Acute intestinal ischemia

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 bowel.

Pathophysiologic mechanisms
Acute thrombosis of pre-existent atherosclerotic disease in the mesenteric arterial circulation Sudden embolic arterial occlusion in artirial circulation compromise of mesenteric arterial blood flow without anatomic occlusion - low cardiac output - in vasospastic disorders - vasculitides Mesenteric venous thrombosis Mechanical external obstruction to blood vessels

Anatomy
Celiac Artery supplies the foreguthepatobiliary system, and spleen Superior Mesentric Artery (SMA) supplies the midgut (ie, small intestine and proximal mid colon) Inferior Mesenteric Artery (IMA) supplies the hindgut (ie, distal colon and rectum).

AnatomyCeliac trunk

Anatomy SMA

Anatomy IMA

Pathophysiology
Damage to the affected bowel portion may range from reversible ischemia to transmural infarction with necrosis and perforation.
Initial vascular oclusion Reactive vasospasm in the SMA region Arterial insufficiancy Tissue hypoxia leading to bowel wall spasm Mucosal sloughing Disruption of musosal bacteria, toxins, and vasoactive substances are released into the systemic circulation
hypoxic damage worsens

vomiting or diarrhea. bleeding into the gastrointestinal tract. septic shock, cardiac failure, or multisystem organ failure before bowel necrosis actually occurs. Fluid is released into the peritoneal cavity

little abdominal tenderness is present, producing the classic intense visceral pain that is disproportionate to physical examination findings.

fever

bowel wall becomes edematous and cyanotic necrosis can occur in 8-12 hours from the onset of symptoms Transmural necrosis Perforation perotinitis

this explains the serosanguineous fluid sometimes recovered by diagnostic peritoneal lavage

Etiology
Arterial embolus (> 50%)-Coronary artery disease, heart failure, valvular heart disease, atrial fibrillation, history of arterial emboli Arterial thrombosis (10%)-Generalized atherosclerosis Venous thrombosis (515%)-Hypercoagulable state, inflammatory conditions (eg, pancreatitis, diverticulitis), trauma, heart failure, renal failure, portal hypertension, decompression sickness Nonocclusive ischemia (25%)-Low flow states (eg, heart failure, shock, cardiopulmonary bypass) and splanchnic vasoconstriction (eg, vasopressors, cocaine) Secondary to mechanical obstruction:hernia with strangulation, volvulus, intussusception, tumor compression Secondary to blunt trauma:Isolated dissection of the superior mesenteric artery (SMA) and lead to intestinal infarction Mesentry tear

Etiology
Cardiac emboli - Mural thrombus after myocardial infarction, auricular thrombus associated with mitral stenosis and atrial fibrillation, septic emboli from valvular endocarditis (less frequent) Emboli from fragments of proximal aortic thrombus due to a ruptured atheromatous plaque Atheromatous plaque dislodged by arterial catheterization Paradoxical embolus from lower extrimity venous thrombi- in patients of L-R cardiac shunt

Arterial Embolism

Arterial thrombosis
Atherosclerotic vascular disease (most common) Aortic aneurysm Aortic dissection Arteritis Decreased cardiac output from myocardial infarction or CHF (thrombotic AMI may cause acute decompensation) Dehydration from other causes

Nonocclusive mesentric ischemia

Hypotension from CHF, myocardial infarction, sepsis, severe hemorrhage, aortic insufficiency, severe liver or renal disease, or recent major cardiac or abdominal surgery, diuretics overuse Paccreatitis Burns Vasopressive drugs Ergotamines Cocaine Digitalis- due to artirial and venous smooth muscle contraction (whether digitalis use causes NOMI or patients who develop NOMI are older and are more likely to have been prescribed digitalis is unclear)

Mesentric venous thrombosis

Hypercoagulability from protein C and S deficiency, antithrombin III deficiency, dysfibrinogenemia, abnormal plasminogen, polycythemia vera (most common), thrombocytosis, sickle cell disease, factor V Leiden mutation, pregnancy, and oral contraceptive use Tumor causing venous compression or hypercoagulability (paraneoplastic syndrome) Infection, usually intra-abdominal (eg, appendicitis, diverticulitis, or abscess) Venous congestion from cirrhosis (portal hypertension) Venous trauma from accidents or surgery, especially portocaval surgery Increased intra-abdominal pressure from pneumoperitoneum during laparoscopic surgery Pancreatitis Decompression sickness

 Age-related differences in incidence frequently considered a disease of people older than 50 years. Younger people with atrial fibrillation or risk factors for MVT, such as oral contraceptive use or hypercoagulable states (eg, those caused by protein C or S deficiency)

Sexual differences in incidence No overall sex preference exists for AMI. Men might be at higher risk for occlusive arterial disease because they have a higher incidence of atherosclerosis. Conversely, women who are on oral contraceptives or are pregnant are at higher risk of MVT.

