1. MESENTERIC VASCULAR INSUFFICIENCY
Preceptors
Dr. Govind Makharia
Dr. Sanjeev Sinha
Speaker
Dr. Deepti

2. OUTLINE Introduction Anatomical Considerations
Classification & Etiology
Clinical Features
Diagnosis
Management

3. Introduction Incidence Mortality Recurrence
1-2/1000 hospital admissions
1% of GI admissions1
Mortality
1960’s %2
1970’s %3
Recurrence
Up to 60%4
Why worry about it?
It occurs relatively rarely among all hospital admissions, and comprises 1% of all GI admissions. Incidence likely to increase with care of older population.
Survival is abysmal, although there has been a reduction in mortality from the 1960’s to the 1970’s,& it has remained around 60-70% since then. Mortality is high because usually the diagnosis is made after infarction, damage proceeds even after revascularization, and concomitant medical problems affect long-term outcomes.
Early diagnosis and aggressive treatment has been credited with lowering these numbers.
There is significant morbidity associated with acute mesenteric ischemia and up to 30% of patients become TPN dependent.
Recurrence of disease is common
1 Ann Surg 2001;233(6):
2 Ann Surg 1982;195:
3 Ann Surg 1978;188;
4 Ann Vasc Surg 2003;17:72-9

4. ANATOMICAL CONSIDERATIONS
The splanchnic circulation receives approximately 25% of the resting and 35%
of the postprandial cardiac output.
The splanchnic circulation is characterized by a vast network of collateral blood
vessels, which impart substantial protection from ischemia or infarction in
settings of segmental vascular occlusion.
The major collateral connections are:
The celiac axis and the SMA, which communicate principally through the junction of the superior and inferior pancreaticoduodenal arteries.
The SMA and IMA, which communicate through several pathways. The middle colic and left colic arteries primarily anastomose through the marginal artery of Drummond, which runs along the mesentery of the splenic flexure of the colon and the arc of Riolan.
Collateralization between the IMA and systemic circulation, which occurs in the rectum, as the superior rectal (hemorrhoidal) vessels merge with the middle rectal vessels from the internal iliac arteries.
The most metabolically active portion of the bowel is the mucosa and submucosa, which receive 70% of the blood flow, and these are the first areas to become ischemic in transmural injury.
Likewise, the mid jejunem the most susceptible to ischemia, as it is farthest away from collateral circulation.

5. MESENTERIC ISCHEMIA ACUTE CHRONIC
MI can be classified as acute or chronic. In the acute form intestinal viability is threatened whereas in the chronic forms blood flow is inadequate to support the functional demands of the intestine.

6. MESENTERIC ISCHEMIA ARTERIAL VENOUS SMA EMBOLUS (SMAE)
NONOCCLUSIVE MESENTERIC ISCHEMIA
SMA THROMBOSIS (SMAT)
FOCAL SEGMENTAL ISCHEMIA (FSI)
MESENTERIC VENOUS THROMBOSIS (MVT)
FOCAL SEGMENTAL ISCHEMIA (FSI)
Acute mesenteric ischemia can be classified into 4 distinct pathophysiologic categories:
Arterial embolic disease 50
Arterial thromboticdisease 10
Venous thromboticdisease 10 And
Non-occlusive disease 25.
Regardless of the cause of the ischemic insult, the end results are similar: a spectrum of bowel injury that ranges from transient alteration of bowel function to transmural gangrene. Clinical manifestations vary with the extent and severity of ischemic injury and, to a lesser degree, with its cause.

7. ACUTE MESENTERIC ISCHEMIA

8. Case Scenario
70/F with h/o AF presents with 3 months h/o near syncopal episodes associated with transient confusion and slurred speech admitted to hospital.
PE normal except for tachycardia 110. ECG AF with FVR. TTE normal. CT brain showed AVM.
Hospital course: successful cardioversion. Not given anticoagulation before cardioversion b/c AVM considered contraindication. Coronary angiography recommended for neurosurgery and underwent cardiac catheterization.
6 hours after catheterization, severe generalized abdominal pain, nausea, vomiting, and diarrhea. Stool tested positive for occult blood. WBC increased to 21K with L shift. Abdominal films revealed normal gas distribution in the small and large bowels without free air.
Sirmon, M. The Invisible Patient. NEJM 334 (14):

