Acute mesenteric ischemia in cirrhosis: Diagnostic and management challenges

Abstract

Acute mesenteric ischemia is a rare but often fatal complication in patients with cirrhosis. A combination of circulatory changes, endothelial dysfunction, and unstable coagulation increases the risk of both occlusive and non-occlusive forms. Yet, due to nonspecific symptoms and clinical overlap with other complications of cirrhosis, diagnosis is frequently delayed. In this review, we describe the pathophysiologic mechanisms that underlie acute mesenteric ischemia in cirrhosis and outline current diagnostic and management strategies. Computed tomography angiography remains the first-line imaging modality, while laboratory findings are supportive but not diagnostic. Medical treatment includes fluid resuscitation, early anticoagulation, and infection control, with vasodilator therapy considered in select cases. Surgical intervention may be required in the setting of bowel infarction or confirmed vascular occlusion, but the risks in patients with cirrhosis are significant and require careful assessment. We also review four published case reports, which illustrate a range of clinical presentations, diagnostic challenges, and outcomes. Together, these cases highlight the need for early imaging, attention to thrombotic risk, and thoughtful use of both medical and surgical therapies. Ongoing research is needed to guide management in this high-risk population.

Key Words: Cirrhosis; Acute mesenteric ischemia; Portal hypertension; Thrombosis; Clinical management

Core Tip: Acute mesenteric ischemia is rare in cirrhosis but often fatal when missed. This review outlines the unique pathophysiology, diagnostic challenges, and therapeutic considerations of acute mesenteric ischemia in cirrhotic patients, who are predisposed to both arterial and portomesenteric venous thrombosis due to portal hypertension and coagulation imbalance. We also highlight lessons from reported cases and propose practical guidance for imaging, medical therapy, and surgical decision-making. Timely recognition and individualized management are essential to improving outcomes in this high-risk group.

INTRODUCTION

Acute mesenteric ischemia (AMI) is a life-threatening condition that is caused by a sudden reduction in intestinal blood flow. This leads to bowel infarction if not quickly diagnosed and managed. Although rare, it carries mortality rates greater than 60% due to delayed recognition in most cases[1,2]. The diagnosis can often be difficult as symptoms are vague and overlap with other causes of acute abdominal pain[3]. AMI can be classified into four main categories: Arterial embolism, arterial thrombosis, mesenteric venous thrombosis (MVT), and non-occlusive mesenteric ischemia (NOMI)[2,4]. Among these mechanisms, portomesenteric venous thrombosis (PMVT) is more commonly implicated than arterial causes of AMI in patients with cirrhosis, likely due to underlying portal hypertension, sluggish venous flow, and a rebalanced yet unstable coagulation profile[5]. In patients with cirrhosis, this picture becomes more complicated. AMI is also increased due to portal hypertension, coagulopathy, and impaired splanchnic autoregulation. On the other hand, other known symptoms of cirrhosis, such as chronic abdominal symptoms, hepatic encephalopathy, and ascites, can mask its presentation, thus leading to delays in diagnosis[6,7].

Although several review articles have discussed AMI in the general population and others have studied portal venous thrombosis in cirrhosis, no prior work has synthesized existing literature specific to AMI in patients with cirrhosis. Further complicating this, the literature on AMI in cirrhosis is limited to a few case reports, making clinical decision-making rather difficult. There are currently no established guidelines tailored to AMI in this high-risk population, and conventional AMI frameworks may be insufficient to manage these patients. To our knowledge, this is the first structured review focused on this intersection. Herein, we explore the pathophysiology, diagnostic challenges, and therapeutic approaches to AMI in patients with cirrhosis. We also highlight a series of published case reports that underscore the variability in presentation and outcomes. Through this, we aim to inform clinicians and identify areas for future research.

