Mesenteric Ischemia - PowerPoint Presentation

Slide1

Mesenteric Ischemia

Dr.hicham

al

mawla

Slide2

Introduction

Mesenteric ischemia is a frequently lethal condition resulting from critically reduced perfusion to the gastrointestinal

tract.

Acute and chronic forms

Involves Arterial and venous sides of circulation

First described in 1500s

Despite remarkable advances in

vascular

surgical technique, vascular imaging, percutaneous intervention, and surgical critical care, mesenteric ischemia remains a complex and often disheartening disease.

Slide3

Statistics

0.1 % of hospital admissions

1%-2% of admissions for abdominal pain

Incidence – 9 in 100,000 person – years

Incidence increases with age

More common in women

Mortality – 24% to 96% with average of 69%

Slide4

Mesenteric vasculature

Comprises of 3 major aortic branches with collaterals

Celiac axis

Superior mesenteric artery

Inferior mesenteric artery

Celiac axis – foregut (distal esophagus to duodenum, hepatobiliary, spleen)

Left gastric artery

Splenic artery

Common hepatic artery

Slide5

Mesenteric vasculature

Superior mesenteric artery – midgut ( Jejunum to mid colon )

Inferior pancreaticoduodenal artery

Jejunal branches

Ileal branches

Middle colic

artery

Right colic artery

Ileocolic artery

Inferior mesenteric artery – hindgut ( mid colon to rectum )

Left colic artery

Sigmoid arteries

Superior rectal artery

Slide6

Slide7

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Slide13

Types

Acute mesenteric ischemia

Chronic mesenteric ischemia

Non occlusive mesenteric ischemia

Slide14

Acute mesenteric ischemia

Acute mesenteric ischemia (AMI) may be defined as an abrupt reduction in blood flow to the intestinal circulation of sufficient magnitude to compromise the metabolic requirements and potentially threaten the viability of the affected organsEmboli (50%) ArrhythmiaValvular diseaseMyocardial infarctionHypokinetic ventricular wallCardiac aneurysmAortic atherosclerotic diseaseIatrogenic

Thrombosis (25%)

Atherosclerotic disease

Nonocclusive

(5% to 15%)

Pancreatitis

Heart failure

Sepsis

Cardiac bypass

Burns

Renal failure

Medications

Slide15

Acute mesenteric ischemia

P

aradoxical

embolus traveling through a patent foramen ovale from a thrombus in the venous system

Venous

occlusion

Hypercoagulable state

Sepsis

Compression

Pregnancy

Portal hypertension

Malignancy

Slide16

Embolic occlusion

Emboli lodge commonly in Superior Mesenteric artery.

>50% - mid to distal segment

The

SMA tapers after major branch

points

Emboli

commonly found distal to the middle colic

artery

<15

% of emboli occlude the SMA at its

origin

Slide17

Embolic occlusion

P

oint

of occlusion affects the magnitude and distribution of the

ischemia

Occlusion at the origin -

ligament of Treitz to the transverse

colon

O

cclusion

distal to the middle colic

artery -

Preserves

the right colon and proximal part of the small bowel

Slide18

Thrombotic occlusion

25% - 30% of acute mesenteric ischemia

Conjunction with chronically diseased arteries

No symptoms/ minimal symptoms until the occlusive event

May be due to rupture of

a previously noncritical atherosclerotic plaque that abruptly occludes the

vessel.

Slide19

Non Occlusive mesenteric ischemia

20% of all cases of acute mesenteric ischemia

Occurs with patent mesenteric arteries

Splanchnic

vasoconstriction

- pathophysiologic

process

P

recipitated

by hypoperfusion from medications, depressed cardiac output, or renal or hepatic

disease

Blood

pressure in the bowel falls below a critical pressure of 40 mm Hg, ischemia develops and eventually leads to infarction and bowel necrosis.