9. Case Scenario
The pain persisted, and the following day the pt passed bright red blood per rectum. Examination revealed mild abdominal distension, hypoactive bowel sounds, and voluntary guarding. She underwent esophagogastroscopy with unremarkable findings, followed by colonoscopy, which revealed bloody mucus but no evidence of ischemic colitis. WBC increased to 29K and metabolic acidosis developed.
Abdominal exploration revealed gangrenous bowel, extending from ligament of Treitz to the hepatic flexure of the colon. No further surgery was performed and the incision was closed. The pt died 12 hrs later.
Sirmon, M. The Invisible Patient. NEJM 334 (14):

10. Acute Mesenteric Ischemia
Diagnosis?
Acute Mesenteric Ischemia
Atheroemboli dislogded during cardiac catherization

11. Early identification of AMI requires a high index of suspicion
HISTORY
Early identification of AMI requires a high index of suspicion
Abdominal Pain Unexplained Abdominal Distension Gastrointestinal Bleeding
Window of opportunity
Almost all patients (95%) with AMI have acute abdominal pain. Early in the course of disease, the pain of AMI is far more impressive than the physical findings. Initially, the pain is severe, but the abdomen usually is flat, soft, and most often not tender or less tender than expected based on the magnitude of the pain.

12. History: Classic Triad SMA embolism
Acute onset abdominal pain
AF, Cardiac disease
(Vomiting, diarrhea)
Gut emptying
The presentation in acute mesenteric ischemia often varies according to etiology. If embolic disease is present, midabdominal pain is usually of sudden onset,
Sudden, severe abdominal pain accompanied by rapid and often forceful bowel evacuation, especially with minimal or no abdominal signs, strongly suggests SMAE.
A more indolent and less striking onset is more typical of MVT, whereas
With NOMI, appreciation of abdominal pain may be overshadowed by the precipitating disorders, such as hypotension, acute congestive heart failure, acute hypovolemia, or cardiac arrhythmias.
Pain is absent in as many as 25% of patients with NOMI.

13. Early identification of AMI requires a high index of suspicion
HISTORY
Early identification of AMI requires a high index of suspicion
ABDOMINAL PAIN UNEXPLAINED ABDOMINAL DISTENSION GASTROINTESTINAL BLEEDING
When pain is absent, especially when due to NOMI, unexplained abdominal distention or gastrointestinal bleeding may be the only indications of AMI
Distension, although absent early in the course of AMI, is often the first sign of intestinal infarction.
The stool contains occult blood in 75% of patients.
Elderly patients with AMI have been reported to develop mental confusion acutely in as many as 30% of cases.[4]
Patients who survive cardiopulmonary resuscitation and who then develop recurrent bacteremia or sepsis should be suspected of having had NOMI, which resulted in a segment of bowel with subacute ischemic injury, acting as a portal for bacterial translocation.[5] Although episodes of sepsis may be treated successfully with antibiotics, the length of damaged bowel must be removed to prevent recurrent sepsis.

14. PHYSICAL EXAMINATION
Sine qua non : Severe abdominal pain out of proportion to physical exam findings early in course of illness
GI:
Early: Abdomen soft, non tender, normal bowel sounds
Ischemia progresses: Guarding, hypoactive bowel sounds, absent bowel sounds, distension, ascites, Hemoccult positive stools, bloody diarrhea
Later: progressive guarding, peritonitis as full-thickness intestinal ischemia, necrosis, perforation. Tachycardia, hypotension, tachypnea, altered mental status
Although abdominal findings early in the course of intestinal ischemia are minimal or absent, increasing tenderness, rebound tenderness, and muscle guarding reflect progressive loss of intestinal viability. Such abdominal findings strongly indicate the presence of infarcted bowel. The rate of progression from the onset of abdominal pain to intestinal infarction varies, not with the specific cause of ischemia but with the severity of the ischemic insult; MVT generally has a more indolent, or so-called tumbleweed, course than do the arterial causes of AMI.

