Acute circulatory disturbances in the mesenteric vessels can lead to ischemic necrosis of the intestinal tract within a short period, resulting in intestinal obstruction. This condition clinically presents as ischemic intestinal obstruction. Due to its high mortality rate and propensity for being misdiagnosed, the condition is associated with serious outcomes and demands significant attention.
The common causes of the condition are as follows:
Superior Mesenteric Arterial Embolism
Embolism is often due to emboli originating from the left atrium, commonly associated with atrial fibrillation, valvular heart disease with mural thrombus, or septic emboli from infective endocarditis. The embolus frequently lodges at natural narrowing points of the superior mesenteric artery, most commonly distal to the origin of the middle colic artery.
Superior Mesenteric Arterial Thrombosis
This typically occurs on the basis of atherosclerotic occlusion or stenosis of the superior mesenteric artery.
Superior Mesenteric Venous Thrombosis
This condition may follow abdominal infections, blood stagnation caused by portal hypertension in liver cirrhosis, hypercoagulable states (as seen in polycythemia vera), or events such as splenectomy, pregnancy, oral contraceptives, trauma, or surgery that lead to vascular injury.
Nonocclusive Mesenteric Ischemia (NOMI)
This condition involves ischemia without vascular occlusion of the mesenteric arteries and veins. It is commonly seen in conditions such as congestive heart failure, acute myocardial infarction, shock, or major cardiac and vascular surgeries. It is related to low blood volume, reduced cardiac output, hypotension, or mesenteric vasoconstriction-induced hypoperfusion.
Clinical Manifestations and Diagnosis
The clinical presentation varies depending on the cause, location, type, extent, and acuteness of the mesenteric vascular obstruction. In general, more acute and extensive blockages result in more severe manifestations.
Superior Mesenteric Arterial Embolism
The onset is often sudden and severe, initially marked by abrupt, intense colicky abdominal pain that is poorly relieved by medication. The pain may be diffuse or localized and is characterized by a disproportion between the severe pain reported and the relatively mild findings on physical examination. As intestinal necrosis develops, the pain becomes continuous, and symptoms such as vomiting of bloody fluid and the passage of dark reddish stools may appear. Initially, the abdomen is soft and non-distended, with mild tenderness and preserved bowel sounds. However, as intestinal necrosis and peritonitis ensue, abdominal distension, absent bowel sounds, tenderness, and abdominal rigidity indicative of peritoneal irritation progressively manifest. Peritoneal fluid obtained through aspiration may be hemorrhagic. Patients may develop signs of septic shock early, with laboratory findings showing a sharp elevation in white blood cell (WBC) counts, often exceeding 20×109/L, even during the early stages of the disease.
Superior Mesenteric Arterial Thrombosis
This typically follows a history of chronic mesenteric ischemia, presenting as postprandial abdominal pain, food aversion with progressive weight loss, and symptoms of chronic diarrhea indicative of intestinal malabsorption. When acute and complete vascular obstruction occurs due to thrombosis, the presentation resembles that of superior mesenteric arterial embolism.
Superior Mesenteric Venous Thrombosis
Symptoms progress more gradually and tend to be non-specific. Prodromal symptoms may include abdominal discomfort, constipation, or diarrhea. After a period of days to weeks, sudden, severe abdominal pain may occur, along with persistent vomiting, hematemesis, or hematochezia. This may be accompanied by abdominal distension, tenderness, reduced bowel sounds, and hemorrhagic peritoneal fluid. Fever and significantly elevated WBC counts are frequently observed.
Nonocclusive Mesenteric Ischemia (NOMI)
The clinical presentation resembles that of acute superior mesenteric arterial obstruction but develops more slowly. Abdominal pain increases gradually, and, in the stage of intestinal necrosis, severe abdominal pain, hematemesis, hematochezia, and peritonitis signs become apparent. Selective mesenteric angiography may demonstrate normal proximal mesenteric arteries with a smooth narrowing of distal branches.
Diagnosis relies primarily on the medical history, clinical features, and auxiliary examinations. Laboratory tests often reveal significantly elevated WBC counts and D-dimer levels. Enhanced abdominal CT and CT angiography (CTA) are useful for precisely diagnosing mesenteric arterial and venous embolisms and assessing the extent and severity of the condition. Although selective angiography of the mesenteric artery is now less commonly used for diagnostic purposes, it may play an auxiliary role during thrombectomy procedures.
Treatment
Early diagnosis and timely intervention are essential, and treatment involves both systemic supportive therapy and surgical management.
Regardless of the presence of shock symptoms, fluid resuscitation should be initiated immediately, along with anticoagulation therapy and broad-spectrum antibiotics. Fluid resuscitation plays a critical role in improving tissue and organ perfusion using crystalloids or blood products. Anticoagulation therapy aims to reduce the formation and propagation of intravascular thrombosis, with low-molecular-weight heparin commonly used. Anticoagulation should continue throughout the course of treatment. Early administration of broad-spectrum antibiotics helps mitigate adverse effects associated with bacterial translocation from the gut.
In the early stages of superior mesenteric artery embolism, if peritonitis has not yet developed, endovascular interventions, including vascular stenting to assist angioplasty, percutaneous thrombectomy, or localized catheter thrombolysis, may be performed. However, the risks of reperfusion injury, systemic inflammatory response, and rethrombosis resulting in bowel necrosis after vascular recanalization must be carefully assessed. If peritoneal irritation symptoms are present, exploratory laparotomy should proceed without delay, conditions permitting. Necrotic bowel segments need to be resected, and blood flow restored through thrombectomy, while preserving any viable intestines. Depending on the extent of bowel resection and the vascular supply at the resection margins, a one-stage bowel anastomosis or an exteriorized intestinal stoma may be performed. Conducting such procedures in a hybrid operating room, where intraoperative angiography can be utilized, is advised to clarify the location and nature of the lesion, evaluate vascular recanalization, and improve the survival rate of ischemic intestinal segments.
For superior mesenteric vein thrombosis, in the absence of peritonitis or complete vascular occlusion, anticoagulation and anti-infective therapies may be selected. However, if peritonitis is present, early exploratory laparotomy and resection of necrotic intestinal segments should be performed. Postoperative anticoagulation therapy should then be continued.
Acute ischemic diseases of mesenteric vessels associated with extensive intestinal ischemia and necrosis carry a poor prognosis and high mortality rate. Following surgical treatment, patients are often admitted to the ICU for ongoing fluid resuscitation, anticoagulation therapy, anti-infective treatment, and close monitoring of clinical status. Postoperative complications are frequently severe and may include short bowel syndrome, recurrent thrombosis, septic shock, multiple organ dysfunction syndrome (MODS), intestinal fistula, gastrointestinal bleeding, and segmental intestinal fibrosis with stricture.