ENDOVASCULAR MANAGEMENT OF MESENTERIC ISCHEMIADr. Ankur BanikPGTDept Of General MedicineBMCH

INTRODUCTION Cokkinis (1921):

“occlusion of the mesenteric vessels is regarded as one of those conditions of which the diagnosis is impossible, the prognosis hopeless, and the treatment almost useless.”

INTRODUCTION Intestinal ischemia occurs when the

splanchnic perfusion fails to meet the metabolic demands of the intestines resulting in ischemic tissue injury

Occlusive or non-occlusive mechanism leads to hypo perfusion of one or more mesenteric vessels

INTRODUCTION Incidence

2-3 per 1 lac population 1-2/1000 hospital admissions 1% of GI admissions increased incidence with age

Mortality 1960’s - 70-100% 1970’s - 60-70% 21st century > 50%

Morbidity Poor quality of life

Recurrence Up to 60% in the long run

BASIC ANATOMY• Celiac artery, SMA, and IMA supply foregut, midgut,

and hindgut, respectively• Splanchnic circulation can receive up to 30% of the

cardiac output• Celiac artery: Supplies lower esophagus, stomach,

duodenum, liver, pancreas, and spleen• SMA : Supplies the ileum, cecum, ascending colon, the

transverse colon and communicates with the IMA.• Communication between superior and inferior

pancreaticoduodenal arteries is an important anastomosis that helps to maintain bowel perfusion in atherosclerotic disease of the mesenteric vessels

• Right and middle colic arteries are an important supply of blood to the marginal artery of Drummond

BASIC ANATOMY...• IMA:

• Smallest mesenteric vessel• Supplies distal transverse, descending, sigmoid

colon, rectum• SMV drains the small intestine, cecum, ascending

colon, transverse colon, stomach, pancreas and duodenum

• IMV drains descending colon, sigmoid colon, rectum • IMV joins the splenic vein, which then joins the SMV to

form the portal vein. The portal vein enters the liver

ETIOLOGYInsufficient blood perfusion of small bowel or colon may result from:

Arterial Embolic Disease (50%)

Arterial Thrombotic Disease (25%)

• Venous Thrombotic Disease (10%)

Non-occlusive Mesenteric Ischemia (20%)

PATHOPHYSIOLOGY• Injury severity is inversely proportional to mesenteric blood flow• Number of vessels involved, mean arterial pressure, duration of

ischemia, and extent of collateral circulation all determine mesenteric blood flow

• SM vessels are more frequently involved than the IM vessels (larger diameter and better collaterals with inferior vessels)

• Damage may range from reversible ischemia to transmural infarction with necrosis and perforation

• Arterial insufficiency causes tissue hypoxia, leading to bowel wall spasm initially(vomiting or diarrhea)

• Injury complicated by reactive vasospasm in SMA after initial occlusion

• Mucosal sloughing may cause bleeding into the GIT

PATHOPHYSIOLOGY• Minimal abdominal tenderness is present despite symptoms

of intense visceral pain• If ischemia persists disruption of mucosal barrier occurs and

bacteria, toxins, and vasoactive substances are released into the systemic circulation

• This can cause septic shock, cardiac failure, or multi-organ failure before bowel necrosis actually occurs

• With worsening hypoxic damage the bowel wall becomes edematous and cyanotic

• Bowel necrosis occurs in 8-12 hours from onset of symptoms • Transmural necrosis leads to peritonitis and indicates grave

prognosis

ACUTE MESENTERIC ARTERIAL EMBOLISM

Majority of cases (>50%): SMA occlusion Location: origin of middle colic artery (ischemia

from proximal jejunam to splenic flexure) Occlusion is sudden and no time to develop

compensatory increase in collateral flow Ischemia is more severe in SMA occlusion Celiac and IMA occlusion usually less severe

and is tolerated Most have underlying stenosis as well

ACUTE MESENTERIC ARTERIAL EMBOLISM

Embolic sources: cardiac (80%), aortic plaques Typical causes: Mural thrombi - MI Atrial thrombi - mitral stenosis and AF, vegetative

endocarditis Aortic thrombi - mycotic aneurysm, thrombi at

sites of atheromatous plaques, sites of vascular aortic prosthetic grafts interposed between heart and SMA