PATHOPHYSIOLOGY

The progression of AMI in cirrhosis is still not entirely clear, but the condition likely results from several overlapping mechanisms. The disorder is the result of abnormalities in hemodynamics, endothelial function, and coagulation. Patients with cirrhosis can develop occlusive as well as non-occlusive forms of AMI due to impaired splanchnic autoregulation, endothelial injury, and a very unstable coagulation system[6,8]. The hyperdynamic circulatory state associated with cirrhosis is primarily characterized by systemic and splanchnic arterial vasodilation, resulting in reduced effective perfusion pressure. In the mesenteric circulation, such physiology raises the possibility of NOMI, especially in the case of concomitant hypotension, vasopressor use, sepsis, gastrointestinal bleeding, or large-volume paracentesis[3,9]. In patients without cirrhosis, NOMI typically results from a perfusion/demand mismatch between mesenteric circulation and the intestinal circulation demands. In cases such as hypovolemia, hypotension, or use of systemic vasoconstrictors, the superior mesenteric artery and its branches vasoconstricts leading to reduced blood flow to the bowel and subsequent ischemia[1]. In patients with cirrhosis, the pathophysiology is slightly different. Patients with cirrhosis, known for hyperdynamic circulation, intrahepatic vasoconstriction, and splanchnic arteriole vasodilatation, are more often intravascularly hypovolemic[10]. With already reduced available arterial blood flow to their mesenteric circulation, these patients are predisposed to ischemic injury with small changes in their arterial tension, potentially leading to bowel ischemia and NOMI.

Furthermore, cirrhosis affects mesenteric blood flow, increasing resistance to venous outflow and favouring the establishment of collateral vessels. These alterations might lead to segmental underpreservation and local ischemia. Alternatively, MVT has been identified in patients with liver cirrhosis; however, it is still a less recognized condition. MVT may remain clinically silent until advanced ischemia occurs[7,11]. Among patients with cirrhosis, PMVT appears more common than arterial or nonocclusive forms, especially in those with advanced portal hypertension and low portal flow[5]. In spite of an elevated international normalized ratio (INR) and thrombocytopenia, cirrhosis patients remain prone to thrombosis. Levels of procoagulant proteins like factor VIII and von Willebrand factor are typically elevated, whereas the levels of natural anticoagulants comprising protein C, protein S, and antithrombin are often low[6,12]. Consequently, the risk for thrombotic events that involve either the arterial or venous systems, including those in the mesenteric vessels, is increased.

In addition, systemic inflammation and dysfunction at the intestinal barrier can further exacerbate injury. Elevated mucosal permeability fosters bacterial translocation and local inflammatory responses. These subsequently cause microvascular thrombosis and further damage epithelial integrity[8]. Any short period of hypoperfusion may lead to irreversible injury if the condition is not recognized and treated promptly[13]. Under such circumstances, AMI reflects the manifestation of circulatory dysfunction, endothelial injury, and thrombotic risk altogether. These overlapping factors can complicate clinical management (Figure 1).

Figure 1 Pathophysiology of acute mesenteric ischemia in cirrhosis. This diagram outlines the multifactorial pathogenesis of acute mesenteric ischemia in patients with cirrhosis. Key contributing factors include impaired splanchnic autoregulation, systemic inflammation, endothelial dysfunction, and a fragile coagulation balance. These changes increase susceptibility to both occlusive and non-occlusive forms of mesenteric ischemia.

In summary, in cirrhosis, portal hypertension and splanchnic arteriole vasodilation alter mesenteric blood flow. As intrahepatic resistance is increased due to impaired sinusoidal blood flow, portal pressure rises and triggers a compensatory splanchnic vasodilation and pathological neoangiogenesis, which increases portal inflow despite the increased resistance[14,15]. In addition, mesenteric arteries and veins become chronically dilated and less responsive to vasoconstrictors due to excess nitric oxide and other vasodilators[14]. As blood continues to pool in the mesenteric vasculature, effective arterial pressure is decreased. If systemic circulation decreases secondary to an insult such as sepsis, paracentesis, or bleeding, the bowel is at risk of hypoperfusion.

In parallel, patients with cirrhosis have a rebalanced hemostasis with altered coagulation balance[16]. Venous congestion within the portal-mesenteric system promotes stasis, completing Virchow’s triad in combination with endothelial dysfunction. Endothelial cells in the splanchnic circulation become dysregulated in portal hypertension, producing excess vasodilators and inflammatory mediators, further promoting thrombosis[17]. Together, these mechanisms suggest a hierarchy in which: (1) Portal hypertension and altered mesenteric hemodynamics create a vulnerable environment; (2) Endothelial cell dysfunction amplifies local injury; and (3) An underlying hypercoagulable state increases the likelihood of thrombosis. Finally, bacterial translocation, a well-recognized feature of cirrhosis, likely exacerbates ischemic injury. Increased intestinal permeability allows bacterial products to enter the portal circulation, leading to high levels of inflammatory markers[18]. Inflammatory states are known risk factors for venous thrombosis and may accelerate the progression of AMI[19].

