Intestinal ischemia: mesenteric infarction, ischemic colitis and abdominal angina

From Wikimedicine
Jump to: navigation, search
  Author(s) : Dr Shanan Khairi
  Last edited on : 25/09/2024

Intestinal ischemias encompass the suffering of the intestinal wall induced by a critical decrease in blood supply of oxygen. They can result from a reduction in arterial flow or an obstruction to venous return. Their clinical manifestations are dominated by abdominal pain. They primarily affect individuals over 60 years old with underlying cardiovascular risk factors.

Chronic intestinal ischemia or abdominal angina is a transient suffering that occurs during an increase in oxygen needs (++ after a meal) and resolves spontaneously. It corresponds to episodic or chronic intestinal hypoperfusion, usually secondary to diffuse sub-occlusive atheromatous arterial lesions. It is difficult to diagnose, does not represent an emergency, but can complicate into acute intestinal ischemia.

Acute intestinal ischemia corresponds to a sudden intestinal hypoperfusion leading to non-spontaneously resolutive suffering. It is an absolute abdominal emergency, infrequent (causing less than 1% of hospitalizations for abdominal pain), difficult and often late to diagnose… However, if sufficient perfusion is not quickly restored, it will lead to mesenteric infarction, which has a mortality rate of 70 to 90%.

Etiologies

Ischemias with vascular lesions (70 to 80% of cases)

  • Obstructions of the superior mesenteric artery (extent of the ischemic territory depending on the level of the lesion) (85%)
    • Embolism (this embolic site accounts for 5% of peripheral arterial embolisms) → the most typical picture (sudden occurrence, absence of collateral circulation, threatens the viability of the small intestine and the right colon).
      • Origins : left heart +++ (valvular lesions and atrial fibrillation ++), aorta (aneurysm, atheroma), iatrogenic (aortic surgery, arterial catheterizations), paradoxical embolism (through interauricular communication, very rare)
    • Acute thrombosis
      • Origins : ++ on tight atheromatous stenosis, Takayasu, necrotizing vasculitis, iatrogenic (surgery, digestive endoscopy, chemotherapy), paraneoplastic (carcinoid, pheochromocytoma)
    • Arterial dissection secondary to aortic dissection, dysplasia, atheroma, connective tissue diseases
    • Compression or invasion by a pancreatic tumor: exceptional
    • Post-surgery, trauma, volvulus, strangulated hernia,…
  • Other arterial lesions (5%) : inferior mesenteric artery and hypogastric arteries → clinical presentation generally more blunt, exacerbated by a decrease in splanchnic flow (vasoconstrictive medications, collapse,…)
  • Obstruction of the superior mesenteric vein (10%)
    • Abdominal infections, coagulation disorders (deficiencies in protein C/S/antithrombin III, dysfibrinogenemias, platelet disorders), hematological pathologies (polycythemia, sickle cell disease, myeloproliferative syndromes), mechanical causes (portal hypertension, pancreatitis or tumor, extensive thrombosis after sclerotherapy of esophageal varices), trauma, postoperative (splenectomy), hormonal disorders (pregnancy, childbirth, contraception), idiopathic

Ischemias without vascular lesions (20 to 30% of cases)

Ischemia is then attributed to low flow and/or splanchnic vasoconstriction. ++ in very fragile patients (recent myocardial infarction, congestive heart failure, severe hypovolemia, aortic surgery, extracorporeal circulation, iatrogenic [diuretics, vasopressors, propranolol, digitalis, cyclosporine], intoxications [phenobarbital, ergot of rye, cocaine], Clostridium infections,…)

Pathophysiology

The major prognostic factor is the duration of ischemia. In cases of total circulatory arrest, irreversible lesions appear after 30 minutes, areas of necrosis after 1 hour, and the epithelium disappears, exposing the submucosa after 4 hours. Muscle lesions become irreversible after 6 hours. These lesions lead to permeability to fluids and bacteria.

General consequences : fluid loss, electrolyte disturbances (metabolic acidosis + hyperkalemia), release of toxins, disruption of microcirculation, disseminated intravascular coagulation (DIC), infections.

Ischemia-reperfusion syndrome : reperfusion, especially if it occurs late, is paradoxically likely to cause a sudden worsening of ischemic lesions with a risk of multi-system failure and shock.

Clinic

Mesenteric ischemia syndrome

It can present in various forms depending on the location, but the clinical picture is generally dominated by pain and is not very evocative. Diagnosis is therefore rarely made at this stage, while lesions are still often reversible.