 PAIN

Symptoms

The pain is disproportionate to physical examination findings. Typically, pain is moderate to severe, diffuse, nonlocalized initially and depending on the particular segment involved, the pain may be more localized to one side of the abdomen in latter stages. SMA : tends to be more diffuse IMA: Ischemic pain toward the left side constant, and sometimes colicky. Pain may be unresponsive to narcotics

Nausea and vomiting -found in 75% of affected patients. Anorexia and diarrhea progressing to obstipation are also common. Abdominal distention and gastrointestinal (GI) bleeding are the primary symptoms in as many as 25% of patients. Fever Rectal bleeding

Clinical presentation
Embolic acute ischemia
Typically has the most abrupt and painful presentation of all types, as a consequence of the rapid onset of occlusion and the inability to form additional collateral circulation. It has been described as abdominal apoplexy and can be labeled as a bowel attack. Severe pain Often, vomiting and diarrhea (gut emptying) are observed. Patients are usually found to have a source of embolization. Because most emboli are of cardiac origin, patients often have atrial fibrillation or a recent myocardial infarction (with mural thrombus). Infrequently, patients may report a history of valvular heart disease or previous embolic episode.

Clinical presentation
Thrombotic acute mesenteric ischemia
AMI caused by a thrombus typically happens when an artery already partially blocked by atherosclerosis becomes completely occluded. Abdominal angina - a syndrome of postprandial abdominal pain that starts soon after eating and lasts for up to 3 hours. The digestion of food requires increased perfusion of the intestine, so the mechanism is similar to that of exercise-induced angina pectoris. Food fear Weight loss, early satiety, and altered bowel habits may be present. Precipitating event- sudden drop in cardiac output from myocardial infarction or congestive heart failure (CHF) or a ruptured plaque. Dehydration from vomiting or diarrhea due to an unrelated illness may also precipitate thrombotic AMI. Gradual progression of arterial occlusion and frequently have a better collateral supply. Bowel viability is better preserved, often leading to a less severe presentation than with embolic AMI. Symptoms tend to be less intense and of more gradual onset. As might be expected, these patients typically have a history of atherosclerotic disease at other sites, such as coronary artery disease, cerebral arterial disease, peripheral artery disease (especially aortoiliac occlusive disease), or a history of aortic reconstruction.

Clinical presentation
Nonocclusive mesenteric ischemia
Occurs more frequently in older patients than other forms of AMI do. patients are already in an intensive care unit (ICU) with acute respiratory failure or severe hypotension from cardiogenic or septic shock, or they are taking vasopressive drugs. Most of them are taking digitalis. Symptoms typically develop over several days, and patients may have had a prodrome of malaise and vague abdominal discomfort. When infarction occurs, the clinical condition of the ICU patient deteriorates with no apparent reason. Patients may report increased pain associated with vomiting. They may become hypotensive and tachycardic, with loose bloody stool. Much younger patient population. An acute or subacute abdominal pain syndrome related to involvement of the small intestine rather than the colon. The symptoms are frequently less dramatic. Diagnosis can be even more difficult, because symptoms may have been present for weeks. Typical symptoms of MVT may have been experienced for a prolonged period with gradual worsening. The chronic form may manifest as esophageal variceal bleeding. History of risk factors for hypercoagulability including oral contraceptive use, congenital hypercoagulable states, deep vein thrombosis (DVT), liver disease, tumor, and portocaval surgery.