15. WHEN TO SUSPECT? MESENTERIC ARTERY EMBOLISM
Atrial or ventricular thrombus
Arrhythmias
Synchronous emboli
MESENTERIC ARTERY THROMBOSIS
Diffuse atherosclerotic disease
H/o chronic mesenteric ischemia with weight loss
The different etiologies of mesenteric ischemia are each associated with a unique set of risk factors.
The development of sudden abdominal pain in a patient older than 50 years of age who have long-standing congestive heart failure (particularly if poorly controlled), cardiac arrhythmias, recent myocardial infarction, or hypotension should suggest the diagnosis of AMI.
Diffuse atherosclerotic disease or a history of chronic mesenteric ischemia with weight loss will usually be present in a patient with thrombotic mesenteric ischemia.
Use of vasospastic medications, myocardial depression, and hypotension can usually be elicited in the history of a patient with nonocclusive mesenteric ischemia.
NON OCCLUSIVE MESENTERIC ISCHEMIA
Use of vasospastic medications
Myocardial depression
Hypotension

16. LABORATORY FEATURES Hemoconcentration
Profound leukocytosis of
High anion gap metabolic acidosis.
Elevated lactic acid levels.
Amylase, AST, LDH, CPK, Phosphate may also be elevated but is fairly non-specific. *
High peritoneal fluid amylase may be present; again non specific
On admission to the hospital, approximately 75% of patients with AMI have leukocytosis above 15,000 cells/mm3. A normal white blood cell count cannot be used to exclude early AMI, just as a high WBC count does not make the diagnosis.
About 50% have metabolic acidemia
Elevated levels of serum phosphate, d-lactate, amylase, and other enzymes have been noted, as have high peritoneal fluid amylase and intestinal alkaline phosphatase activity, but the sensitivity and specificity of these markers of intestinal ischemia have not been established.
More specific intestinal enzymes including diamine oxidase, hexosaminidase, glutathione S-transferase,[7] and intestinal fatty acid binding protein[8] also lack sufficient sensitivity and specificity to diagnose AMI.
Moreover, serum markers, when elevated, usually indicate late-stage disease.
No clear markers to establish or exclude AMI and labs are generally not helpful.
* Kurland B et al  Surg Clin North Am  1992; 72:85. .

17. RADIOLOGY PLAIN X-RAY ABDOMEN ULTRASOUND ABDOMEN CT ABDOMEN
CT ANGIOGRAPHY
MR ANGIOGRAPHY
DOPPLER
SELECTIVE MESENTERIC ANGIOGRAPHY

18. X-RAY ABDOMEN Rule out other causes
Often normal in AMI ; positive findings are usually late and non-specific
“THUMBPRINTING” Bowel wall thickening
“PNEUMATOSIS INTESTINALIS” Bowel infarction
“AIR IN PORTAL VENOUS CIRCULATION, BILIARY TREE, FREE PERITONEAL AIR”
Late findings c/w bowel necrosis
“PAUCITY OF BOWEL GAS AND ADYNAMIC ILEUS”
Most frequent finding in MVT
Although poorly sensitive (30%) and nonspecific, plain films of the abdomen still are obtained in evaluating patients with suspected AMI. The primary purpose of plain films (or CT scans) is to exclude causes of abdominal pain other than ischemia that might mandate a different therapeutic approach.
Plain films of the abdomen usually are normal in AMI before infarction. Later on, formless loops of small intestine, ileus, “thumbprinting” of the small bowel or right colon ( Fig ), or still later, pneumatosis and portal or mesenteric vascular gas may be seen

19. The plain abdominal x-ray shows thumbprinting, an indication of mucosal edema,
associated with ischemic colitis. Found in approximately 30% of patients with mesenteric
ischemia, it is associated with a poor prognosis.

20. PNEUMATOSIS INTESTINALIS

21. X-RAY ABDOMEN Abdominal X rays
Rule out other causes: perforated viscus, small or large bowel obstruction
Often normal in AMI ; positive findings are usually late and non-specific
“THUMBPRINTING” Bowel wall thickening
“PNEUMATOSIS INTESTINALIS” Bowel infarction
rarely seen (5%)
Also associated c other benign findings (e.g. COPD, IBD, mechanical ventilation)
“AIR IN PORTAL VENOUS CIRCULATION, BILIARY TREE
FREE PERITONEAL AIR”
Late findings c/w bowel necrosis
“PAUCITY OF BOWEL GAS AND ADYNAMIC ILEUS”
Most frequent finding in MVT
Although poorly sensitive (30%) and nonspecific, plain films of the abdomen still are obtained in evaluating patients with suspected AMI. The primary purpose of plain films (or CT scans) is to exclude causes of abdominal pain other than ischemia that might mandate a different therapeutic approach.
Plain films of the abdomen usually are normal in AMI before infarction. Later on, formless loops of small intestine, ileus, “thumbprinting” of the small bowel or right colon ( Fig ), or still later, pneumatosis and portal or mesenteric vascular gas may be seen