ARTERIAL THROMBOTIC DISEASE

• 15%-25% of acute intestinal ischemia• Pre-existing atherosclerotic disease

― Worsening chronic mesenteric ischemia― Late complication of pre existing visceral atherosclerosis

• Found at ostium of SMA • More delayed onset of symptoms - Slow process of

atherosclerotic stenosis before acute occlusion allows time for development of collateral circulation

ACUTE MESENTERIC ARTERIAL THROMBOSIS

• Symptoms do not develop until 2 of 3 arteries are stenosed or completely blocked

• Patients usually have history of atherosclerotis at other sites (eg, CAD, strokes, PVD) or other vascular disease (Aortic Aneurysms, dissections, trauma)

• Patients frequently present with history of chronic mesenteric ischemia and symptoms of intestinal angina before acute event

MESENTERIC VENOUS THROMBOSIS

• 5-10% of intestinal ischemia• Younger patient population• 80% have hypercoagulable state

(Secondary MVT)• Primary MVT occurs in the absence of any

identifiable predisposing factor

MESENTERIC VENOUS THROMBOSIS

• Common Causes:• Malignancy• Blood disorders - Sickle cell disease, Protein C & S

deficiency• Post surgery • oral contraceptives, previous DVT/PE• Nephrotic syndrome

MESENTERIC VENOUS THROMBOSIS• Decreased venous outflow impedes inflow of

arterial blood and also causes bowel wall edema leading to bowel ischemia

• Fluid sequestration and bowel wall edema are more pronounced than in arterial occlusion

• Infarction rarely observed with isolated SMV thrombosis, unless collateral flow in peripheral arcades or vasa recta is also affected

• Colon rarely involved due to good collateral supply

NONOCCLUSIVE MESENTERIC ISCHEMIA 20-30% of acute intestinal ischemia Precipitated by severe reduction in mesenteric

perfusion secondary to arterial spasm or decreased cardiac output

-Sympathetic adrenergic system mediated Visceral vasoconstriction/shunting for cerebral

protection Bowel perfusion, like cerebral perfusion, is

preserved till late in hypotension therefore NOMI represents a failure of autoregulation

NONOCCLUSIVE MESENTERIC ISCHEMIA

• Causes:• Cardiac failure• Shock• Use of potent vasopressors in critically ill patients

• Vasoactive drugs (eg, digitalis, cocaine, diuretics, and vasopressin) may also cause regional vasoconstriction

• Gross pathologic arterial or venous occlusions are not observed

PROGNOSIS• All-cause mortality 71% (59-93%)• Once bowel wall infarction has occurred the mortality

is as high as 90%• Survivors have a high risk of re-thrombosis and poor

QOL due to short-gut syndrome• Predictors of mortality: older age, hepatic and renal

impairment, metabolic acidosis, hypoxia, intramural pneumatosis, and sepsis

• Mortality is highest for thrombotic AMI followed by NOMI and embolic AMI.

• Venous thrombotic AMI carries a relatively better prognosis

PROGNOSIS• Early and aggressive diagnosis and treatment

shown to reduce mortality if diagnosis made before onset of peritonitis.

• The timeliness of diagnosis and treatment is the most significant indicator of survival.

• Madrid study - described 21 patients with SMA embolus• Intestinal viability achieved in 100% of

patients if symptoms <12 hours, 56% if <12-24 hours, and 18% if > 24 hour

CLINICAL PRESENTATION: RISK FACTORS

J Vasc Surg 2002;35:445-52

CLINICAL PRESENTATION: RISK FACTORS

Ann Surg 2001;233(6):801-808

CLINICAL PRESENTATION:PHYSICAL EXAMINATIONArterial Thromboembolic, Non-Occlusive

• Severe abdominal pain • Sudden onset

Venous Thrombotic Less severe pain Subacute

• Symptoms variable• Abdominal pain• vomiting• Peritonitis (late)• Hypotension, tachycardia

CLINICAL PRESENTATION: LABORATORYLimited clinical utility arterial lactate1

amylase2

CK, CK-BB3

Serum phosphate4

Other markers shown to be of use: LDH, PAF, TNF-α, AP, AST/ALT, α-glutathione

1 Eur J Surg 1994;160:381-42 Br J Surg 1986;73:219-213 Dig Dis Sci 1991;36:1589-934 Br J Surg 1982;69:S52-3

DIAGNOSIS:

