Introduction

Acute MI continues to remain an elusive disease to diagnose despite clinicians being taught in medical school and residency about the classic pain out of proportion with examination presentation. Although a rare case of abdominal pain, with an annual incidence of 0.09% to 0.2% per year and approximately 1% of acute abdomen hospitalizations, this is offset with a 60% to 80% mortality within the first 24 hours. It is imperative that there is no delay in diagnosis because delays in diagnosis lead to increased mortality and morbidity in terms of amount of bowel requiring resection. The presentation of patients with MI is usually nonspecific with a falsely reassuring objective abdominal examination, which can lead to a false sense of security because the late findings of this disease process (absent bowel sounds, positive fecal occult blood test, focal/generalized peritonitis from visceral ischemia, elevated lactate, hypotension, fever, and so forth) have not evolved. In general, a high degree of clinical suspicion should be based on a combination of history, examination, laboratory results, and imaging studies to arrive at the diagnosis of acute mesenteric ischemia.

Anatomy

The abdominal aorta gives off 3 major branches to the intestines (foregut, midgut, and hindgut), which are the celiac artery (CA), superior mesenteric artery (SMA), and inferior mesenteric artery (IMA). The CA perfuses the foregut (distal esophagus to second portion of duodenum). Acute MI of the foregut is rare because the CA is a short, wide artery with good collateral flow. The SMA perfuses the midgut (duodenum to distal transverse colon), which encompasses nearly the entire small bowel and two-thirds of the large bowel. This is the most common embolic site of MI due to favorable takeoff angle (approximately 45°) from the aorta. The IMA perfuses the hindgut (transverse colon to rectum) and is rarely the sole vessel involved in MI. Collateral circulation from the CA or IMA generally allows sufficient perfusion in reduced SMA occlusion states.

Pathophysiology

In addition to the abdominal aortic anatomy, it is important to understand how the bowel layers are affected by MI, starting from the innermost to outermost layers (mucosa, submucosa, muscularis, and serosa). Early in the course of MI, the furthest layer from the blood supply (mucosa) is the first to become ischemic and is the reason for extreme pain, which is visceral in origin. Because the outer structures (muscle and serosa) have not become ischemic, however, there is minimal irritation of the parietal peritoneum when the examiner indents down against the serosa and the external layers of the bowel. Hence, there is pain out of proportion with the examination early on in the disease process. Over a period of hours, the muscularis and serosal layers become ischemic and infarct, leading to peritoneal irritation and guarding with rigidity. At this point, the pain is in proportion with the examination. It is also important to consider that between the early and late presentations (discussed previously), there is a deceptive pain-free interval of approximately 3 to 6 hours caused by a decline in intramural pain receptors from hypoperfusion.

Etiology

MI can be classified as acute versus chronic or as occlusive versus nonocclusive. The following are the major 4 causes of acute MI :

• •
  

  Acute arterial emboli – the most frequent cause of MI, accounting for 40% to 50% of cases; the embolus usually lodges in the SMA. The proximal branches of the SMA (jejunal and middle colic arteries) are usually preserved because the embolus lodges 3 cm to 10 cm distally from the SMA takeoff, where the artery tapers off and is just after the first major branch of the SMA (the middle colic artery). As a result, the proximal small and large bowels are usually spared. Due to poorly developed collateral circulation, the onset of symptoms in cases of emboli is usually severe and dramatic pain. When the bowel becomes ischemic, it has a propensity to empty itself, leading to vomiting or diarrhea, so-called gut emptying. This is one of the reasons that MI is often misdiagnosed as gastroenteritis. Common predisposing factors include atrial fibrillation, cardiomyopathy, recent angiography, and valvular disorders, such as rheumatic valve disease. One-third of patients have had a previous embolic event, such as an embolic renal infarct, embolic stroke, or peripheral arterial embolus.

  
  
• •
  

  Acute arterial thrombosis – patients with long-standing atherosclerosis may develop plaque build-up at the origin of the SMA, a site of turbulent blood flow. This subsequent stenosis may lead to long-standing postprandial pain (intestinal angina) and food fear with resultant weight loss. These symptoms of chronic MI can be seen in up to 80% of patients who develop arterial thrombosis. If the plaque acutely ruptures or the stenosis reaches a critical level, patients may present with acute pain, similar to those with arterial emboli.

