36: Acute Mesenteric Ischemia


CHAPTER 36
Acute Mesenteric Ischemia


Rami O. Tadros1 and Chien Yi M. Png2


1 Icahn School of Medicine at Mount Sinai, New York, NY, USA


2 Harvard Medical School, Boston, MA, USA


Background


Definition of disease



  • AMI is defined as a sudden loss of blood flow to the small intestine.
  • The loss of intestinal flow may be due to superior mesenteric artery or portal venous obstruction, although arterial etiologies predominate.

Disease classification


There are four classifications within AMI:



  • Acute mesenteric arterial embolism (AMAE).
  • Acute mesenteric arterial thrombosis (AMAT).
  • Non‐occlusive mesenteric ischemia (NOMI).
  • Mesenteric venous thrombosis (MVT).

Incidence/prevalence



  • AMI is seen in around one out of every 1000 hospital admissions, and has an annual incidence of between 0.1% and 0.2% per patient year.
  • Because it primarily affects older patients, the incidence of AMI is expected to rise with the aging population.

Etiology



  • AMAE is most commonly caused by an embolus in a patient with atrial fibrillation, but also can be iatrogenic or from arterial–arterial embolization.
  • AMAT is most often the result of progressive atherosclerosis. Less common causes include spontaneous superior mesenteric artery (SMA) dissection, aortic dissection, aneurysm, and arterial vasculitis.
  • NOMI can be caused by secondary hypotension from septic shock, heart failure, and the use of vasoactive medications.
  • MVT has several etiologies, including abdominal tumors, gastrointestinal infection, and portal hypertension.

Pathology/pathogenesis



  • AMAE: Emboli, most frequently of cardiac origin or from a ruptured thrombus, lodge in mesenteric arteries (most commonly in the SMA) leading to acute ischemia.
  • AMAT: Thrombosis of the mesenteric arteries due to chronic atherosclerosis leads to ischemia. Arterial aneurysms, dissections, and vasculitis can all also lead to acute thrombosis.
  • NOMI: Secondary vasoconstriction caused by hypovolemia, shock, and vasoactive drugs leads to decreased mesenteric perfusion.
  • MVT: Virchow’s triad – namely hypercoagulability, venous stasis, and endothelial damage – can result in thrombosis.

Predictive/risk factors
















Risk factor Odds ratio
Atrial fibrillation 1.2
Diabetes 2.4
Coagulopathies 8.1

Prevention


Screening



  • Lactic acid elevation is useful for diagnosing and trending possible ischemic bowel.

Primary prevention



  • Anticoagulation of patients with atrial fibrillation.
  • Antiplatelet agents, antihypertensive medications, and cholesterol management, particularly statins in patients with known atherosclerosis and atherosclerosis risk factors.
  • Hydration of patients at risk for MVT.

Secondary prevention



  • In patients with new onset atrial fibrillation who have been treated for embolism, continued anticoagulation is needed.
  • Anticoagulation will help prevent progression and recurrence of MVT.
  • Intra‐arterial papaverine may relieve and prevent recurrence of NOMI.

Diagnosis


Differential diagnosis

























Differential diagnosis Features
Gastroenteritis Vomiting
Diarrhea
Ischemic colitis Different clinical setting
Pain LLQ
History of aortic manipulation
Ruptured abdominal aortic aneurysm Sudden hypotension
Pulsating abdominal mass
+ FAST exam
History of aneurysm
Bowel obstruction Prior surgery
Distention
Vomiting
Appendicitis RLQ pain
Cholecystitis RUQ pain

Typical presentation



  • It is classically taught that patients with AMI present with abdominal pain that is out of proportion to the physical exam (due to the lack of initial peritoneal signs).
  • The onset of pain varies with the etiology of the AMI; typically AMAE and AMAT present in an acute setting, NOMI is more of a slowly progressive process, while MVT can fall in either category.
  • Patients also commonly present with nausea, vomiting, diarrhea, and subsequent constipation. Hematochezia is another potential presentation of AMI. AMI tends to occur in older patients (age >60 years) with the exception of MVT which is seen in patients in their forties.

Clinical diagnosis


History



  • Because of the non‐specific physical exam findings associated with AMI, clinicians should take a detailed history.
  • A past medical history of previous embolic events or recent myocardial infarction would be concerning for AMAE, while a long history of atherosclerotic disease is more indicative of AMAT.
  • Infection/sepsis can predispose to NOMI and less commonly AMAT.
  • A patient’s past surgical history can provide additional insight, specifically recent abdominal surgeries in the case of MVT and vascular bypass surgeries in the setting of AMAT.
  • The use of oral contraceptives, liver disease, malignancy, and congenital hypercoagulable states should be explored when MVT is suspected.