DIAGNOSTIC WORKUP

Diagnosing AMI in cirrhosis is challenging. Clinical signs are often subtle, and symptom onset may be gradual. In this population, delayed diagnosis is common and strongly associated with worse outcomes[3,9]. Acute portal vein thrombosis (aPVT) may present with abdominal pain and can resemble AMI, but it typically lacks signs of bowel ischemia. Distinguishing between these conditions is critical, as the urgency and management strategies differ.

Computed tomography (CT), CT angiography (CTA) remain the gold standard for imaging. It provides fast, high-resolution evaluation of both arterial and venous mesenteric circulation and can assess bowel viability. Multiphase scans are preferred, and the use of oral contrast is not necessary[1,11]. The major findings may be vascular occlusion, bowel wall thickening, hypoenhancement, pneumatosis intestinalis, and portal venous gas[4,20]. Dilatation of small bowel loops, typically greater than 2.5-3.0 cm, is also commonly associated with AMI[21]. In patients with liver cirrhosis, ascites, splenomegaly, or the formation of collateral vessels may occur and thus should be taken into account together with the clinical context[7]. CTA also remains the most sensitive modality for detecting PMVT, which may present subtly but carries the risk of progression to bowel ischemia[22]. If the suspicion of AMI is strong, concerns regarding renal function should not result in imaging delays[1,23]. In the case of NOMI, where thrombus is not visible in the arterial or venous circulation, CT diagnosis can be more challenging. Radiologic findings such as the presence of narrowing of the superior mesenteric artery, in comparison to prior CT scans, can be a supportive finding[24]. Notably, the absence of bowel wall enhancement is the most commonly associated CT finding suggestive of transmural necrosis in NOMI[25]. The distribution of ischemic changes characteristic of this pathology includes extensive and diffuse patterns[4]. Furthermore, indicators of potential mortality include findings of pneumatosis intestinalis, pale mesentery, and thin bowel wall[25].

In patients with contraindications to iodine contrast, such as severe chronic kidney disease or prior anaphylaxis, alternative imaging modalities may be used. Magnetic resonance imaging (MRI) using T1-weighted, T2-weighted, or diffusion-weighted protocols can help evaluate the health of the patient’s bowel, while contrast-enhanced MR angiography is particularly helpful in assessing vasculature[26]. Alternatively, duplex ultrasonography is particularly useful in ruling in vascular occlusion, but may be of less use to rule it out[26]. Furthermore, duplex ultrasonography is operator dependent and may miss important markers of bowel ischemia, such as pneumatosis intestinalis that would normally be seen on a computed tomography scan[26].

Laboratory findings are supportive but nonspecific. Lactate may be elevated in later stages, but is often normal early in the disease course. Leukocytosis and acidosis levels can be seen in AMI but lack sensitivity in cirrhosis[9,22]. D-dimer, a common marker of coagulopathy, has been shown to be elevated in up to 70% of patients with cirrhosis, due to multifactorial reasons such as decreased renal clearance[27]. Therefore, if baseline D-dimer exists, we suggest evaluating the delta and tracking it over the course of hospitalization, as absolute values may be less indicative. Furthermore, lactate, a commonly used biomarker to assess for ischemia, can be mildly elevated in patients with cirrhosis, though often not to the same degree[28]. These markers may help guide repeat imaging or escalation of care when trends worsen.

Ultrasound with Doppler can assist in evaluating portal or mesenteric vein thrombosis, but is limited by patient body habitus and operator experience. In order to overcome ascites, ultrasonographers may utilize the lateral decubitus position to shift ascites away from the intended area or increase compression. Its accuracy decreases in patients with ascites[11,22]. MRI and MR angiography may be useful in select cases but are generally not suitable in acute settings due to limited speed and spatial resolution[9,20]. In cirrhosis, where the signs of ischemia may be atypical or delayed, early CTA should be pursued when clinical suspicion arises. If the initial study is inconclusive, repeat imaging and early consultation with radiology, hepatology, and surgery should be considered[3,13].