  
  
• •
  

  Mesenteric venous thrombosis (MVT) – generally found in patients with an underlying hypercoagulable state; MVT accounts for 10% to 15% of cases. Patients typically present with less severe and more insidious pain than those with arterial occlusion. A majority of patients present after more than 24 hours of symptoms. In 1 study, the mean symptom duration was 5 to 14 days, with many patients experiencing pain for 1 month prior to diagnosis. Predisposing risk factors include malignancy, sepsis, liver disease or portal hypertension, sickle cell disease, and pancreatitis. Many patients have heritable hematologic disorders, including protein C and protein S deficiency, antithrombin III deficiency, and factor V Leiden mutation. One-half of patients with MVT have a personal or family history of venous thromboembolism.

  
  
• •
  

  Nonocclusive MI (NOMI) – this type of MI occurs in 20% of patients due to failure of autoregulation in low-flow states, such as hypovolemia, potent vasopressor use, heart failure, or sepsis. The underlying ischemia from splanchnic vasoconstriction can further lead to hypotension from endogenous substances, perpetuating a vicious cycle. This accounts for the extremely high mortality rate, usually due to the poor health of the affected population, with multiple comorbidities, combined with the difficulty in treating the primary cause of diminished intestinal blood flow. Patients who present with abdominal pain postdialysis may have NOMI secondary to intradialytic hypotension, leading to vasospasm.

Clinical Findings

The presentation of MI is typically acute severe abdominal pain with a paucity of physical examination findings. There is a widely variable range of performance characteristics of the history and physical examination, which underlines the diagnostic challenge. History and physical examination findings, such as acute abdominal pain, pain out of proportion, peritoneal signs, guaiac-positive stool, acute abdominal pain, heart failure, and atrial fibrillation, have a wide range of sensitivities and are frequently absent. Therefore, clinicians should be vigilant in considering MI in the differential diagnosis of abdominal pain of unclear etiology. Assessing a patient’s pretest probability for disease, actively searching for known risk factors, and adding in clues based on a patient’s history and physical examination findings are an important process for wary clinicians. Early and aggressive imaging based on this process has been demonstrated to decrease overall mortality from MI.

Laboratory Studies

Numerous laboratory abnormalities have been described in MI, including elevated amylase, lactate dehydrogenase, large base deficit, and metabolic acidosis. None of these findings is sensitive or specific for MI. Troponin I levels are often elevated. This finding is not specific for MI and has been shown to lead to delays in definitive care of these patients and inappropriate cardiology consultations. Common laboratory abnormalities, such as hemoconcentration, leukocytosis, and high anion-gap metabolic acidosis with elevated lactate (specifically d -lactate), are neither sensitive nor specific enough to be diagnostic and usually late findings.

Diagnostic biomarkers are a tool that should bear a high sensitivity and specificity, especially in MI, where early symptoms are nonspecific and mortality rises with delayed or missed diagnosis. Many laboratory tests have been studied in AMI, including d -lactate, intestinal fatty acid–binding protein, glutathione S-transferase, ischemia-modified albumin, and D-dimer. Although some have shown promising early results, none is sufficiently well established to either make or exclude the diagnosis of AMI. The serum marker that practicing clinicians are most familiar with is lactate. Although MI mortality is associated with high lactate serum values, a normal serum lactate value does not exclude AMI. Early in the disease process, lactate is generally normal as it travels through the portal venous system to the liver, where it is converted into glucose via the Cori cycle. As the ischemia load increases and the liver is not able to keep up with the demand, lactate spills over into the systemic circulation, where it eventually increases in late stages.

Imaging Studies

Various imaging methods have been studied and used in the diagnosis of MI, including lower GI endoscopy, radionuclide imaging, peritoneal fluid analysis, MRI, and peritoneoscopy. Imaging that is insensitive or low yield should be avoided, and any imaging that is performed should be pursued in as expeditious a manner as possible, given the time-sensitive nature of the disease. It has been shown that a multidisciplinary approach to suspected cases of AMI with streamlined protocols and early involvement of consultants can have an impact on overall mortality. The following are common diagnostic modalities often described:

• •
  

  Plain radiographs: the findings on a plain abdominal radiograph are usually nonspecific (ie, small bowel distention with air-fluid levels or ileus), and 25% of patients may have normal findings. Patients with normal plain radiographs have a lower mortality rate, presumably because the findings that are visible on plain radiographs are late findings seen in more advanced disease. Characteristic findings, such as thumb printing or thickening of bowel loops, occur in less than 40% of patients. Later findings, such as air in the bowel wall (pneumatosis intestinalis) and portal venous system, are ominous signs portending a poor prognosis.