Slide20

Pathophysiology

Intestinal blood flow accounts for 10 to 20% of the resting cardiac output but may, on occasion, exceed 30%.

R

egulated

by a variety of mechanisms, including

T

he

autonomic nervous system,

Neurohormonal factors

G

astrin

,

Glucagon

Secretin

B

radykinin

, serotonin, histamine, and the prostaglandins

.

Of

the blood reaching the intestinal wall, most is directed toward the mucosa, the layer with the greatest metabolic demand and highest rate of cell turnover

.

Slide21

Pathophysiology

Sudden

reduction of the blood supply to the

viscera

changes

associated with organ ischemia

Specifically

compromises the mucosal barrier function.

Changes

follow with an inflammatory cell

infiltrate

Bowel

wall edema ensues as a result of loss of capillary

integrity

Slide22

Pathophysiology

Absence

of this natural barrier

bacterial

translocation,

promotion

of endotoxemia,

exudation

of fluid into the bowel lumen.

Injured

mucosa sloughs, leaving ulcerations of the bowel wall.

T

he

bowel may still be viable when the mucosa is

threatened

Prolonged

interruption of blood

flow

N

ecrosis

of the muscularis and

serosa

C

ompromised segment

is no longer salvageable.

Slide23

Pathophysiology

Interruption

of mesenteric blood flow initiates tissue injury and systemic illness,

D

eleterious

effects catalyzed by oxygen free radicals and other

toxins.

Myocardial

depression,

P

rogressive

inflammatory

response

G

eneralized

increase in capillary permeability,

Edema

and organ dysfunction.

Slide24

Diagnosis

Classical -

Abdominal pain out of proportion to the findings on physical examination and persisting beyond 2 to 3 hours

Diarrhoea

Nausea

Vomiting

Anorexia

Abdominal distention

Melena /

hematochezia

/

occult fecal blood – 15%

Full thickness bowel involvement

Acute abdomen

Distention, guarding, rigidity, hypotension – peritonitis – septic consequences

Slide25

Diagnosis

Complete hemogram

Hemoconcentration – dehydration and hypovolemia

Leucocytosis

Evaluation

of renal and hepatic function,

Blood

urea nitrogen,

Creatinine

,

amylase

, lipase,

prothrombin

time, activated partial thromboplastin

time

cardiac

enzymes

Slide26

Diagnosis

M

etabolic

acidosis

Hyperamylasemia

Elevation of

lactate dehydrogenase, aspartate aminotransferase, and creatine

phosphokinase.

Hyperkalemia

and hyperphosphatemia are

present -

B

owel infarction

ECG - cardiac

rhythm.

Slide27

Diagnosis

Plain x rays - Non diagnostic

Ultrasonography – Limited utility in acute mesenteric ischemia

CT scan

Magnetic resonance angiography – Not a choice in acute state

Arteriography – Method of definitive diagnosis

Slide28

Plain x-ray

Supine / erect

Chest – AP view

Suspicious findings

Non specific ileus

Dilated bowel loops

Thumb printing

Separation of bowel loops

Intramural gas

Free air

Majority of the cases plain films are non diagnostic

Slide29

CT scan

I

ndirect

findings of arterial bowel ischemia and may show the arterial occlusion or mesenteric venous thrombus

.

Dilation

of the bowel lumen,

Bowel

wall

thickening

A

bnormal

bowel wall enhancement,

A

rterial

occlusion,

V

enous thrombosis

I

ntramural

or portal venous

gas

Slide30

CT scan

Symmetrical bowel wall thickening greater than 3 mm in a distended segment of bowel suggests ischemia

Greater

degrees of bowel wall thickening should raise suspicion of mesenteric venous thrombosis (MVT).