Physical examination



  • A focused abdominal exam should be done, with particular attention to auscultation and palpation. Depending on the progression of the disease, peritoneal signs such as abdominal distension, rebound tenderness, and guarding may be appreciated. In addition, bowel sounds might be absent.
  • Other physical exam findings are dependent on the etiology of the AMI and the corresponding risk factors. Irregularly irregular heart sounds may be appreciated on cardiac auscultation in the case of AMAE.

Laboratory diagnosis


List of diagnostic tests



  • The following laboratory tests should be drawn for all patients:
  • d‐dimer: d‐dimer is elevated early in the course of AMI, although the magnitude of elevation does not correlate with severity.
  • CBC: Leukocytosis is seen in around half of patients with AMI.
  • ABG: Metabolic acidosis is a late laboratory finding in patients with AMI, while metabolic alkalosis can be an early finding if the patient has vomited excessively. An elevated lactate is common.
  • PT/PPT/INR: These tests are used to evaluate patients for hypercoagulable states.

List of imaging techniques



  • CT angiography: This is the gold standard and preferred imaging technique with high sensitivity and specificity.
  • Ultrasound: US is less sensitive than CT, but can be done if MVT is the suspected etiology or CT is contraindicated. This modality is made more difficult by the deep location of the mesenteric arteries, compounded by the abdominal distention that may accompany AMI.
  • MRI: Because of the time taken to perform an MRI, it is not considered first line for an emergent condition like AMI.
  • Arteriogram: This used to be a first line diagnostic test, and may still be considered if initial CT angiography is equivocal. A benefit of this technique is that it may also allow therapeutic intervention.

Potential pitfalls/common errors made regarding diagnosis of disease



  • The most common error is mistaking AMI for gastroenteritis.

Treatment


Treatment rationale



  • Initial management regardless of etiology involves anticoagulation and antibiotics, in addition to hemodynamic stabilization and pain management.
  • Next, patients should undergo appropriate imaging to determine the surgical approach for treatment.
  • Exploratory laparotomy is required in all cases of AMAE and AMAT, and should be performed selectively in NOMI and MVT.
  • Necrotic bowel should be resected (Figure 36.1). Delayed bowel reconstruction is preferable after a second‐look exploration.
  • AMAE: Embolectomy is the first line. Infusion of thrombolytic is second line but only if the patient has not been symptomatic for a sustained period of time (<8 hours).
  • AMAT: Mesenteric bypass or endarterectomy with patch angioplasty. Retrograde stenting may be possible in select cases.
  • NOMI: Treat underlying cause.
  • MVT: Continuous anticoagulation.
  • A second‐look operation should be performed to minimize removal of viable gut.

Table of treatment













Treatment Comments
Medical
AMAE and AMAT: heparin 80 U/kg bolus followed by 18 U/kg/h infusion
AMAE: thrombolytic infusion can be considered if patient has been symptomatic for <8 hours
NOMI: vasodilators can be used. Papaverine infusion 60 mg/h selectively in the superior mesenteric artery
MVT: heparin 80 U/kg bolus followed by 18 U/kg/h infusion
Heparin monitoring should be performed by trending aPTT
Papaverine should not be administered in the same setting as heparin or its derivatives
Surgical
AMAE: laparotomy followed by embolectomy. Bypass if embolectomy fails
AMAT: laparotomy followed by bypass. Endarterectomy if bypass is not an option
AMAE, AMAT: endovascular treatments, including thrombectomy, thrombolysis, and/or angioplasty and stenting can be considered alongside surgical therapy. Second‐look operation should be done between 24 and 48 hours after initial procedure
NOMI and MVT: laparotomy in very select cases
MVT: can consider TIPS with directed thrombectomy and thrombolysis in very select cases that are refractory to anticoagulation

Prevention/management of complications



  • Heparin can cause bleeding and heparin‐induced thrombocytopenia; in the latter case, heparin should be discontinued and substituted for an alternative anticoagulant.
  • As a side effect of resection, patients may suffer from short gut syndrome, for which treatment is individualized but ranges from total parenteral nutrition to taking anti‐diarrheal medication.
  • Another potential complication is myocardial infarction, especially in patients with AMAT. This can be avoided by close hemodynamic monitoring during the perioperative period.
  • AMI has a poor prognosis, and, therefore, a prolonged hospital course and possible death are not uncommon.
Nov 20, 2022 | Posted by in ANESTHESIA | Comments Off on 36: Acute Mesenteric Ischemia
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