - a bruit caused by compression of the coeliac axis, elicited by deep expiration

=== '''Investigations:''' ===

* Endoscopy - diffuse small ulcerations in the stomach or proximal duodenum, or patchy areas of ischaemia in the colon
* DUS
** Good sensitivity
**
* CT
** Necessary for planning operative intervention

=== '''Diagnosis''' ===


=== '''Treatment''' ===

* '''Goals:'''
** Resolve abdominal symptoms
** Promote weight gain
** Prevent deterioration to AMI
* '''Indications for revascularisation (SVS practice guidelines)'''
** Weight loss
** Food fear
** Diarrhoea
** Post-prandial pain
** Prophylactic revascularisation in asymptomatic patients is controversial - limited to those with severe three-vessel disease, especially those in remote areas
* '''Selective a procedure'''
** SMA is primary target for revascularisation
** Stent angioplasty preferred where possible (80% of patients)
** Patients with difficult anatomic lesions should undergo open procedures if comorbidities permit
** Ideal lesion for endovascular is a short, focal stenosis/occlusion with minimal calcification/thrombus
** Flush occlusions with aorta, severe eccentric calcification, longer occlusions, small outflow vessels, and tandem lesions affecting branches all make angioplasty harder
** Proceed to open procedures in patients with failed endovascular procedure, recurrent in-stent stenosis after multiple re-interventions, and for non-atherosclerotic lesions
* '''Endovascular'''
** Routine stenting recommended
** For short-segment focal arterial lesions
** Brachial access better, especially if acute SMA origin is present
** Recanalising occlusions often requires through-and-through access
** Complications:
*** Cardiac events
*** GIT bleeding
*** Bowel ischaemia (distal embolism, thrombosis or dissection)
*** Access
*** AKI
*** Late restenosis
* Endarterectomy
** Limitation - can only extend 2cm beyond origin
** Consider only in hostile conditions such as contaminated field
* Open bypass grafting
** For patients with long segment stenosis or occlusion not amenable to endovascular stent angioplasty
** Should probably do at least two reconstructions while you're at it
** The standard approach is for a bifurcated polyester graft from supracoeliac aorta to both CA and SMA
** Complications:
*** Ileus
*** High-risk wound
*** Early graft thrombosis (technical issue)


[[Category:Vascular]]