Intravenous

contrast is useful in demonstrating the heterogeneity of the ischemic bowel wall (lack of bowel wall enhancement

)

and may show occlusion of mesenteric arteries if given by rapid bolus administration

Slide31

CT scan

Pathologic Damage

CT Findings

Vasoconstriction

Wall

hyper density

Absence of wall enhancement

Increased capillary permeability

Wall thickening

Bowel dilation

Mucosal cellular necrosis

Pneumatosis

Gas in mesenteric vein branches

Gas in portal vein branches

Transmural bowel necrosis

Pneumoperitoneum

Retropneumoperitoneum

Ascites

Slide32

CT scan

S

ensitivity -

64%

Specificity -

92%

CT

is the diagnostic technique of choice for acute

MVT

sensitivity exceeding 90

%.

3D recon

of the aorta and its branches show additional

detail

sensitivity

and specificity to 94% to 96

%

The

limitations and risks of CT angiography

renal

insufficiency or contrast

allergies

limitations

of contrast volume, and metal

artefacts

obscuring the area of interest

Slide33

Arteriography

D

efinitive

diagnosis

-

acute and chronic mesenteric ischemia

.

Arteriograms

E

stablish

the

diagnosis

A

ssist

in differentiating between acute embolic, thrombotic, or nonocclusive mesenteric ischemia

A

llow

proper planning of the revascularization

procedure.

AP

and lateral views of the aorta and the mesenteric branches

are

required for proper arteriographic evaluation.

The

lateral view is particularly important to examine the proximal celiac artery and SMA, which overlap the aortic contrast column on AP views

.

Slide34

Arteriography

Acute

embolic occlusion of the SMA is

abrupt

occlusion of the artery, usually at a branch point where the vessel tends to narrow

If

imaged acutely, a meniscus sign (crescent) is often observed.

If

secondary thrombosis occurs proximal to the embolus, the classic meniscus sign of embolic occlusion will be obscured.

Slide35

Management

Effective management

Early diagnosis

Aggressive resuscitation

Early revascularization

On going supportive care

Medical treatment

Surgical treatment

Endovascular Treatment

Slide36

Treatment

F

luid

resuscitation

Systemic

anticoagulation

- Heparin

Significant

metabolic acidosis not responding to fluid resuscitation should be corrected with sodium bicarbonate.

A

central venous catheter, peripheral arterial catheter, and a Foley catheter should be placed for hemodynamic status monitoring.

Appropriate

antibiotics are given before surgical exploration.

Primary

goal of surgical treatment in embolic mesenteric ischemia is to restore arterial perfusion with removal of the embolus from the

vessel

Slide37

Surgical treatment

Operative intervention remains the mainstay of management

The

surgeon's goal is to confirm the diagnosis

Assess

bowel viability,

Determine

the responsible

etiology

,

Perform

revascularization where

possible

Resect

nonviable bowel

Slide38

Surgical treatment

The abdomen is explored

-

midline

incision - reveals

variable degrees of intestinal ischemia from the

mid jejunum

to the ascending or transverse colon.

The

SMA is approached at the root of the small bowel

mesentery.

Once

the proximal SMA is identified and controlled with vascular clamps, a transverse

arteriotomy

is made to extract the embolus, using standard balloon

embolectomy

catheters.

Slide39

Surgical treatment

Following the restoration of SMA flow,

A

ssessment

of intestinal viability must be made,

Nonviable

bowel must be resected.

Several

methods

Intraoperative

IV fluorescein injection and inspection with a Wood's

lamp

Doppler

assessment of antimesenteric intestinal arterial pulsations.

A

second-look procedure

- 24

to 48 hours following embolectomy.

The

goal of the procedure is reassessment of the extent of bowel viability, which may not be obvious immediately following the initial embolectomy.

Slide40

Surgical treatment

Thrombotic mesenteric ischemia

- severely

atherosclerotic

vessel

Typically

the proximal CA and SMA.

Require

a reconstructive procedure to the SMA to bypass the proximal occlusive lesion and restore adequate mesenteric flow.

The

saphenous vein is the graft material of

choice

Prosthetic

materials should be avoided in patients with nonviable bowel, due to the risk of bacterial contamination if resection of necrotic intestine is performed.