Non-Invasive Imaging Plain X-ray Computed Tomography (helical/angiography) Ultrasound MRI/MRAInvasive Endoscopic procedures Angiography

DIAGNOSIS: X-RAYPlain Films pneumatosis portal venous gas thumbprinting →

Findings late, associated with high mortality

DIAGNOSIS: CT ANGIOGRAPHY

Sensitivity: 96%Specificity: 94%

Criteria• pneumatosis• venous gas• SMA/celiac/IMA occlusion

w/distal disease• arterial embolism

OR

• bowel wall thickening + one of following:

– lack of bowel wall enhancement

– solid organ infarction– venous thrombosis

1 Radiol 2003;229:91-98

Ct Angio with 3D reconstruction is a highly sensitive test for intestinal ischemia

Radiol 2003;229:91-98

COMPUTED TOMOGRAPHY

DIAGNOSIS: ULTRASOUND

A mesenteric duplex scan demonstrating a high peak velocity of flow in SMA is associated with 80% PPV of mesenteric ischemia

More significantly, a negative duplex scan virtually precludes the diagnosis of mesenteric ischemia

Body habitus is an important limitation of duplex scan. Poor yield in obese patients

Mainly used as a screening test Confirmed with angiography

DIAGNOSIS: MRI Poor delineation of smaller vessels Limited clinical application Perfusion flow contrast studies show

promise1

1 Radiol 2004;234:569-575

DIAGNOSIS: ENDOSCOPIC PROCEDURES Endoscopic techniques using visible light

spectroscopy can be used in the diagnosis of chronic ischemia

When suspecting mesenteric ischemia involving the colon performing an endoscopy to evaluate up to the splenic flexure is high yield

This is an excellent diagnostic tool in pts with chronic renal insufficiency who cannot tolerate iv contrast

DIAGNOSIS: ANGIOGRAPHY

Gold Standard Anatomic delineation of

occlusion and collaterals

Plan operative revascularization

Allow infusion of therapeutic agents (thrombolytics, vasodilators)

1 Ann Surg 2001;233(6):801-808

TREATMENT : PRINCIPLES Diagnosis

Supportive Care

Restoring Blood Flow

Resection of non-viable gut

Second-Look

THERAPY

Supportive measures IV resuscitation

Optimize cardiac status

Broad-spectrum antibiotics (no data)

Nasogastric decompression

Correction of electrolyte imbalances

THERAPY: PHARMACOLOGIC

Anticoagulation Heparin IV

Prevents clot propagation Systemic vs. intra-arterial Restart 48 hrs after any surgical intervention

Warfarin Prevents clot propagation Give for 6-12 mos if no clotting disorder (no data)

1 Surg Gynecol Obstet 1981;153:561-5692 Vascular Emergencies. 1982;553-561

THERAPY: PHARMACOLOGIC

Vasodilators Papaverine

Increases cAMP, relaxes smooth muscle Primary indication: Non-occlusive arterial disease Early SMA infusion reduces mortality to 40-50% Directed infusion via angiography Not commonly used nowadays

Criterion for use: Peritoneal signs absent Cannot undergo surgery Must have good distal perfusion bed

THERAPY: PHARMACOLOGIC

Thrombolysis urokinase>streptokinase, rtPA

Short t½, easily reversed Dose: high vs. low

5,000 U/hr - 600,000 U/hr Direct SMA infusion vs. operative placement

THERAPY: PHARMACOLOGIC

Thrombolysis Duration: minutes – 48 hrs1

Risk of bowel necrosis if treatment delayed Treat to re-establish flow vs. complete dissolution > 48 hrs-Greater risk of bleeding

Discontinue if Worsening abdominal symptoms without evidence of

thrombolysis Bleeding No angiographic improvement

1 JVIR 2005;16:317-329

JVIR 2005;16:317-329

Outcomes

• Technical success: 43/48• Technical failure: 5/48• Outcome most dependent on age of thrombus/embolus• Improvement of abd pain in 1st hour is a favorable prognostic sign• Technical success does not equal clinical success• Survival: 43/48• Safety

THERAPY: PHARMACOLOGIC

Thrombolysis Criterion for use:

Embolic/thrombotic disease Poor operative candidates No contraindications to fibrinolytics No bowel infarction (no peritonitis/acidosis)

Expansion of use to all patients without bowel infarction and without contraindications to thrombolysis

ENDOVASCULAR MANAGEMENTEndovascular therapy includes: Embolectomy Catheter based thrombolysis Angioplasty and stenting

ENDOVASCULAR STENTINGIndications Simple stenotic lesions - ideal Complex lesions (long-segment, irregular, heavily

calcified)without distal disease Total occlusion of short segment

Contraindications Suspected bowel necrosis (peritonitis, acidosis, etc) Diffuse distal disease Median arcuate ligament compression syndrome

ENDOVASCULAR MANAGEMENT OF CMIAdvantages Significantly low peri-procedure mortality Shorter hospital stay Technical success rate 91% Immediate symptom relief 82%Disadvantages One third developed restenosis at 26months Long term outcome better in open repair (5 year

patency rate was 3.8 times greater in open repair) Potential serious complication of endovascular

repair is occlusion of stent itself which manifests as AMI

ENDOVASCULAR MANAGEMENT OF CMIStenting Outcomes (Chronic, SMA/Celiac)

1999: Primary patency 74% at 18 mos (n=12)1

8.3% mortality <30 days2003: Technical success 96% (n=26)2

Clinical success 88% Primary patency at 34 mos 65% Restenosis at 34 mos 12%

2013: Technical success 91% (n=292) Clinical success 82% Restenosis at 26 mos 30%

1 JVIR 1999;10(7):861-8672 J Vasc Surg 2003;38:692-8I

ENDOVASCULAR MANAGEMENT OF CMI

J Vasc Surg 2003;38:692-8

ENDOVASCULAR MANAGEMENT OF AMIIndications Prohibitive operative risk No clinical signs of peritoneal inflammation Those with no autologous vessel available for

graft even with contaminated peritoneal cavity

ENDOVASCULAR MANAGEMENT OF AMIAdvantages Technical success rate 87% Significantly lower in hospital mortality and morbidity Lesser complications Outcomes (both short term and long term) comparable to

open repair Successful endovascular repair resulted in a mortality rate

of 36% which was significantly lower compared to that of 50% in those treated surgically

Patients who failed endovascular repair had a mortality rate of about 50% which was equivalent to that of traditional surgical repair

Disadvantages There is a slight theoretical risk of ischemia reperfusion

injury which might lead to worsening clinical outcome

ENDOVASCULAR MANAGEMENT: SUMMARY

Angioplasty/Stenting Ideal for thrombotic lesions

Calcified ostial lesions Chronic or acute occlusion

Advanced techniques for embolic lesions Embolectomy w/distal protection

Long-term durability questioned vs. surgical repair Utility in acute ischemia setting Advantages:

Shorter duration of treatment than thrombolysis Definitive treatment

TECHNIQUE OF ENDOVASCULAR REPAIR Prior heparinisation Trans femoral or trans brachial puncture Visceral vessels are selectively cannulated and

visualised in lateral view Lesion identified and crossed with 0.014-0.032 inch

guide wire Balloon angioplasty with appropriate size balloon

performed Balloon expandable stent is preferred over self-

expanding stent Following intervention patient is to be put on dual

antiplatelet therapy for 3 months at least Follow up surveillance by ultrasound Doppler or upper

gi endoscopic ultrasound to check for patency

SURGERY

Anyone with peritonitis needs to be explored Midline incision Evaluate extent of ischemia Doppler of entire SMA if possible Revascularization (embolectomy vs.

bypass) Re-evaluate ischemia Lastly, non-viable bowel must be resected

http://drkeyurbhatt.blogspot.com/2012/12/case-acute-mesenteric-ischemia-due-to.html

http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082010000500007

CONCLUSION : TAKE HOME MESSAGES Mesenteric ischemia is diagnosis which is often

missed and even today it carries a relatively grim prognosis.

Mesenteric ischemia is to be suspected in any patient presenting with pain abdomen out of proportion to the physical findings.

The timeliness of diagnosis and treatment is vitally important.

Surgical procedures have been the mainstay of treatment over the years but the advent of endovascular treatment options offer great promise in reducing the mortality and morbidity without compromising on the efficacy of treatment.

THANK YOU!