Acute mesenteric ischemia in elderly patients

KEYWORDS:

• Acute mesenteric ischemia
• acute on chronic
• elderly
• revascularization
• computed tomography
• diagnosis

1. Introduction

Acute mesenteric ischemia (AMI) is more common than generally thought, and the disease is often caused by mesenteric atherosclerotic occlusive disease especially in the elderly. The atherosclerotic etiology is as common as the embolic etiology, if not more so. Approximately half of the patients with atherosclerotic etiology present with acute thrombotic occlusion of the superior mesenteric artery (SMA), while the other half develop acute ischemia upon chronic occlusive multivessel disease of the mesenteric arteries. The symptoms and clinical findings are often obscure. Clinical suspicion is a major factor in the correct interpretation of computed tomography (CT) findings as some patients develop acute ischemia gradually from previously symptomatic or asymptomatic chronic mesenteric ischemia, and the ischemia-specific signs may not yet have been developed at the time of the imaging. Patients with symptomatic chronic mesenteric ischemia require urgent treatment before the disease culminates in AMI with much worse prognosis.

2. Acute mesenteric ischemia is more common than expected in the elderly

AMI due to arterial occlusive disease is generally considered a rare condition with hospital incidence rates ranging from 4.5 to 5.4 per 100,000 person-years [1–3]. On the other hand, it has been shown that AMI is 1.5 times more common abdominal emergency than ruptured abdominal aortic aneurysm [1,4]. Rare or not, AMI should never be overlooked as a possible cause of acute abdomen especially in the elderly. The incidence of AMI increases exponentially with age. In patients aged 75 years or older, AMI is a more prevalent cause of acute abdomen than appendicitis [1]. The incidence of AMI is roughly 10-fold in an 80-year-old than in a 60-year-old patient [1,4].

3. Atherosclerotic occlusive disease may currently be the most common cause of AMI

Decades ago, SMA embolism was determined as the most common cause of AMI [5]. Based on contemporary data, however, it would seem that atherosclerotic occlusive disease of the mesentery is currently the most common etiology [6,7]. Unfortunately, population-based studies with high autopsy frequency have not been performed in the current century, so there is no definitive proof of any change in the etiological spectrum of AMI. Even so, the population is getting older (which means more atherosclerosis), and the use of anticoagulation therapy has increased (less embolic events) [8]. Nowadays, the classic presentation of AMI, i.e. ‘severe, poorly localized abdominal pain that is out of proportions to the physical examination’, is becoming a rarity, while the so-called ‘acute on chronic’ presentations of mesenteric ischemia are more common, and probably underdiagnosed. The classical characterization of AMI seems to apply only when AMI is caused by acute embolic occlusion of previously unobstructed SMA. Patients who develop AMI upon atherosclerotic occlusive disease of the mesenteric arteries often present with insidious onset of obscure symptoms such as vague abdominal pain, vomiting, and diarrhea, and the diagnosis can be incredibly difficult.

It is important to recognize that there is only ‘a thin red line’ between chronic mesenteric ischemia and AMI. Patients with symptomatic chronic mesenteric ischemia (abdominal angina) are at high risk of developing AMI. In one study, more than 80% of patients with acute on chronic mesenteric ischemia had been previously hospitalized or evaluated at hospital for the same complaints, often within half year before the final admission [9]. Therefore, patients with clearly symptomatic chronic mesenteric ischemia need to be evaluated and revascularized preferably within days or, if anyhow possible, with equivalent urgency as if the patient had acute coronary syndrome. If symptoms persist for hours after meal, the patient may already have gone into an irreversible state of bowel ischemia, and emergency revascularization may be necessary (even though fluid resuscitation and correction of anemia may sometimes reverse the acute symptoms). Any unnecessary delay will risk the patient developing fulminant AMI.

4. Clinical suspicion is a key factor in early diagnosis of AMI

The diagnostic accuracy of imaging alone in AMI should not be overestimated. In two systematic reviews, CT was associated with as high as 89–100% sensitivity and specificity in AMI [10,11]. Unfortunately, there is a discrepancy between the study setting and practice. First, the studies were performed exclusively on patients with clinical suspicion of AMI prior to the imaging, and the CTs were performed in optimal (biphasic) imaging protocols. Second, the majority of the study patients seemed to have advanced intestinal ischemia (proving to be fatal or requiring bowel surgery). These factors make the CT findings in AMI more prominent and easier to detect, but the reality is different in the daily life of the emergency department where AMI is found unexpectedly in the CT (without prior clinical suspicion) in two-thirds of the cases, and the CTs of acute abdominal pain are often performed in venous phase alone unless the clinician has specifically inquired for AMI [7]. Furthermore, we should aim to detect AMI before irreversible bowel injury has occurred. In ‘still reversible’ phase of bowel ischemia, the CT findings are more subtle and difficult to detect, and especially because of this, clinical suspicion is a major factor in the correct CT interpretation [7,12].

There are few studies on the diagnostic accuracy of CT in AMI that have been performed in patients with unclear acute or subacute abdominal pain in the clinical routine (based on the duty radiologist’s report) [7,12,13]. These studies showed no more than 67–86% rate of correct CT diagnosis, and roughly half of the AMI patients in these studies had advanced bowel ischemia, whereas the other half had reversible ischemia.