MEDICAL MANAGEMENT

The medical management of AMI along with cirrhosis is aimed at early patient stabilization and preventing subsequent bowel injury. The first treatment that should be administered is fluid resuscitation to restore effective perfusion. This procedure is necessary as low blood pressure and low intravascular volume cause splanchnic hypoperfusion to worsen and could lead to bowel infarction at a faster rate[9,13]. In cirrhosis, fluid shifts, low oncotic pressure, and third spacing can render resuscitation more difficult.

It is best to start anticoagulation early, especially in the case of MVT, unless bleeding or other contraindications are present[1,29]. The American Gastroenterological Association 2025 guidelines recommend immediate anticoagulation in patients with cirrhosis with ischemic bowel in order to improve mortality and decrease surgical resection of bowel[5]. A recent multicenter study reinforces this notion, showing improved survival with urgent full-dose anticoagulation in intensive care unit patients with AMI, including those with liver failure[30]. However, the choice of anticoagulant is nuanced in patients with cirrhosis due to their coagulopathy, and little is known in the case of patients with cirrhosis with AMI. Low molecular weight heparin provides excellent safety profiles and a predictable effect in patients with cirrhosis[31], leading it to be the anticoagulant of choice in patients with cirrhosis with venous thromboembolism[32]. Additionally, the risk of heparin-induced thrombocytopenia is less than with unfractionated heparin[33]. Direct oral-anticoagulants are another option in patients with cirrhosis, although their safety profiles are unique with each medication. Dabigatran’s safety profile is unclear in patients with cirrhosis, while apixaban, rivaroxaban, and edoxaban are all contraindicated in severe hepatic decompensation[33]. Furthermore, fondaparinux may be an option, but only in mild or moderate liver disease[33]. Dosing of these individual agents must be guided by several patient factors, including disease severity, renal function, and the risk of hemorrhage. The American Association for the Study of Liver Disease recommends patient-tailored individual decisions to guide the use of therapeutic anticoagulation in patients with liver failure or thrombocytopenia[32].

Monitoring anticoagulants in these patients may also pose unique difficulties due to altered coagulation markers such as increased INR and thrombocytopenia[3]. American guidelines caution against using standard coagulation assays to guide therapy[34]. While viscoelastic testing, including thromboelastography and rotational thromboelastometry have been proposed as a method of monitoring anticoagulation, there is limited evidence to support their use in guiding therapy. Multiple randomized controlled trials have been done showing that viscoelastic testing guided management does not alter bleeding, transfusion, or mortality[34]. Ultimately, there continues to be a lack of evidence-based practice to assess the coagulation parameters and guide the management of anticoagulants in patients suffering from liver disease[27].

The implementation of broad-spectrum intravenous antibiotics is another crucial step. Liver cirrhosis can lead to increased gut permeability and dampening of the immune system. Thus, there is increased risk of bacterial translocation and sepsis[2,9]. During an episode of active ischemia, bowel rest is recommended while further treatments are initiated. In the case of prolonged bowel rest, parenteral nutrition can be considered. Enteral feeding should resume only when ischemia has been resolved and perfusion has been restored.

In NOMI patients, vasodilator treatment such as intra-arterial papaverine may relieve vasospasm[35]. This phenomenon is more closely linked to cirrhosis, where baseline splanchnic vasodilation and impaired autoregulation can lead to regional ischemia. The elimination of potential causes such as vasopressors, hypovolemia, or sepsis plays a critical role in those cases[13]. Fluid resuscitation is often necessary in these patients, as they can often present in a state of shock; it must be guided by overall hemodynamics. At baseline physical exam can be utilized to assess fluid status in combination with a bedside ultrasound assessing cardiac function and inferior vena cava diameter[32]. Furthermore, continuous assessment utilizing stroke volume and pulse pressure can further guide therapy[32]. It is generally recommended to target a mean arterial pressure of > 60 mmHg in patients with cirrhosis who are critically ill[36].