22. US Doppler Noninvasive assessment of portomesenteric flow
Inexpensive especially in cases of MVT
Exclude other differential causes including cholecystitis, or pancreatitis.
Useful in chronic mesenteric ischemia
Distended bowel loops limits role in AMI
Does not exclude embolic phenomenon, but absence flow and ascites highly suggestive MVT

23. LIMITATIONS
Only the proximal portions of the major splanchnic vessels can be studied reliably, not the peripheral vasculature.   
Vessel occlusions are not diagnostic of intestinal ischemia since complete occlusions can be seen in asymptomatic individuals.  
Blood flow though the SMA is highly variable, which makes interpretation difficult.   
NOMI, which accounts for approximately 25% of AMI,
cannot be diagnosed reliably by ultrasound.

24. COMPUTED TOMOGRAPHY
Multi-detector row CT allows for 92% specificity and 64% sensitivity in determining the presence of mesenteric ischemia.*
Offers the ability to perform 3D reconstructions.
Diagnostic modality of choice in MVT, sensitivity 90%
CT has largely replaced plain film study of the abdomen for diagnosis today and is used to identify arterial and venous thromboses as well as ischemic bowel. [10] [11] [12] [13]
In a study comparing CT findings in 39 patients who had AMI proven at surgery with 24 patients suspected of AMI that was disproved at surgery, the detection of at least one of these signs
Arterial or venous thrombosis
Intramural /Portal venous gas
Focal lack of BW enhancement
Liver or spleen infarcts
resulted in a sensitivity of 64% (25 of 39; confidence interval, 0.49, 0.79),
a specificity of 92% (22 of 24; confidence interval, 0.81, 1.00), and
an accuracy of 75% (47 of 63; confidence interval,0.64, 0.86).
Diagnostic choice in MVT, sensitivity 90%
Superior mesenteric or portal vein enlarged c central areas of attenuation suggestive of thrombus.
BW thickening and presence of ascites also suggestive.
*Taourel PG, et al:  Radiology  1996; 199:632

25. Normal anatomy

26. FINDINGS ON CT Colon dilatation Bowel wall thickening
Abnormal bowel wall enhancement
Lack of enhancement of arterial vasculature
with timed intravenous contrast injections,
Arterial occlusion
Venous thrombosis
Engorgement of mesenteric veins
Intramural gas and mesenteric or
portal venous gas
Infarction of other organs
Ascites
Findings on CT include colon dilatation, bowel wall thickening, abnormal bowel wall enhancement, lack of enhancement of arterial vasculature with timed intravenous contrast injections, arterial occlusion, venous thrombosis, engorgement of mesenteric veins, intramural gas and mesenteric or portal venous gas ( Fig.111-6)
infarction of other organs, ascites, and signs related to the cause of the infarcted bowel such as hernia.[10]

27. Figure 7.  Bowel dilatation in a 54-year-old woman with mesenteric venous thrombosis. CT image shows multiple loops of distended, fluid-filled small intestine (B) secondary to SMV thrombosis (arrowhead). There is no pneumatosis or free intraperitoneal air. Trace ascites is also present (arrow).

28. Contrast-enhancedtransverseCTscanshowssegmental
small-bowelwithpronouncedwallthickening(arrowheads)andmild
periserosalhazinessinvolvingileumandcoloninapatientwithgener-
alizedautoimmunevasculitisduetosystemiclupuserythematosus

29. a/b.Unenhanced aspects of ischemic bowel loops (arrowheads) compared to normal bowel loops (arrows)
c. Jejunal art normal arrows but ileal arteries are poorly represented

30. pneumatosis

33. Gas in the bowel wall or portal system Acute embolic infarction of other intra-abdominal organs Thrombi in the mesenteric vessels
There are three relatively specific findings of AMI that are better depicted on CT scans compared with plain films:
gas in the bowel wall or portal system;
(2) acute embolic infarction of other intra-abdominal organs; and
(3) thrombi in the mesenteric vessels.
Unfortunately, the early signs on CT are nonspecific and the late signs reflect necrotic bowel.