Mesenteric venous thrombosis

Clinical presentation
Strangulated hernia- a sudden increase in pain and other symptoms irreducible, tender to the touch and accompanied by symptoms of nausea, vomiting and fever. Volvulus &intussusception- sudden increase of signs and symptoms in patient with intestinal obstruction and patient suddenly detoriates

Physical Examination

The different etiologies notwithstanding, physical examination findings are generally similar in patients with bowel ischemia The main distinction is between early and late presentation.
Early presentation - in the absence of peritonitis Physical signs are few and nonspecific Tenderness is minimal to nonexistent. Stool may be guaiac positive. Late presentation - Peritoneal signs develop infarction with necrosis or perforation occurs. Tenderness becomes severe and may indicate the location of the infarcted bowel segment. A palpable tender mass may be present. Bowel sounds range from hyperactive to absent. Voluntary and involuntary guarding appears. Fever, hypotension, tachycardia, tachypnea, and altered mental status are observed. Foul breath may be noted with bowel infarction, from the putrefaction of undigested alimentary material accumulated proximal to the pathologic site. Signs reflecting risk factors for AMI may be noted.

Diagnostic Considerations
Because of unclear initial presentation, serious morbidity, and a high mortality rate without proper treatment, clinical suspicion should remain high. Early intervention if any suspicion exists. Subsequent treatment should be initiated as rapidly as possible. No patient in whom ischemia is suspected should be discharged unless it can be ruled out. A diagnosis of int. ischemia is considered in all elderly patients with abdominal pain, especially if the pain is disproportionate to physical examination findings. Patients with atrial fibrillation, cardiovascular disease, or peripheral vascular disease, especially those with recent myocardial infarction, are at higher risk.

Differentials
Abdominal Abscess Abdominal Aortic Aneurysm Acute Abdomen and Pregnancy Aortic Dissection Appendicitis Biliary Colic Biliary Disease Biliary Obstruction Boerhaave Syndrome Cholangitis Cholecystitis Choledocholithiasis Cholelithiasis Colonic Obstruction Diverticulitis Ectopic Pregnancy Esophageal Rupture Gastric Volvulus Helicobacter Pylori Infection Ileus Intestinal Perforation Intestinal Pseudo-obstruction: Surgical Perspective Multisystem Organ Failure of Sepsis Acute Pancreatitis Acute Intermittent Porphyria, Pyelonephritis, Septic Shock Testicular Torsion

Blood Studies
The complete blood count (CBC) - Leukocytosis and/or leftward shift are observed in over 50% of cases. The hematocrit is elevated initially from hemoconcentration due to third-spacing, but it decreases with gastrointestinal (GI) bleeding. Amylase levels are moderately elevated in over 50% of patients, but this finding is nonspecific. Phosphate levels were initially thought to be sensitive, but later studies showed a sensitivity of only 25-33%. Metabolic acidosis is observed late in disease course, but this is a nonspecific finding. Lactate is elevated late in the clinical course. levels that are persistently within the reference range strongly indicate a diagnosis other than AMI (sensitivity 96%, specificity 60%). D-dimer has been suggested as possibly helpful. Coagulation profile

Plain X-Ray of Abdomen

It often appear normal however, they are warranted to exclude identifiable causes of abdominal pain, such as perforated viscus with free intraperitoneal air. late and nonspecific findings
Ileus edematous or thickened bowel walls paucity of gas in the intestines.

Pneumatosis intestinalis (ie, submucosal gas), Thumbprinting of the bowel wall Portal vein gas Radiograph may show bowel spasm, an early sign of ischemia.

Radiograph showing bowel spasm, an early sign of ischemia.

Gas in the colon wall, typical of advanced ischemia

Pneumatosis intestinalis (black stripes of air) in advanced acute mesenteric ischemia (AMI) with gangrenous bowel

Air in portal vein

perforated viscus with free intraperitoneal air

Computed Tomography and CT Angiography

CT scanning helps exclude other causes of abdominal pain. It may show pneumatosis intestinalis, portal vein gas, bowel wall or mesenteric edema, abnormal gas patterns, thumbprinting, streaking of mesentery, and solid organ infarction. Bowel wall edema is the most common finding, representing submucosal infiltration of fluid or hemorrhage into ischemic bowel. Arterial occlusion may show nonenhancement of the vessels. Mesenteric venous thrombosis (MVT) usually shows a thrombus in the superior mesenteric vein (SMV) or portal vein.