At all stages, multidisciplinary input from hepatologists, interventional radiologists, surgeons, and critical care teams is crucial[37]. Laboratory indicators such as lactate and leukocyte count can help with progress monitoring; however, they are not diagnostic. Early re-imaging should be pursued if clinical worsening or stagnation of the supportive care[1,3]. In select patients with extensive PMVT, particularly when associated with signs of intestinal ischemia, catheter-directed thrombolysis via a transjugular intrahepatic portosystemic shunt (TIPS) may be considered. This approach delivers local thrombolytics, such as alteplase, into the portal system, often as part of a stepwise regimen including thrombectomy. Reports suggest this method may reduce clot burden while minimizing systemic bleeding risk[38,39]. Though data are limited, this strategy has been successfully applied in acute settings and may serve as a bridge to recovery in centers with appropriate expertise[40,41]. While limited data exists on TIPS for PMVT, there is substantial evidence regarding TIPS in PVT, which was historically contraindicated in patients with liver disease[42]. However, careful patient selection is often done through multidisciplinary discussions at expert centers[42].

SURGICAL MANAGEMENT

Surgical management remains the mainstay of treatment for patients suffering from AMI[43]. While operative management may offer the only chance at survival, this decision can be particularly difficult for patients with cirrhosis whose perioperative risk of mortality is up to 3 × higher than the general population[44]. Several scores that use basic laboratory markers have been proposed to assess perioperative risk in these patients, including the Child-Turcotte Pugh, model for End-Stage Liver Disease, Mayo risk score, and VOCAL-Penn model[45]. In a situation where the risks of death from AMI outweigh the risks of patients with cirrhosis undergoing surgery, operative management is necessary.

Three principal goals guide surgical intervention for AMI: Restore blood flow to the bowel, remove non-viable bowel, and preserve the remaining healthy intestine[1]. While these goals are universal, patients with cirrhosis present unique challenges that complicate both intraoperative decision-making and postoperative outcomes. Removing non-viable bowel in patients with cirrhosis with AMI requires complex decision-making based on clinical presentation. In its most severe presentation, AMI presents with transmural bowel infarction. In these cases, patients will present with typical peritonitic signs, and emergency laparotomy is the standard of treatment[46]. However, cirrhosis complicates the technical and physiological aspects of resection with increased risks of bleeding, infection, wound dehiscence, and postoperative decompensation[44].

For some patients who present with AMI, with equivocal signs of necrotic bowel, there may be a benefit in proceeding with laparoscopy to assess intestinal damage[1]. This is particularly relevant in patients with cirrhosis, where laparoscopic interventions on the intestines have been shown to reduce perioperative mortality and morbidity compared to open procedures[47,48]. Laparoscopy may also be beneficial as a second-look approach to assess for ischemic bowels after primary operation[38]. When a non-viable bowel is identified, resection remains unavoidable[49]. However, if a viable bowel is identified using laparoscopy, endovascular techniques may be better alternatives than proceeding with laparotomy initially. Furthermore, if laparotomy is already indicated for the assessment/removal of necrotic bowel, several options are available. Open revascularization methods such as bypass grafts, open embolectomy, endarterectomy, and patch angioplasty have been proposed[50]. Nonetheless, these procedures carry substantial risk in patients with cirrhosis due to bleeding and post-operative physiologic stress.

ENDOVASCULAR MANAGEMENT

In recent years, endovascular techniques have emerged as alternatives for patients without signs of frank peritonitis. These techniques include aspiration, embolectomy, stenting, and endovascular thrombolysis[1,46]. In AMI, endovascular techniques have been shown to reduce 30-day mortality rates, decrease hospital length of stay, decrease total parenteral nutrition, and result in shorter lengths of bowel resection compared to their open counterparts[51]. A study comparing open vs endovascular revascularization demonstrated that only 14% of patients with endovascular treatment required bowel resection compared to 33% in the open revascularization group[52]. Although no studies to our knowledge have directly compared endovascular vs open management of AMI in patients with cirrhosis, extrapolation from related surgical fields suggests that endovascular techniques may be advantageous in this population. Patients with liver fibrosis have lower mortality and morbidity when treated endovascularly compared to open for peripheral arterial disease[53]. Similarly, endovascular aortic repair has been recommended for patients with Child-Turcotte Pugh class B[54].