34. CT ANGIOGRAPHY
CT angiography has been shown to be promising in the diagnosis of AMI, and in one study, the added CT angiographic findings were believed to alter clinical management in 19% of 62 patients by making the diagnosis of AMI when CT alone did not.*
Note complete occlusion and lack of IV contrast filling the superior mesenteric artery from its origin from the aorta (Arrows).
*Kirkpatrick IDC et al  Radiology  2003; 229:91

35. MRA SHOWING INFERIOR MESENTRIC ARTERY STENOSIS
MR ANGIOGRAPHY
MRA Magnetic resonance (MR) angiography is another of the newer imaging techniques used to diagnose AMI.
Major drawbacks are expense and time.
MRA SHOWING INFERIOR MESENTRIC ARTERY STENOSIS

36. SELECTIVE MESENTRIC ANGIOGRAPHY
Selective mesenteric angiography, frequently with papaverine infusion, currently is the mainstay of diagnosis and initial treatment of both occlusive and nonocclusive forms of AMI
Sensitivity and specificity of mesenteric angiography for diagnosing AMI in most studies are 90% to 100% and 100%, respectively.*
Selective mesenteric angiography, frequently with papaverine infusion, currently is the mainstay of diagnosis and initial treatment of both occlusive and nonocclusive forms of AMI, and should be performed promptly if AMI is suspected or diagnosed on other imaging tests.
*Brandt LJ, Boley SJ: AGA  Gastroenterology  2000; 118:954.

37. Hemodynamic stabilisation should be achieved prior to the study since angio will demonstrate mesenteric vasoconstriction , even in the absence of mesentric ischemia, in the setting of hypotension or hypovolemia.

38. ARTERIOGRAPHY FINDINGS BASED ON ETIOLOGY
ACUTE EMBOLIC OCCLUSION
A rounded filling defect with nearly complete obstruction to flow.
SMA, other mesenteric vessels, abdominal aorta relatively undiseased
Poor collaterals, multiple emboli
ACUTE THROMBOTIC OCCLUSION
Origin of SMA or celiac axis with opacification of short segment of these vessels; may see collaterals
Diffuse atheromatous disease in abdominal aorta

39. Note complete lack of contrast in mesenteric vessels in AP view (left)
Note complete lack of contrast in mesenteric vessels in AP view (left). The occluded origins of the celiac axis and superior mesenteric artery are demonstrated in the Lateral view (right).

40. ARTERIOGRAPHY FINDINGS BASED ON ETIOLOGY
MVT
Not as helpful esp. segmental venous thrombosis.
Most importantly can exclude embolus, thrombus, NOMI.
NOMI
Mesenteric vessels may be patent with or without evidence of chronic disease.
Intermittent areas of narrowing and dilatation (“string of sausages”) c/w arterial vasoconstriction of spasm.
Diagnostic test: Direct infusion of papaverine (60mg) into SMA can reverse vasoconstricion and confirms diagnosis. Can leave catheter in place for continuous therapeutic infusion.

41. NOMI intermittent spasm and dilatation of vessels “string of sausages”

42. ARTERIOGRAPHY FINDINGS BASED ON ETIOLOGY
MVT
Not as helpful esp. segmental venous thrombosis.
Most importantly can exclude embolus, thrombus, NOMI.
NOMI
Mesenteric vessels may be patent with or without evidence of chronic disease.
Intermittent areas of narrowing and dilatation (“string of sausages”) c/w arterial vasoconstriction of spasm.
Diagnostic test: Direct infusion of papaverine (60mg) into SMA can reverse vasoconstricion and confirms diagnosis. Can leave catheter in place for continuous therapeutic infusion.

43. THERAPEUTIC OPTIONS DURING ANGIOGRAPHY
Administration of intraarterial vasodilators or thrombolytic agents
Angioplasty
Placement of a vascular stent, and
Embolectomy

44. ROLE OF LAPAROSCOPY
Laparoscopy may be useful, but it can be misleading because early in ischemic injury, blood may be shunted to the serosa, giving a normal appearance to the outside of the bowel while the mucosa may be necrotic.
Laparoscopy is potentially dangerous because SMA blood flow decreases when intraperitoneal pressure exceeds 20 mm Hg.

45. OTHER STUDIES ECHO - Confirm source of emboli EKG – MI or AF
Endoscopy - dx ischemic colitis but does not visulaize much of small bowel which is frequently involved
Barium studies
Contraindicated as increased intraluminal pressure -> perforation and residual barium may obscure crucial angiographic findings