Abdominal angina (small intestine involvement generally predominant, chronic clinical picture) is characterized by intense postprandial abdominal pain, predominantly peri-umbilical and spontaneously resolutive. These pains can be relieved by nitroglycerin. Diarrhea is infrequent (20%). A malabsorption syndrome may exist.

Ischemic colitis (colonic involvement, generally acute clinical picture): intense acute abdominal pain, suddenly appearing, in the form of colicky paroxysms, predominantly in the iliac fossae. It is usually accompanied by nausea, vomiting, diarrhea (sometimes bloody). Possible tenesmus without diarrhea. Pain may be interspersed with deceptive calm, often of short duration. The onset can, however, be insidious (painful abdominal cramps). At this stage, palpation is generally normal except for abdominal tenderness, auscultation may detect exaggerated peristalsis. Moderate tachycardia, generally normal blood pressure (sometimes briefly lowered), and generally normal temperature.

Mesenteric infarction

This stage may follow a few hours after the previous one. The pain becomes continuous and is accompanied by bloody diarrhea, eventually leading to a picture of ileus (cessation of stool and gas). The abdomen is then distended, atonic, and silent. The evolution rapidly progresses to the appearance of peritoneal signs, shock, and deterioration of consciousness.

Diagnostic clarification

The medical history (cf vascular risk factors, embolic conditions and history, triggering modes,…) and clinical picture are essential. Any acute abdomen in an elderly person should evoke this diagnosis.

In rare cases, the diagnosis may be complicated by the existence of another abdominal pathology (increasing oxygen needs on already compromised vascular terrain).

Imaging

Essential for early diagnosis, do not hesitate to perform an angiography if available.

  • Abdominal X-ray (AAB) : not very indicative at first (absence of gas), later: distension of the loops with hydro-aerial levels, pneumoperitoneum in case of perforation. The presence of air in the portal vein is a very poor prognostic sign.
  • Abdominal Doppler ultrasound : not very effective, yet it remains the recommended first-line examination.
  • Angiography (Gold Standard) : its early performance is associated with improved prognosis.
  • Abdominal CT scan : allows the exclusion of other pathologies, may show nonspecific images (hydroaerial distension of the loops, thickening of the walls).
  • Abdominal Angio-CT scan : less effective than angiography but more widely available.

Biology

No diagnostic interest, but shows general repercussions in case of late stage : hyperleukocytosis, inflammatory syndrome, hemoconcentration, metabolic acidosis, hyperphosphatemia, increased liver enzymes/LDH/CK/amylase.

However, the diagnostic interest of measuring FABP and D-lactate, if available, is discussed.

Colonoscopy

Has only shown its usefulness for postoperative ischaemias of the left colon.

Laparoscopy / exploratory laparotomy

Diagnostic utility (++ in case angiography is unavailable or doubts about the coexistence of several intra-abdominal pathologies) and therapeutic.

Therapeutic Management - Treatments

Chronic Ischemia (Abdominal Angina)

It is necessary to discuss with a vascular surgeon the appropriateness of simple follow-up + prevention of atherosclerosis + progressive enteral nutrition or an intervention depending on clinical presentation, age, comorbidities, and the patient's autonomy status. In case of intervention, endovascular treatment is the first choice (sometimes impractical due to the extent of the lesions → consider surgery).

The same attitude applies when discovering significant asymptomatic lesions incidentally, generally favoring a non-interventional approach.

Acute Mesenteric Ischemia and Mesenteric Infarction

These are absolute medical-surgical emergencies :

  • Resuscitation if needed (cf shock states) and supportive measures.
  • General measures to be discussed between the surgeon and intensivist: gastric aspiration to combat intestinal distension, fluid resuscitation, transfusions, routine preventive broad-spectrum antibiotics, IV heparin at therapeutic doses under supervision to prevent extension and recurrence.
  • Surgery: surgical techniques depending on intraoperative findings (intestinal viability tests) and angiography. Endarterectomy, bypass, in-situ thrombolysis, resection of infarcted areas (in this case: systematic reintervention 24 hours postoperatively to verify viability). Postoperative: prolonged mechanical ventilation, hydration and diuretics (renal protection), antacids, various treatments depending on context (antiarrhythmics, treatment of shock,…), parenteral nutrition…

Mortality is high even with appropriate management, and complications are frequent.

Bibliography

EMC, traité de gastro-entérologie, Elsevier, 2018

Hawkey CJ et al., Textbook of clinical Gastroenterology and Hepatology, 2d edition, Wiley-BlackWell, 2012

Tendler DA, Overview of intestinal ischemia in adults, UpToDate, 2024