CT angiography
Sensitivity of 71-96% and a specificity of 9294% for AMI. In clinical practice, CT angiography is ordered much more frequently than classic angiography. CT angiography is noninvasive, readily available, and the preferred modality for MVT (90% sensitivity). Serial CT angiograms can be used to monitor

Angiography
The gold standard to aid in diagnosis and preoperative planning. It also plays an important role in pharmacologic infusion therapy. An embolus appears as a sharp cutoff of flow. Thrombus appears as a more tapered occlusion. NOMI is characterized by narrowing of the origins of multiple SMA branches, alternating dilation and narrowing of the intestinal branches (ie, the string of sausages sign), spasm of the mesenteric arcades, and impaired filling of the intramural vessels. Findings with MVT include thrombus in the SMV, reflux of contrast into the aorta, prolonged arterial phase with accumulation of contrast and thickened bowel walls, extravasation of contrast into bowel lumen, and filling defect in the portal vein or complete lack of venous phase

Ultrasonography
Duplex ultrasonography is highly specific (92-100%) but is not as sensitive (70-89%) as angiography. The examination cannot detect clots beyond the proximal main vessels, nor can it be used to diagnose NOMI. Ultrasonography is considered a second-line study for AMI. It is often less useful in the presence of dilated loops of bowel. In MVT it may show a thrombus or absent flow in the involved arteries or veins. Other possible findings include portal vein gas, biliary disease, free peritoneal fluid, thickened bowel wall, and intramural gas

Magnetic Resonance Imaging and Magnetic Resonance Angiography

Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) yield findings similar to those of CT scanning MRA has a sensitivity of 100% and a specificity of 91%. It is particularly effective for evaluating MVT. The main drawbacks are the expense and the time required. In the future, rapid MRA may supplant angiography.

Other Studies
Echocardiography
Electrocardiography (ECG) Diagnostic peritoneal lavage (DPL) may recover the serosanguineous fluid associated with bowel infarction; with the availability of CT scanning or magnetic resonance angiography (MRA), DPL is not a preferred study if AMI is suspected. In patients with intestinal angina, percutaneous transluminal angiograph, angioplasty and stenting of the celiac and/or mesenteric arteries

Initial Treatment
Resuscitation
Every effort should be made to improve patients cardiovascular status. Vasopressors should be avoided, because they worsen ischemia. Oxygen should be provided to maintain a saturation between 96-99%, by endotracheal intubation if needed. Fluid resuscitation is accomplished with isotonic sodium chloride solution, and blood products are provided as needed. Adequacy of resuscitation can be monitored by urinary output, central venous pressure, or Swan-Ganz pressure monitoring. Insert a nasogastric tube optimize cardiac status by treating arrhythmia, congestive heart failure (CHF), or myocardial infarction. Start broad-spectrum antibiotics early. Provide pain control while maintaining stable blood pressure.

 Papaverine infused through the angiography catheter at the affected vessel is useful for all arterial forms of AMI. Relieves reactive vasospasm in occluded arterial vessels and is the only treatment of NOMI other than resection of gangrenous bowel. Infusion of 30-60 mg/h after angiography, and adjust the dose for clinical response. Continue this for at least 24 hours. If the catheter slips into the aorta, significant hypotension can occur. Papaverine is incompatible with heparin. Thrombolytics infused through the angiography catheter can be a life-saving therapy for selected patients with embolic AMI. Bleeding is the main complication. Thrombolytic administration is risky and should only be undertaken if peritonitis or other signs of bowel necrosis are absent. The infusion must be started within 8 hours of symptom onset. If symptoms do not improve within 4 hours or if peritonitis develops, stop the infusion and perform surgery.

Infusion of papaverine and thrombolytics

Angioplasty after thrombolysis

A very select group of patients who have atherosclerotic plaques at the origin of the superior mesenteric artery (SMA) after thrombolysis is eligible for angioplasty. Angioplasty is technically difficult because of the anatomy of the SMA. Restenosis rates are 20-50%.

Heparin anticoagulation
Heparin anticoagulation is the main treatment of MVT. If no signs of bowel necrosis exist, the patient may not even need an operation. Heparin may increase the chance of bleeding complications. the use of enoxaparin or other low-molecular-weight heparins as a potential substitute for heparin in the treatment of MVT. Administer heparin as a bolus of 80 U/kg, not to exceed 5000 U, and then as an infusion at 18 U/kg/h until full conversion to oral warfarin. Appropriate monitoring of anticoagulation using activated partial thromboplastin time (aPTT) is mandatory.