Slide41

Slide42

Endovascular treatment

Catheter-directed thrombolytic therapy is a potentially useful treatment

modality

Initiated

with intra-arterial delivery of thrombolytic agent into the mesenteric thrombus at the time of diagnostic angiography.

Various

thrombolytic medications, including

urokinase

or recombinant tissue plasminogen activator

have

been reported to be successful

Catheter

-directed thrombolytic therapy has a higher probability of restoring mesenteric blood flow success when performed within 12 hours of symptom onset.

Slide43

Endovascular treatment

Successful resolution of a mesenteric thrombus

- facilitate

the identification of the underlying mesenteric occlusive disease process

.

Subsequent

operative mesenteric revascularization or mesenteric balloon angioplasty and stenting may be performed electively

Main

drawbacks

Percutaneous

, catheter-directed thrombolysis (CDT) does not allow the possibility to inspect the potentially ischemic intestine following restoration of the mesenteric flow.

Prolonged

period of time

- achieve

successful CDT,

An

incomplete or unsuccessful

thrombolysis

Slide44

Acute Mesenteric venous thrombosis

MVT

- 5

% to 15% of

patients

The

superior mesenteric vein is most

commonly

frequently

with extension of thrombus into the portal vein.

The

inferior mesenteric vein is most often spared

.

Clinical

findings

–

extent

of thrombosis,

the

mesenteric veins

involved

degree

of bowel wall ischemia.

M

ortality

rate

- up

to 50

%

Slide45

Clinical features

Midabdominal

colicky

pain

D

iffuse

and nondescript nature of their

symptoms

- delay

Nausea

,

vomiting

,

D

iarrhea

, and

anorexia

Occult

blood in the stool are present in half of the patients

,

H

ematemesis

, hematochezia, or melena

-

15

%.

Slide46

Past

medical history or family history -

informative because venous

thromboembolism

Physical findings

- early

arterial mesenteric ischemia.

Abdomen

soft,

Early stage – No tenderness/ peritoneal signs

Advanced disease - Fever

,

muscular guarding, rebound tenderness

Bowel

infarction ultimately develops in 30% to 60% of patients with acute MVT.

Slide47

Fluid

sequestration within the bowel wall and lumen and the development of ascites, hypotension with hemodynamic instability is often part of the clinical picture. Patients first seen in this advanced clinical condition have a poor prognosis

.

Blood tests are obtained but are not generally helpful. Elevation of the white blood count with a shift toward immature white cells can be found in 50% to 65% of patients.

[51]

Serum amylase is usually normal, and serum lactate is elevated only in patients with advanced bowel ischemia and suggests necrosis.

Plain abdominal films are often the initial diagnostic test and are generally of little value. Although abnormalities can be found in 50% of patients,

[47]

the findings are nonspecific. Thumbprinting, when seen, is indicative of the mucosal edema resulting from venous congestion. Pneumatosis intestinalis, portal vein gas, and free air in the abdomen usually represent bowel infarction.

[52]

Slide48

CT of the abdomen with intravenous contrast is the diagnostic test of choice for patients with suspected acute MVT. A definitive diagnosis can be made in more than 90% of patients. Harward et al.

[50]

reported 90% sensitivity of abdominal CT with observation of a luminal venous thrombus. However, if one includes other characteristic findings of the bowel wall, such as thickening, pneumatosis, or streaking of the mesentery, CT sensitivity increases to nearly 100%.

[33,52]

Magnetic resonance venography is used less commonly, but when properly performed, it is highly sensitive.

Depending on the timing of the examination, color duplex ultrasound of the mesenteric veins can be helpful. If performed early, before significant bowel distention, a sensitivity of 80% or greater can be anticipated.

