Seminar on mesenteric ishcemia

1. Mesenteric Ischemia
CHAIRMAN – DR. ANIL P BELLAD
CO CHAIRMAN – DR. BINITA MALLAPUR
PRESENTER – DR S S K KANTH KAVIPURAPU

2. 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.

3. 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%

4. 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

5. 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

13. Types
 Acute mesenteric ischemia
 Chronic mesenteric ischemia
 Non occlusive mesenteric ischemia

14. 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 organs
 Emboli (50%)
 Arrhythmia
 Valvular disease
 Myocardial infarction
 Hypokinetic ventricular wall
 Cardiac aneurysm
 Aortic atherosclerotic disease
 Iatrogenic
 Thrombosis (25%)
 Atherosclerotic disease
 Nonocclusive (5% to 15%)
 Pancreatitis
 Heart failure
 Sepsis
 Cardiac bypass
 Burns
 Renal failure
 Medications

15. Acute mesenteric ischemia
 Paradoxical embolus traveling through a patent foramen ovale from a
thrombus in the venous system
 Venous occlusion
 Hypercoagulable state
 Sepsis
 Compression
 Pregnancy
 Portal hypertension
 Malignancy

16. 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

17. Embolic occlusion
 Point of occlusion affects the magnitude and distribution of the ischemia
 Occlusion at the origin - ligament of Treitz to the transverse colon
 Occlusion distal to the middle colic artery - Preserves the right colon and
proximal part of the small bowel

18. 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.

19. Non Occlusive mesenteric ischemia
 20% of all cases of acute mesenteric ischemia
 Occurs with patent mesenteric arteries
 Splanchnic vasoconstriction - pathophysiologic process
 Precipitated 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.

20. Pathophysiology
 Intestinal blood flow accounts for 10 to 20% of the resting cardiac output but may,
on occasion, exceed 30%.
 Regulated by a variety of mechanisms, including
 The autonomic nervous system,
 Neurohormonal factors
 Gastrin,
 Glucagon
 Secretin
 Bradykinin, 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.

21. 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

22. 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.
 The bowel may still be viable when the mucosa is threatened
 Prolonged interruption of blood flow
 Necrosis of the muscularis and serosa
 Compromised segment is no longer salvageable.

23. Pathophysiology
 Interruption of mesenteric blood flow initiates tissue injury and systemic
illness,
 Deleterious effects catalyzed by oxygen free radicals and other toxins.
 Myocardial depression,
 Progressive inflammatory response
 Generalized increase in capillary permeability,
 Edema and organ dysfunction.

24. 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

25. 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

26. Diagnosis
 Metabolic acidosis
 Hyperamylasemia
 Elevation of lactate dehydrogenase, aspartate aminotransferase, and creatine
phosphokinase.
 Hyperkalemia and hyperphosphatemia are present - Bowel infarction
 ECG - cardiac rhythm.

27. 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

28. 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

29. CT scan
 Indirect findings of arterial bowel ischemia and may show the arterial occlusion or mesenteric venous
thrombus.
 Dilation of the bowel lumen,
 Bowel wall thickening
 Abnormal bowel wall enhancement,
 Arterial occlusion,
 Venous thrombosis
 Intramural or portal venous gas

30. 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

31. 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

32. CT scan
 Sensitivity - 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

33. Arteriography
 Definitive diagnosis - acute and chronic mesenteric ischemia.
 Arteriograms
 Establish the diagnosis
 Assist in differentiating between acute embolic, thrombotic, or nonocclusive mesenteric ischemia
 Allow 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.

34. 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.

35. Management
 Effective management
 Early diagnosis
 Aggressive resuscitation
 Early revascularization
 On going supportive care
 Medical treatment
 Surgical treatment
 Endovascular Treatment

36. Treatment
 Fluid 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

37. 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

38. 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.

39. Surgical treatment
 Following the restoration of SMA flow,
 Assessment 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.

40. 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.

41. Suspected Acute
mesenteric ischemia
Mesenteric
arteriogram
Normal arteriogram
R/O
mesenteric
venous
thrombosis
Peritone
al signs
No
observe
Yes
Exploratory
laparotomy
Non-occlusive
mesenteric ischemia
(vasoconstriction)
Anticoagulation
SMA catheter
with papaverine
infusion
Peritoneal
signs
Yes
Exploratory
laparotomy
Continue
papaverine
Repeat
arteriogram Clinical
evaluation
Second look
laparotomy
No Continue
papaverine Clinical
evaluation
Repeat
arteriogram
Small branch
occlusion/embolus
Anticoagulation
Vasoconstriction
Yes
No Peritoneal
signs
Yes Exploratory
laparotomy
No Continue
anticoagulation
observe
Aggressive resuscitation
Swan ganz catheter, volume
repletion/blood, antibiotics

42. 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.

43. 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

44. 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.
 Mortality rate - up to 50%

45. Clinical features
 Midabdominal colicky pain
 Diffuse and nondescript nature of their symptoms - delay
 Nausea,
 vomiting,
 Diarrhea, and anorexia
 Occult blood in the stool are present in half of the patients,
 Hematemesis, hematochezia, or melena - 15%.

46.  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.

47.  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]

48.  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]

49.  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.

50.  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.

51. Chronic Mesenteric ischemia
 Commonly 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

52. 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.

53. Chronic Mesenteric ischemia
 Occlusive 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

54. Clinical features
 Classic picture
 Postprandial abdominal pain
 Weight loss.
 Pain - intestinal angina / intestinal claudication
 Diffuse - Midabdominal, midepigastric, and crampy in nature.
 Develops within 15 to 45 minutes after eating,
 Severity - size of the meal ingested.
 Early-onset pain with foregut (celiac artery distribution) ischemia,
 Later-onset pain - diffuse ischemic disease.

55. Clinical features
 Nausea,
 Vomiting
 Diarrhea
 Bloating
 Constipation
 Occult blood in stool and ischemic colitis - hindgut ischemia.

56. Diagnosis
 Non invasive mesenteric duplex scan
 Fasted state
 Sensitivity – 75%, Specificity – 92%
 Aortography
 CT angiogram
 Magnetic resonance angiography

57. 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.76

58. 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.80