Endovascular management of AMI contains a large spectrum of catheter-directed therapies, with the goal of obtaining reperfusion to the bowel, while avoiding the morbidity associated with open surgical intervention. The choice of intervention is guided by the mechanism of ischemia (thrombotic vs vasospastic) and patient characteristics. In patients with contraindications to open surgery, endovascular suction thrombectomy may be an appropriate choice of treatment. While limited data exists on this method, several studies have shown promising results in patients who were not candidates for open surgery or who had previously failed thrombolytic therapy[55,56]. Additionally, aspiration thrombectomy with concomitant catheter-directed thrombolytic therapy has also been proposed as a potential intervention with promising results in small-scale case series[57]. The American College of Radiology notes that most studies involving aspiration thrombectomy also include catheter-directed thrombolysis, with variable results on mortality and morbidity, ultimately stating this therapy is “usually appropriate” in non-peritonitic patients[58].

In addition to thrombolysis and thrombectomy, percutaneous stenting and angioplasty is another treatment methods proposed in the literature. One case series of 3 patients demonstrated successful angioplasty and stenting in patients with AMI and no peritoneal signs with follow-up of 12 months[59]. Similarly, a patient with acute on chronic mesenteric ischemia who was treated with angioplasty and stenting at early stages of AMI had complete symptom resolution[60]. Notably, all of these cases present patients with AMI, without signs of bowel infarction.

Similarly, endovascular techniques have begun to emerge in the treatment of NOMI, with the catheter-directed injection of vasodilators into splanchnic arteries. One study comparing conservative treatment (n = 31) to papaverine catheter-directed vasodilation (n = 35) in NOMI demonstrated 34% survival in endovascularly treated patients compared to 3% survival in conservative management over 30 days[61]. Similarly, in patients without cirrhosis, a meta-analysis including 335 patients demonstrated the potential use of endovascular directed vasodilator therapy in AMI, with high technical success rates[62].

Ultimately, surgical management of AMI in patients with cirrhosis requires an individualized patient-centred approach. While the fundamental goals of revascularization and saving viable bowel remain the same, the presence of cirrhosis poses a significant risk of compounding morbidity and mortality even when intervention is successful. Future research is needed to clarify the role of endovascular techniques in this population, particularly concerning the benefits of endovascular procedures and which patients can benefit from them. Based on the current literature, it appears that endovascular treatment modalities would be beneficial in patients without peritonitis. Until then, decisions to operate on these patients must be made with multidisciplinary groups, weighing the pros and cons related to the patient's unique physiology.

CASE SERIES OVERVIEW

AMI and cirrhosis have been highlighted in a small number of case reports. Different pathophysiological mechanisms, such as MVT and NOMI, were involved in these cases. However, some common features extend beyond their diverse presentations that may provide the basis for the diagnosis and management of this high-risk group. A PubMed search using the terms “acute mesenteric ischemia” AND “cirrhosis” yielded 67 results. Of these, four case reports were included as reviewed by authors Hassan AS and Laor B (Table 1).

Table 1 Summary of published case reports of acute mesenteric ischemia in cirrhosis.

Ref.	Cirrhosis etiology	AMI type	Clinical presentation	Imaging modality	Management	Outcome
Bawany et al[63], 2010	Alcohol-related	Non-occclusive	Abdominal pain, hypotension	CT	Fluids supportive care	Deceased despite supportive care; NOMI with multi-organ failure
Hughes et al[64], 2014	NAFLD	Portomesenteric venous thrombosis	Abdominal pain post-bariatric surgery	CT	Anticoagulation	Full recovery; recanalization confirmed post-anticoagulation
Mitev et al[7], 2023	Wilson’s disease	SMV thrombosis	Abdominal pain, nausea, vomiting	CT + Doppler ultrasound	Anticoagulation, antibiotics, fluids	Clinical improvement; complete SMV recanalization on imaging
Wang et al[65], 2024	Alcohol and chronic hepatitis	SMV thrombosis post-variceal embolization	Abdominal pain, nausea	CT	Anticoagulation, antibiotics, fluids	Resolved symptoms; partial SMV thrombus resolution radiographically

Key clinical features, diagnostic findings, management decisions, and outcomes from published case reports of acute mesenteric ischemia in patients with cirrhosis. AMI: Acute mesenteric ischemia; CT: Computed tomography; NOMI: Non-occlusive mesenteric ischemia; NAFLD: Non-alcoholic fatty liver disease; SMV: Superior mesenteric vein.