[53]

Selective mesenteric arteriography is not frequently used to establish the diagnosis of MVT, although it may be helpful in the management of these patients. Findings such as incomplete filling of the mesenteric veins, prolonged opacification of the arterial arcades, and the presence of thrombus or nonfilling of the superior mesenteric, splenic, or portal vein (Fig. 84-5) are seen in these patients. Most report a sensitivity of 70% to 80%.

[54,55]

Slide49

Treatment is generally directed at limiting progressive venous thrombosis, reducing the risk for bowel necrosis, and performing timely resection in those with irreversible bowel ischemia. Unfortunately, because of delay in diagnosis, the diffuse nature of the thrombosis, and the rarity of this condition, treatment directed at restoring patency to the thrombosed veins is unusual. In light of the rapid technologic advances in percutaneous interventions, which incorporate pharmacologic and mechanical methods of thrombus dissolution/extraction, it appears reasonable, if not advisable to initiate a strategy of thrombus dissolution/extraction to restore venous drainage because with the traditional care of anticoagulation alone, these patients continue to face a mortality rate ranging from 15% to 50%.[48,50,55,56] The diagnosis of MVT should trigger a search for an underlying thrombophilia. Such an evaluation includes factor V Leiden, prothrombin gene mutation, antiphospholipid/anticardiolipin antibodies, antithrombin III, protein C, protein S, factor VIII levels, hyperhomocysteinemia, paroxysmal nocturnal hemoglobinuria, and assessment for an underlying myeloproliferative disorder.

Rapid initiation of systemic anticoagulation is important. In patients with localized or diffuse peritoneal irritation, exploratory laparotomy is indicated. Laparoscopy should be avoided in these patients because the increased abdominal pressure associated with the pneumoperitoneum further diminishes mesenteric blood flow.

Slide50

On entering the abdomen, the superior mesenteric and portal veins should be assessed to determine the relative age of the thrombus. If the large veins appear to have an acute thrombus within them, thrombectomy is recommended, followed by bolus infusion of a recombinant tissue plasminogen activator (rt-PA) solution. The authors use a high-volume, low-dose solution of rt-PA, typically diluting 2 mg in 50 ml and infusing the entire 2-mg dose. Necrotic bowel is conservatively resected with preservation of viable intestine. The patient is treated with heparin intraoperatively and anticoagulation is continued postoperatively.

Associated arterial vasospasm should be evaluated by arteriography and treated with catheter-directed papaverine into the SMA, which improves perfusion to the ischemic bowel and reduces the necessity for additional resection. Patients treated for MVT have a high risk of recurrence (35% to 70%),[49] most frequently within 30 days, thus emphasizing the need for early and persistent anticoagulation.

Patients surviving the acute episode of MVT face chronic mesenteric venous hypertension with a subsequent risk for varices. This post-thrombotic venous hypertension occurs most commonly in patients with persistent large-vein mesenteric thrombosis, which further supports a strategy to remove the thrombus in patients with acute large-vein MVT. Some have reported success with transhepatic portography and instillation of a plasminogen activator directly into the thrombus.[57,58] Unfortunately, thrombolytic agents have been used infrequently in these patients because of the perceived risk for hemorrhage. The success of thrombolysis is often compromised by the delay in diagnosis. Intrathrombus thrombolytic therapy and, alternatively, intra-arterial thrombolytic therapy via the SMA should be considered in patients with thrombosis of large mesenteric veins when the potential benefit outweighs the risk of bleeding.

Slide51

Chronic Mesenteric ischemia

C

ommonly

the result of advanced atherosclerotic disease of multiple mesenteric arteries.

Good

collateral circulatory

- symptomatic

chronic mesenteric ischemia is rare.

Risk

factors

a

positive family history,

smoking,

hypertension,

hypercholesterolemia

.

More common in females

Slide52

Chronic Mesenteric ischemia

Non atherosclerotic

causes - less frequent

inflammatory

arterial disease,

middle

aortic syndrome,

celiac

artery compression (median arcuate ligament syndrome),

chronic

aortic dissection, aortic coarctation,

fibromuscular

dysplasia,

neurofibromatosis

.