  
  
• •
  

  Ultrasound: the use of ultrasound to detect significant stenosis (>50%) in mesenteric vessels has been shown and has a role in chronic MI, but the role of ultrasound in making the diagnosis of acute ischemia is less well established. This likely is due to limited operator experience in AMI and the abnormality in patient bowel gas patterns that often accompanies AMI, which make visualization of the mesenteric vessels more difficult.

  
  
• •
  

  CT scan: CT is the most commonly used diagnostic tool in suspected MI; the initial sensitivity was 64% but has now improved to 93% with the use of dynamic contrast-enhanced CT. The addition of multidetector row CT (MDRCT) technology has further improved results ( Fig. 1 ). The use of MDRCT angiography does not require oral contrast, which has been shown to increase time to image acquisition to 2 to 3 hours, a potentially lethal delay in cases of suspected MI.

  
  

  
  

  
  

  
  

  
  

  Sagittal reconstruction of MDRCT angiography of normal celiac artery ( arrowhead ) and normal SMA ( arrow ).

  
  
  
  
• •
  

  Angiography: angiography was once the diagnostic gold standard in work-up due to its high accuracy and therapeutic role; today it is used primarily as a confirmatory tool when noninvasive radiological studies do not produce conclusive results. Catheter-based therapy and vasodilation still play a large role in management, especially in those patients who are deemed too risky for open surgical techniques. In addition, patients who undergo successful revascularization procedures may still require intra-arterial vasodilators to treat associated vasospasm.

  
  
• •
  

  Laparoscopy: depending on the institution, the availability of experienced radiologists to interpret CT angiograms and endovascular specialists to perform diagnostic and therapeutic angiography may be limited. In addition, acute renal failure from MI or those with known contrast allergy may prohibit obtaining a contrast study. Furthermore, a CT scan may not show vascular/intestinal pathologies in patients with a high pretest probability of MI. As a result, a diagnostic laparoscopy can fill this diagnostic gap. Studies have shown that the mean time between admission and diagnostic laparoscopy (10.2 h) was significantly shorter in patients who underwent successful revascularization and in those who survived with or without developing short bowel syndrome.

Treatment

Treatment of AMI should be initiated while the diagnostic evaluation is commencing. Treatment often requires a multidisciplinary approach involving general and vascular surgeons as well as interventional radiologists. Aggressive fluid resuscitation should be started to correct fluid deficit and metabolic derangements. Broad-spectrum antibiotics are generally given as well. Early surgical consultation is warranted, even before definitive testing is performed, especially in cases of high pretest probability. The presence of peritoneal signs is usually an indicator of late stages of the disease requiring emergency laparotomy and may obviate any confirmatory imaging.

Once a diagnosis is established, surgical treatment of the underlying cause should be performed (ie, embolectomy, thrombectomy, endarterectomy, or bypass). Anticoagulation should be started, in consultation with the treating surgeon. An important part of the postsurgical care involves reducing the profound vasospasm that accompanies AMI. This is typically accomplished through intra-arterial papaverine infusion via an indwelling catheter in the SMA. A growing area of research involves minimizing ischemia-reperfusion injury.

Summary

MI is a vascular emergency, which all emergency physicians must consider early in their abdominal pain differential. It continues to remain a diagnostic challenge, and any delay in diagnosis can contribute to the increases in the already high mortality rate. Clues to the diagnosis should be sought for in the patient history ( Table 1 ). Although the underlying cause varies, early diagnosis and prompt effective treatment can lead to improved clinical outcome. Time is bowel, so if there is a high clinical suspicion for MI, surgical and interventional radiology consultants should be involved early and in parallel with an expeditious diagnostic evaluation.

Table 1

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

Lower Abdominal Pain Anorectal Complaints in the Emergency Department The Vomiting Patient Acute Abdominal Pain in the Bariatric Surgery Patient Abdominal Pain Mimics The Opioid Epidemic in the United States

Stay updated, free articles. Join our Telegram channel

Join