In nearly all cases, patients had severe, acute abdominal pain often accompanied by nausea or vomiting. Leukocytosis and elevated lactate levels were observed, yet they were non-pathognomonic. Diagnostic imaging via contrast-enhanced CT played a leading role, often detecting superior mesenteric vein thrombosis or evidence of NOMI[7,63-65]. In some cases, ultrasound was used to evaluate the portal or mesenteric veins; however, technical limitations reduced sensitivity in patients with ascites or a high body mass index. Cases of mesenteric vein thrombosis were successfully medically managed with anticoagulation and supportive care. The use of genetic testing in one case revealed the genotype of PAI-1 4G/4G, indicating a thrombophilic predisposition despite the presence of cirrhosis-associated coagulopathy[7]. These cases suggest the pursuit of therapeutic anticoagulation despite elevated INR and thrombocytopenia except in cases of active bleeding[64,65].

Bawany et al[63] introduced a case of NOMI in a patient with concomitant cirrhosis without evidence of vascular occlusion. Clinical presentation, hemodynamic instability, and imaging that failed to demonstrate thrombosis supported the diagnosis. Patient was treated with cautious fluid resuscitation, vasopressor tapering, and antibiotics[63]. This observation is a prime example of the importance of low-flow states recognition as a different mechanism of AMI in cirrhosis. Indeed, splanchnic vasodilation and impaired autoregulation can lead to regional ischemia even if vessels are patent. Interestingly, procedures were identified as potential triggers of AMI. PMVT was described in one case following sleeve gastrectomy[64], whereas another patient developed AMI following esophageal variceal ligation[65]. These two cases highlight heightened thrombotic risk in susceptible patients undergoing abdominal or endoscopic procedures, where endothelial injury, increased intra-abdominal pressure, and altered blood flow may all be contributing factors.

Taken together, these reports highlight a few key points. AMI in cirrhosis may have a subtle presentation and, therefore, must be considered in patients with unexplained abdominal pain. Early imaging, such as CTA, plays a crucial role. Management should be guided by the clinical context, with anticoagulation used early in venous cases and supportive care prioritized in NOMI. Notably, several cases involved PMVT, reinforcing its relative frequency in this population. Across cases, early recognition and individualized treatment led to good outcomes, reinforcing the need for vigilance in patients with cirrhosis presenting with acute abdominal pain.

While these case reports provide valuable clinical insight, their heterogeneity limits the ability to draw broad conclusions. The small sample size, variability in cirrhosis etiology and AMI mechanisms, and differences in diagnostic timing or intervention strategies prevent definitive recommendations. Nonetheless, a few generalizable patterns emerge: Early imaging, particularly CTA, appears crucial; venous causes such as PMVT are not rare and respond well to timely anticoagulation; and NOMI often follows hypotensive or procedural triggers and requires hemodynamic correction. Larger studies are needed to clarify risk stratification and optimal treatment strategies.

CONCLUSION

AMI in cirrhosis is difficult to diagnose and manage. Delays in recognition remain common, given the overlap with other complications of advanced liver disease. A low threshold for imaging, particularly with contrast-enhanced CT, is warranted in any patient with cirrhosis with new or worsening abdominal symptoms. When identified early, supportive care, anticoagulation, and antibiotics can prevent progression and may avoid the need for surgery. In cases where surgery is required, individualized decision-making that accounts for both the severity of ischemia and underlying liver disease is essential. Minimally invasive and endovascular techniques may reduce risk in selected patients. Future studies should also clarify the role of targeted interventions such as TIPS-directed thrombolysis in patients with venous causes of AMI. While individual case reports offer valuable perspectives, clinical decision-making must account for their limited generalizability, and larger studies are needed to inform care. Future work should aim to characterize risk factors and outcomes better and to develop cirrhosis-specific diagnostic and treatment strategies.