Surgical Care general considerations

Before operative management stabilize patients by means of intravenous (IV) fluid administration, antibiotic prophylaxis covering the colonic flora, nasogastric tube decompression, and bladder catheterization, with heparin or papaverine administered as indicated. Blood should be available. Resection of necrotic bowel may be required if signs of peritonitis develop. Differentiation of nonviable from viable bowel by intraoperative fluorescein administration. During laparotomy, 1 g of fluorescein is infused. Viable bowel fluoresces brightly under a Wood lamp, thus allowing the surgeon to better evaluate the segments that need resection. A second-look operation 24- to 48-hour latter to assess for viability of the remaining bowel. Intraoperative fluorescein administration may be performed either at the primary operation or during the second-look operation.

Surgical care
laparotomy should not be unduly delayed in the compromised patient because, in most cases, surgical exploration allows accurate identification of the responsible pathologic process and operative delay is the most important determinant of an adverse outcome.

The operating room should be equipped with a Woods lamp, fluorescein, and a continuous-wave Doppler ultrasound unit

Surgeons Goal
is to confirm the diagnosis of mesenteric ischemia assess bowel viability determine the responsible etiology perform revascularization where possible resect nonviable bowel.

Surgery Thrombectomy
For embolic ischemia, unless the involved bowel is clearly gangrenous, an attempt at reperfusion is necessary. SMA is isolated location of the blockage is determined by palpation of pulses. A proximal transverse arteriotomy thrombectomy using Fogarty catheter (size 3 or 4) passed distally. arteriotomy can be closed primarily or vein-patched to prevent lumen compromise. A bypass may be required if thrombectomy is unsuccessful. Observe the intestines for 10-15 minutes after restoration of flow to assess viability of bowel. This can be enhanced by intraoperative duplex ultrasonography, fluorescein use, and palpation of pulses distal to the occlusion.

Surgical revascularization
For thrombotic AMI, emergency surgical revascularization is indicated. Simple thrombectomy has little or no benefit, because most patients have clinically significant atherosclerosis at the time of the acute decompensation. Unlike patients with embolic AMI, these patients have a lesion at the origin of the SMA, and no SMA pulsation is detected at the origin. If the gut is not gangrenous, proceed with revascularization.

Antegrade aortomesenteric bypass is the best technique. Transaortic endarterectomy is an alternative when no vein
is suitable for harvesting or when a prosthetic graft is contraindicated (eg, with massive fecal contamination). After revascularization and thrombectomy, reevaluate bowel viability

Confirming viability of the bowel

Peristalsis bowel wall edema discoloration of the bowel and mesentery mucosal hemorrhage bleeding from cut bowel edges Resection of nonviable bowel is done The challenge is to resect all nonviable bowel while leaving the patient with sufficient intestinal length to avoid development of the short bowel syndrome

Post-Operative care
Vigorous cardiopulmonary resuscitation Correction of electrolyte imbalance and arrhythmias Pharmacologic inotropic support, if necessary (especially in patients with NOMI) Acidosis correction Parenteral broad-spectrum antibiotics, with anaerobic coverage to prevent sepsis Prolonged gastrointestinal decompression for proper healing of intestinal anastomoses Early Parenteral nutrition Formal anticoagulation with its potential benefit weighed against the risk for gastrointestinal hemorrhage. Long term anticoagulation to prevent recurrence

Complications
Acute renal failure - in the immediate postoperative period(prevented by keeping the patient well hydrated) Other possible complications include
Bleeding Infection Bowel infarction Prolonged ileus Anastomosis leak Graft infection Short bowel syndrome

Interventional radiology
Other interventional radiologic techniques used recently include -Catheterdirected thrombolysis -Percutaneous transluminal angioplasty(PTA) -Fenestration of aortic dissection When spontaneous dissection of the SMA is diagnosed before the onset of intestinal infarction, percutaneous stent placement has been successful

Suspicion of intestinal ischemia

Clinical Suspicion Of Ischemia

Take home message:

High index of suspicion is the key to early diagnosis and decreases morbidity and mortality High risk patient ( Af, old age, hypercoagulation state) PE: Localized pain Lab: CBC/DC, BCS+e, ABG,amylase ,lipase Imageing-Angiography, X-RAY, CT-Scan Tx: Antibiotics, fluid + electrolyte correction, surgery or intervention and long term anticoagulation

Thankyou For Your Kind Attention