5. Disregarding the elderly in patient selection is a major bias in the literature on AMI

The treatment outcome in AMI depends highly on patient selection. If you treat only relatively young and low-risk patients with mild peritoneal signs, you obviously get better results than if you would treat all the high-risk elderly patients and those with severe peritonitis. The problem with many reports regarding AMI treatment outcomes is that, too often, it is not clearly disclosed what percentage of all patients with AMI in the population was actively treated with revascularization, and how many patients were treated with bowel resection alone, or with mere comfort care.

Currently, the most often referred papers regarding open and endovascular therapy in AMI are probably the studies by Schermerhorn and Arthurs [8,14]. The paper by Schermerhorn et al. provided outcomes of endovascular and open therapy in acute and chronic mesenteric ischemia based on the National Inpatient Sample. It is a database that contains a 20% sample of hospital stays in approximately 1000 hospitals in the United States; thus, the huge numbers of patients in that study actually represented weighted estimates for the entire population. Nevertheless, the study showed lower mortality rate after endovascular therapy than after open revascularization for patients with AMI (16% vs. 28%). The problem, however, was that the overall revascularization rate of all patients with AMI in that study was probably very low. Although this was not discussed directly in the paper, the suspicion was raised by another study based on the same database by Bealieu et al.; the total revascularization rate in AMI in the National Inpatient Sample was less than 3%, while 17% were treated with bowel resection alone, and disturbingly, 80% received no intervention whatsoever [15].

In the single-center report by Arthurs et al., 70 consecutive patients received primarily endovascular (n = 56) or open (n = 14) revascularization for AMI with commendable results (39% overall mortality) [14]. However, the mean age of the patients, 64 years, was very low compared to the mean age of approximately 80 years in other studies that include unselected patients with AMI (due to arterial occlusive etiology) [1,4]. Thus, the patient population in the Arthurs’ study does not represent the majority of AMI patients.

This problem is uniform in the current literature on AMI, and the Arthurs’ and Schermerhorn’s papers are just two examples of extremely well-performed studies, but even so, these factors must be taken into account when interpreting the results of AMI treatment modalities.

6. When publishing outcomes of AMI treatment, it is mandatory that all cases with AMI are reported, not just those selected for active treatment

In our institution, we see nearly all patients with acute abdomen from a well-defined population of 250,000 inhabitants. Between the years 2009 and 2013, we treated 66 patients with arterial occlusive AMI of whom 50 (mean age 79 ± 9 years) received attempt at endovascular therapy constituting a 76% revascularization rate and proving technically successful in 44 (88%) of the cases. Thus, these were fairly unselected AMI patients. The 30-day mortality of the 50 patients who received either successful or failed attempt at endovascular revascularization was 32%, and the overall mortality of all 66 patients with AMI was 42%. Resection of gangrenous bowel was required in one-third of the patients, and more than half avoided laparotomy altogether [16]. Our current treatment algorithm is presented in Figure 1.

Figure 1. The current treatment algorithm of AMI in our hospital. In stable patients, we seek to revascularize by endovascular means first; we convert to laparotomy if the endovascular approach is unsuccessful or unfeasible, or if the symptoms do not resolve soon after successful endovascular revascularization. In patients with septic peritonitis, laparotomy is always required.

During our 5-year study period, only half of the patients with atherosclerotic occlusive etiology of AMI presented with a clearly visible thrombotic clot in the contrast-enhanced CT. Thus, half of the patients developed AMI upon chronic mesenteric ischemia either due to microthrombosis (that is not clearly visualized in CT) or due to some other sudden decrease in the bowel perfusion (dehydration, hypovolemia, and anemia). Although all our AMI patients with atherosclerotic etiology had severe occlusive disease of the mesentery, oftentimes, it could only be speculated why the chronic state suddenly manifested as AMI; in some cases, even the thrombotic clot that was clearly seen in the CT proved to be a chronic thrombus (based on earlier CT scans), and yet, the patient had acute bowel necrosis [7]. If this is not confusing enough, one-third of our patients with atherosclerotic AMI presented without any specific CT sign (defined as thrombotic clot of the SMA, decreased bowel wall enhancement, or pneumatosis). But if it is of any comfort, all patients did have at least some abnormal, however, unspecific intestinal signs in their CT examinations such as luminal dilatation (i.e. paralysis), bowel wall thickening, and mesenteric fat stranding (i.e. mesenteric edema), and these findings together with occlusion or subtotal occlusion of the SMA might help the clinician to make the diagnosis [17].

Finally, the diagnosis of AMI must be based on clinical findings, laboratory findings, and CT findings, all together. High suspicion of AMI is encouraged in elderly patients with acute or subacute abdominal pain, especially in those with prior cardiovascular risk factors, occlusive mesenteric atherosclerosis, and abnormal intestinal signs (specific or unspecific) in contrast-enhanced CT. Patients who slowly develop AMI upon chronic mesenteric ischemia are difficult to diagnose but seem to have very good survival after (endovascular) revascularization even despite several days’ duration of symptoms and high inflammatory marker values [9,16,17]. In contrast, decreased bowel wall enhancement, pneumatosis, and metabolic acidosis are strong signs of advanced bowel ischemia and indicate the need for surgical intervention.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Acknowledgments

The author was funded by the Interventional Radiologists of Finland society.

Additional information

Funding

This paper was not funded.