Slide53

Chronic Mesenteric ischemia

O

cclusive disease – more common

Obliterative

disease of the celiac or mesenteric artery

-14

% to 24

%.

Visceral

artery stenosis -

frequent,

Symptoms - uncommon (extensive

collateral

circulation)

As

imaging techniques - common - stenosed visceral arteries detected more

frequently

Slide54

Clinical features

C

lassic picture

Postprandial

abdominal

pain

W

eight

loss.

Pain -

intestinal angina

/ intestinal claudication

D

iffuse - Midabdominal,

midepigastric, and crampy in nature.

D

evelops

within 15 to 45 minutes after eating

,

S

everity - size

of the meal ingested.

E

arly-onset

pain with foregut (celiac artery distribution) ischemia,

L

ater-onset

pain -

diffuse ischemic disease.

Slide55

Clinical features

N

ausea,

Vomiting

D

iarrhea

Bloating

C

onstipation

O

ccult

blood in

stool

and ischemic colitis

-

hindgut ischemia.

Slide56

Diagnosis

Non invasive mesenteric duplex scan

Fasted state

Sensitivity – 75%, Specificity – 92%

Aortography

CT angiogram

Magnetic resonance angiography

Slide57

Treatment

The therapeutic goal in patients with chronic mesenteric ischemia is to revascularize mesenteric circulation and prevent the development of bowel infarction. Mesenteric occlusive disease can be treated successfully by either transaortic endarterectomy or mesenteric artery bypass. Transaortic endarterectomy is indicated for ostial lesions of patent CA and SMA. A left medial rotation is performed, and the aorta and the mesenteric branches are exposed. A lateral aortotomy is performed, encompassing both the CA and SMA orifices. The visceral arteries must be adequately mobilized so that the termination site of endarterectomy can be visualized. Otherwise, an intimal flap may develop, which can lead to early thrombosis or distal embolization.

For occlusive lesions located 1 to 2 cm distal to the mesenteric origin, mesenteric artery bypass should be performed. Multiple mesenteric arteries are typically involved in chronic mesenteric ischemia, and both the CA and SMA should be revascularized whenever possible. In general, bypass grafting may be performed either

ante grade

from the supraceliac aorta or retrograde from either the infrarenal aorta or iliac artery. Both autogenous saphenous vein grafts and prosthetic grafts have been used with satisfactory and equivalent success. An

ante grade

bypass also can be performed using a

small-calibre

bifurcated graft from the supraceliac aorta to both the CA and SMA, which yields an excellent long-term result.

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Slide58

Endovascular treatment

Endovascular treatment of mesenteric artery stenosis or short segment occlusion by balloon dilatation or stent placement represents a less invasive therapeutic alternative to open surgical intervention, particularly in patients whose medical comorbidities place them in a high operative risk category. Endovascular therapy is also suited to patients with recurrent disease or anastomotic stenosis following previous open mesenteric revascularization. Prophylactic mesenteric revascularization is rarely performed in the asymptomatic patient undergoing an aortic procedure for other indications.

79

However, the natural history of untreated chronic mesenteric ischemia may justify revascularization in some minimally symptomatic or asymptomatic patients if the operative risks are acceptable, because the first clinical presentation may be acute intestinal ischemia in as many as 50% of the patients, with a mortality rate that ranges from 15 to 70%.

79

This is particularly true when the SMA is involved. Mesenteric angioplasty and stenting is particularly suitable for this patient subgroup given its low morbidity and mortality. Because of the limited experience with stent use in mesenteric vessels, appropriate indications for primary stent placement have not been clearly defined. Guidelines generally include calcified ostial stenoses, high-grade eccentric stenoses, chronic occlusions, and significant residual stenosis greater than 30% or the presence of dissection after angioplasty. Restenosis after PTA is also an indication for stent placement.

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Slide59

Thank

you